Tag: Cancer

Benefits of Joining the American Cancer Society

Networking Through Health Care Associations

Find a health care association you would be interested in joining and follow it on LinkedIn® or subscribe to its newsletter. Gather details about membership fees and any discounts available with the membership. Identify current association members via social media and reach out to them to find out more about their experiences with and the benefits of having a membership.

Read also How to Effectively Network Within the the Hospital Setup

Write a proposal to your employer outlining the benefits of joining the selected health care association and the benefits of attending a meeting, convention or conference in-person. Provide a rationale of how your membership to the health care association and attending its event(s) will benefit your employer, contribute to your job responsibilities, and promote your own professional development. Include insight from the relationships you established to reinforce your rationale.

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Benefits Of Joining The American Cancer Society (ACS) And Attending Related Meetings, Conventions, And Conferences

A proposal to  management and the Chief Executive Officer (CEO) outlining the benefits of joining the American Cancer Society (ACS) and attending related meetings, conventions, and conferences.

            The American Cancer Society (ACS) is a leading healthcare association devoted to eradicating the scourge of cancer in the United States and internationally. It is currently classified as a voluntary health organization with volunteers spanning the entire expanse of Continental America and the 48 adjoining states.  ACS’s coordinates activities from its headquarters in Atlanta, Georgia with the aim of streamlining operations and contributing to the fight against cancer while supporting research endeavors aimed at finding a cure. The organization offers the following membership options; First-tier membership ($10), Star’s circle ($25), Patron’s circle ($75), Leader’s circle ($250), Hero’s circle ($500), Champion’s circle ($1,000), and the President’s circle ($3,000) (American Cancer Society Cancer Action Network, 2020). I firmly believe that our organization would benefit a great deal from liaising with and joining ACS due to its level of professionalism and the fact that its goals align with our structural objectives. Although our stakeholders have invested heavily in ensuring that the organization makes cumulative gains within its scope of practice, it is fundamental to strive for higher ideals such as those espoused by ACS when endeavoring to serve humanity. The following is a rationale of how the organization’s membership to ACS will benefit management and how attending related events will contribute to employee’s job responsibilities and promote individual professional development for posterity.

Read also American Nursing Association – Professional Organization for Nurses

Benefits of joining the American Cancer Society (ACS)

            Over the past four decades, cancer has emerged the bane of contemporary society and a leading cause of death globally. The Centers for Disease Control (CDC) currently estimates that a total of 606,520 people will succumb to cancer in 2020 which represents a 24% increase in recorded cases (Centers for Disease Control and Prevention, 2020). Cancer is a major public health issue within the United States owing to it indiscriminate nature. One of the main benefits of joining ACS will be in steering our organization in the right trajectory with regard to addressing major health challenges facing the wider greater population in the United States. It will also accord a unique opportunity to management to participate directly in health promotion initiatives to underscore the importance of early screening and lifestyle choices. Furthermore, persons occupying key positions in our organization will benefit greatly from insight on how best to manage chronic ailments while involving employees within the decision-making framework.

            Active membership at ACS will also contribute to our job responsibilities, especially as it relates to responding appropriately to major health challenges and coordinating such activities with community leaders. It is integral for healthcare practitioners to build rapport with communities ravaged by chronic ailments such as cancer and the novel corona virus (COVID-19) to develop an appropriate response. Community involvement in healthcare has long been hailed as a suitable framework to addressing modern-day healthcare challenges and one of the most effective methods of fostering care-seeking behavior (Elk & Landrine, 2014, p. 513). This will go a long way in ending decades-long health disparities which hinder access to care options among minority communities such as non-White Hispanic Americans, Native Americans, and Native Americans. Participating in ACS-led programs will allow employees to gain a comprehensive understanding of the extent to which cancer has affected society through current research. This will allow individual employees within our organization to adopt groundbreaking innovations proposed as a major step towards addressing cancer while building capacity among clinical staff.

            Joining ACS also presents an important opportunity for the organization to benefit from tax breaks provisions provided under section 501(c) (3) of the internal revenue code (IRC). This will allow the organization to save a considerable amount of revenue which will be put to use in a wide range of initiatives meant to benefit management, individual employees, and the public. For instance, these funds will play an important role in enabling the organization to plan for ACS events organized in different localities across the United States on an annual basis. The Childhood Cancer Leaderboard Campaign a, Coaches vs. Cancer Preseason Luncheon, Relay for Life, A Night at the Chef’s Table, A Taste of Hope, and the Associate Board of Ambassadors are some of the main meetings, conventions, and conferences which will greatly benefit the organization (The American Cancer Society, 2018, p. 34). It will provide an apt environment for employees to rub shoulders with like-minded practitioners in the field which ultimately facilitates the exchange of significant information linked to healthcare. Upper management will also develop strong links with major actors in the healthcare sector; allowing them to network and strike lasting relationships for mutual benefit.  This will allow employees to obtain important information in relation to career development, ultimately rekindling their love for the medical profession

Read also Basic Biology of Cancerous Cells

Conclusion

ACS is a one of the main voluntary organizations tasked with addressing cancer in the United States. Membership within the organization is bound to benefit our organization by creating a sense of direction, gaining insights key to individual responsibilities, and benefiting from tax breaks under section 501(c) (3). It is, therefore, imperative for the organization to consider joining ACS since it is bound to improve employee’s expertise leading to elevated patient outcomes.

Lung Cancer – Pathophysiology of the Diagnosis

Lung cancer is one of the leading causes for morbidity and mortality related with cancer worldwide. Also known as bronchogenic carcinoma, lung cancer is any cancer that arises from the bronchi or from the lung parenchymal tissue. A gene locus that determines vulnerability to lung cancer has been described. The causes of cancer include environmental carcinogens such as asbestos, as well as cigarette smoking (Chirieac & Kobzik, 2017). The latter has been identified as the main etiology for lung cancer. There are various types of lung cancer, based on pathological classification. These include small cell lung cancer, squamous cell carcinoma, and adenocarcinoma. A clear understanding of the pathophysiology of lung cancer is crucial for proper diagnosis and management.

Read also The Relationship Between Indoor Air Pollution And Lung Cancer

The pathophysiology of all types of lung cancers is related to either the inactivation of tumor-suppressor genes or the activation of oncogenes by various carcinogens. The mutations that are caused by the carcinogens or the tumor-suppressor genes lead to the development of the cancerous cells. Close to 30 percent of all adenocarcinomas are caused by mutations in the proto-oncogene known as K-ras. Inactivation of the tumor-suppressor genes may result from epigenetic changes such as histone modification or DNA methylation (Zheng, 2016). The epidermal growth factor receptor plays a role in the regulation of tumor invasion and apoptosis. Small cell carcinomas of the lung cause mutation of the epidermal growth factor receptor (EGFR).

Read also Basic Biology of Cancerous Cells

The classical pathophysiology of lung cancer usually starts with the introduction of the carcinogen into the lung. This carcinogen may accumulate to a level where it causes obstruction of the walls of the lung. The next stage is the development of the obstructive emphysema of the lung. The resulting infection of the lob transforms into abscess formation. The abscess then enlarges and involves the pleura of the lung. The next stages are the extension to the chest wall which leads to the inversion of the bronchi or the intercostal nerves. This process leads to extreme compression of neighboring structures. The patient presents with severe chest pains, as well as severe difficulty in breathing. The lung cancer may then metastasize to other regions.

Causes of Throat Cancer at Cellular Organelle Level

The human cell is one of the critical components in the human body that forms the basis of life. The diseases that affect human beings can be traced to the impact it has on cells in the body. Severe cell infections or alteration like it occurs with cancer can cause diseases that can be hard to cure. Cancer is considered one such infection that has become one of the leading killer diseases in the world. According to Pecorino (2012) cancer is considered as a disease that originates from cells growth that is unregulated and which spreads from the primary site to other parts of the body. The author points that research has documented over 100 types of cancer and include throat cancer, lung cancer, neck cancer, skin cancer, and colorectal cancer among other types.  

Read also The Environment and Cancer – My Biomedical Perspective – Descriptive Essay

Throat cancer occurs in a multi-step process that leads to genetic alteration and metastasis. At the cellular level, the process starts through mutation and cell selection and increased proliferation, survival, invasion, and metastasis. The initial step is the tumor initiation where the cells in the throat undergo genetic alteration resulting in proliferation of a single cell. Due to cell proliferation, an outgrowth of population of clonally derived tumor cells is formed. The tumors continue with growth within the tumor cells population through mutations causing cancer.

Read also Cancer Diagnosis and Staging, Complications And Treatment Side Effects

            The cells in the human body reproduce through a process called mitosis that leads to production of identical cells. The process occurs through a controlled replication process that are typically in four stages that involves growth of the cells, synthesis and replication of DNA, growth in preparation of division, and finally the actual mitosis process. The process of cell growth and division into identical cells is controlled by the cell cycle gene called gene p53, also referred as the “guardian of the genome” (Mandinova & Lee, 2015).In addition, as cells divide and grow their reproduction and differentiation is controlled within the normal range through the density-dependent inhibition. The combination of the gene p53 and the density-dependent inhibition ensures cells division, reproduction rate, and differentiation is kept normal in the body and thus suppresses the formation of neoplasms. 

Read also Survivorship Care Plan – Colorectal Cancer

            The throat cancer occurs due to cancerous tumors that occur in the cells that lines the throat. The discovery of throat cancer at an early stage can be critical in providing effective treatment. The abnormal growths that are attributed to tumors responsible for throat cancer can be treated in a number of ways. Early stage throat cancer can be treated through surgery, where the tumors are removed through specialized surgical process referred to as endoscopy. This will allow the elimination of the cancerous cells from the throat lining. Advanced stage throat cancer can be treated using a combination of radiation and chemotherapy.         

Read also The Molecular Basis of Cancer   

Cancer remains one of the leading killer diseases that affect the cells in different parts of human body. Since the disease results from abnormal cell division, its treatment can be complex. Cancer can be benign or malignant, where the later is restricted to specific part of the body while malignant form spreads to other parts of the body. The malignant form of cancer is complex and can be difficult to treat. Although surgery, chemotherapy, and radiation have been developed in the treatment of cancer, they have not been effective methods. There remains the need to identify treatments that can possible reverse or regulate the production of cells that are responsible for various types of cancers.

Read also Breast Cancer – Detailed Research Paper

Survivorship Care Plan – Colorectal Cancer

Task Description and Case Study Resources

This Essay is based on an EdCaN Case Study on Colorectal cancer . You are the Cancer Care Coordinator at the hospital where John receives his adjuvant chemotherapy for colorectal cancer. John is currently receiving his last cycle of chemotherapy and you will be meeting with him to provide education with regards to his discharge and self-management planning following the end of his active treatment.

Discuss the content you would include in a Survivorship Care Plan, and outline your approaches to education and collaboration with John and his wife to develop this plan. Your plan should consider:

  • The recommended follow up regimen after curative treatment for
    colorectal cancer, having critically reviewed the available evidence.
  • Signs and symptoms associated with colorectal cancer recurrence.
  • Strategies to prevent survivorship issues that John may experience
    across all domains of health (including physical, psychological, social
    and spiritual health) after treatment for colorectal cancer.
  • Evidence-based communication strategies and theories of behaviour
    change to facilitate effective education about health behaviours and
    promote a healthier lifestyle.

Survivorship Care Plan For John A Colorectal Cancer Patient

Introduction

Colorectal cancer is one of the most common malignant diseases in the world (Seagel, DeSantis & Jemal, 2014). The risk for the development of the disease increases with age and for many years its prognosis remained poor. However, with developments in such advances as early detection, surgical treatment and adjuvant chemotherapy regimens, the survival rate beyond 5 years has increased (Seagel et al., 2017). It has therefore become paramount that post-treatment issues are addressed and this has led to the development of survivorship care plans and elaborate discharge protocols and patient education. This paper focuses on the survivorship care plan for 65-year-old John who is a survivor of colorectal cancer.

Discharge Planning

Mr. John is a 65 year old male who has been suffering from colorectal cancer. He was specifically diagnosed with a poorly differentiated adenocarcinoma infiltrating the serosa.  Mr. John had surgery of the colon as a treatment option to remove the section that had been adversely affected by the cancer. The surgery was specifically for high anterior resection for the tumour that had been found during a colonoscopy. After a recommendation by the multidisciplinary team that John receives adjuvant chemotherapy regimen, the patient agreed to it following a through deliberation between him and the caregivers. The treatment that he has been on consist of the following: Calcium folinate  (Leucovorin) 50mg IV administered on day 1, Fluorouracil 400mg/m² IV administered on Day 1, Fluorouracil 2400mg/m² by IV infusion over 46 hours that commenced on day 1. The frequency of these adjuvant therapies was after every 14 days and has been given for 12 cycles.

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Considering that there exists a risk of recurrence of colorectal cancer as well as development of other kinds of tumor after the treatment of colorectal cancer, it is important to discuss with the patient the recommended follow up regimen after the curative treatment that he has had. It would be important that I inform John and his wife of the kind of post-treatment surveillance screening that include carcinoembryonic antigen (CEA) test, pelvic CT, periodic abdominal and chest CT scans. The CEA test is significant for diagnosis of rectum and colon cancers while the mentioned scans are for detection of metastatic cancers to the respective regions (Schreuders et al., 2015). These tests would be occasionally done in order to detect second primary tumors and/or detect colorectal cancer recurrence (Rex et al., 2017). It has been found that the incidence for the adenomatous polyps and metachronous primary colorectal cancers four years post-curative surgery to be about 60 percent and 8 percent respectively (Jayesekara et al., 2017). A third of those who receive curative surgery for colorectal cancer normally die to recurrence of the disease. It is therefore significant that there be tests to detect recurrence early when they can be handled.

Read also The Molecular Basis of Cancer

I would also inform John and his wife of the signs and symptoms associated with colorectal cancer recurrence. These include back and pelvic pain, diarrhea, and constipation and belly pain (Vega, Valentin & Cubiella, 2015). The patient could also experience malaise, lack of appetite and difficulty in breathing. The patient should also look out for any sudden and unexplained weight, especially one that lasts for more than 6 months (Meyerhardt et al., 2017). Finally, it would be important to remind the patient of the essence of carrying with them their medical records whenever visiting a general practitioner for checkups as this helps in coordinating the continued management of the patient.

Collaborative approaches to education and planning for self-management

Colorectal cancer survivors face concerns that traverse spiritual, social, psychological as well as physical. There are many effects associated with the management of colorectal cancer and these are categorized into late effects and long-term effects of treatment. It is therefore significant that there be an elaborate communication and coordination of care that the patient can provide to themselves as well as those that take care of them at home and the clinical caregivers at the hospital. In this case, it would be significant to handle some of these issues concerning Mr. John and also involve her wife in the entire elaboration in order to empower her to fully participate in her husband’s post-treatment care.

Read also What Scientific Community Is Doing To Eliminate Most Common Forms Of Cancer

Physical issues that may confront the patient include the development of lymphedema, which is one of the most common presentations that occur long after the treatment of colorectal cancer has occurred (Stanton, Rowland & Ganz, 2015). Surgery may lead to the disruption of flow of lymph through formation of scars in the lymphatic system. Chemotherapeautic agents also predispose to the same condition (Stanton, Rowland & Ganz, 2015). Lymphedema develops very late after these events and therefore the patient should be informed about them. Another issue of concern is reduced function due to frequent feeling of fatigue which may last upto three months after treatment of cancer. The best way to prevent and reduce the effects of fatigue is to reduce activity level and only engage in light duties. Lymphedema can be prevented by the patient through taking part in regular light exercises.

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Psychological issues that I will address with John include possible concerns about his body image and appearance. There exist concerns and challenges regarding appearance and body image after the rigorous chemotherapy and its consequence on the body such as reduced body size and hair loss (Santin et al., 2015). These concerns could be there from the time during the treatment or others may set in during the post-treatment period. To prevent these concerns from affect John, I would advise him to visit a psychologist who may help him to recover confidence in himself and appreciate that his appearance post-treatment is a worthy sacrifice that had to be incurred if he was to be healed from cancer.

The main social issue that I would touch on while discussing with John would be about his financial concerns. Cancer treatment and the monitoring that occur after treatment is a costly affair financially and may take a toll on a person’s capital which may reduce their contribution to their families (Ramsey et al., 2016). This could be a major cause for distress and personal esteem. I would advise Mr. John to consider acquiring an elaborate insurance scheme that would be able to help him take care of his financial concerns.

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Spiritual concerns that could confront Mr. John include the fear of recurrence of the colorectal cancer as well as the risk of development of new primary tumors of the colon (Jeffery et al., 2016). Talking with the patient about this issue is significant in allowing the patient to appreciate the spectrum of the disease and the risk that he faces going forward. It has been shown that psychological preparation contributes a lot towards the patient’s health and the care post-treatment. Given that John is above 60 years and had been diagnosed with a poorly differentiated adenocarcinoma infiltrating the serosa, he is at a high risk of experiencing recurrence and therefore this knowledge is important to him. Included in this context would be the signs and symptoms of recurrence as well as for the development of new primary tumors in order to enable the patient and the wife to note them when they occur. The preventive measure would be to insist to the patient on the need for frequent and regular checkups which would serve to give him reassurances and therefore reduce his fears.

Mr. John would require an elaborate health education that would enable him to continue to recover and also to help him reduce the risk of recurrence or for development of new primary tumors of the colon and rectum (Senore et al., 2015). The education provided would focus on how he would take care of himself as far as such factors as diet and physical activity are concerned (Baenas & Salinas, 2015). This information would be shared with him and his wife Carol because she is an integral caregiver in the health of her husband. I would advise that he avoids red and processed meat because they are associated with increased risk for the development of colorectal cancer (Bouvard et al., 2015). This therefore means that they could predispose John to the recurrence of colorectal cancer, development of new primary colon tumors or metastasis to distant areas. I would also advice that the patient increases his body activity in order to improve on his avoidance of insulin resistance as part of a lifestyle change (Li et al., 2016). Insulin resistance is associated with increased insulin in blood, which increases risk of tumor development. It also induces and increases the activity of insulin-like growth factors (IGFs) which promote the growth of cancer cells (Sanchez-Lopez et al., 2016). The patient should also avoid cigarette smoking as this affects blood vessels and thus inhibiting optimal healing from colorectal cancer. Cigarette smoking is also associated with increased risk for the development of cancers, including colorectal cancer.

Read also Cancer Diagnosis and Staging, Complications And Treatment Side Effects

Communication strategies are important especially when it comes to addressing survivorship issues in cancer patients post-treatment. One of the communication strategies would involve employing motivational interviewing. The patient in this case would require a lot of motivation in order to adhere to the necessary follow up therapy and screenings. This type of interview helps the patient hear themselves while they express their commitment to the agreed regimen and hence enhances their motivation to act on these commitments (Miller et al., 2017). I would also employ trans-theoretical model of change to enhance the patient’s commitment to change their lifestyle (Magnan & McCaul, 2019). The intention of the post-treatment survivorship plan is to ensure that the patient develops and maintains a healthy routine that includes avoidance of risk factors that predispose to cancer such as smoking, developing a good cancer screening routine as well as close monitoring of any signs that may indicate recurrence of colorectal cancer. The maintenance stage of the trans-theoretical model is the most significant stage as it allows patients to adhere to a given lifestyle that is beneficial to their health (Magnan & McCaul, 2019).

Conclusion

From the case study and the elaboration provided above, it is clear that proper survivorship care plans are integral in taking care of survivors of colorectal cancer. Discharge planning captures the patient’s diagnosis and the treatment that they have received. This is important for future references and in the coordination of the patient’s care. Collaborative approaches to the patient’s care helps to bring everyone concerned on board as well as address all the areas of concern as regards the patient’s health. All these are important measures and help to cater for such issues as risk of recurrence of the disease and the impact the disease has on the overall well-being of individual and social life.

Cancer Prevention – Healthy People 2020 Objectives

Exploring a community related health issue identified in the Healthy People 2020 objectives – Assignment Instructions

You will explore a community related health issue identified in the Healthy People 2020 objectives. The goal of this study is to go beyond the basic framework on the Healthy People 2020 internet sources and thoroughly research printed professional literature. You will write a 15–20 page research paper that includes a title page and abstract as well as a thorough discussion of the science behind the issue using the theory, political and policy challenges, and resources for meeting the objective.

Cancer Prevention – Sample Paper

Introduction

Cancer is the second leading cause of premature death and suffering in the United States7. According to the most recent available data on cancer, 1633390 new cancer cases were reported in 2015, a total of 595919 death cases were reported in the same year in the United State. There were 438 reported new cases of cancer for every 100000 individuals and 159 cancer related deaths. Cancer is a serious health issue in the United States with every one out of four death being as a result of cancer in the country. The CDC latest approximations propose that over 1.9 million people in America will be diagnosed with cancer every year by 2020.  Although the Healthy People 2020 goal is to lower the number of new cases of cancer, the older adult population continuous growth ensures that the cancer burden will increase, especially with the new research findings that demonstrate cancer to be more prevalence among adults. The overwhelming impact of cancer on Americans health creates a domineering need to identify missing chances to delay or prevent the cancer development among the population in the country.

Read also The Molecular Basis of Cancer

In an effort to ensure health people and to limit the spread of cancer, Health People 2020 initiative defined a cancer objective, which is to lower the quantity of new cancer cases and death, disability and illness caused by cancer. The Health People 2020 focus on a 10 to 15% decline in specific cancer death rates by 2020. A huge number of researches have been employed to define ways to prevent specific forms of cancers based on their major causes and how they manifest in the body. This research reviews various cancer risks and measures that are being employed to reduce the spread of cancer, other than the common measures of regular screening and early diagnosis. The paper also reviews barriers to effective cancer prevention in the country.

Cancer Prevention Efforts

There are various measures employed to fight cancer among the population in the United States. One of these measures is cancer prevention. Cancer prevention focuses on reducing the number of new cancer cases, especially in the types of cancers caused by preventable measures. There are different approaches employed to enhance cancer prevention in the society based on the targeted population and availability of these measures. One of these measures includes collaboration among interested stakeholders. Collaboration among the community, government agencies, and nongovernmental organizations is one of the most successful ways of cancer prevention in the society. Collaboration is done with intention of identifying and implementing suitable activities, initiatives and policy that can enhance reducing the cancer related risks in the society. The collaborative measure was successful employed in the New York, in a cancer prevention strategy that was initiated in 2012 and implemented from 2013 to 2017. 

Read also What Scientific Community Is Doing To Eliminate Most Common Forms Of Cancer

New York employed a population-founded cancer prevention activities and strategies which prioritize on cancer early detection and prevention. The project which commenced on 2013 January and was to run up to 2017, aimed at mobilizing communities to support strategies which center on environmental, system, an policy changes to lower the cancer risks among community residents. The success of this program was attributed to community coalitions that were supported by nongovernmental and governmental resources and organizations. They employed evidence-based techniques employed at community level to enhance population health.  These coalitions integrated different partners that included healthcare providers, local businesses, community-founded organizations and health plans.

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 Every partner conducted a suitable role to implement and support three cancer prevention strategies. The first strategy involved environmental modification and it focused on increasing nutritious foods access by enhancing standards of food procurement within the area covered by the project. There was change of food procurement policy that described nutrition standards and that hoped to mold social norms, by altering eating habits for people visiting or working in a certain area. This hoped to eliminate cancers initiated by poor diet and food carcinogens. The second initiative involved the change of system and it focused on encouraging at least four obstetric and pediatric offices to implement policies that eliminate the free formula samples distribution among other sponsored materials that include gifts, notepads, or pamphlets which have logos of company, so as clinicians do no unintentionally endorse formula feeding against breastfeeding. Breast feeding is associated with low rate of breast cancer and lower childhood level of obesity. The third approach was a policy based approach that focused on eliminating barriers for obtaining timely recommended screenings of cancer, by collaborating with more than one municipality to enhance level of municipal workers policies. The recent research demonstrated that workers in a paid leave were highly probable to go through cancer screenings as recommended compared to workers without it. The project was created around four main activities that include engaging and educating communities, empowering and mobilizing communities, involving organizational decision makers and offering education to decision makers in the government. Although the program was regarded to be successful, its analyzers called for individual education as one of the measures that should be integrated in the future cancer prevention plans. This program demonstrated the power of collaboration of different agencies and the community in enhancing cancer prevention.  

Another common approach employed to prevent the spread of cancer is fighting health disparity in the United States. According to the research, cancer is highly prevalent among white compared to blacks in the country. However, in instances where cancer is caused by infectious agents, African-Americans lead in cancer incidences. This demonstrates the effect of health disparity on cancer preference among minority groups, especially individual living in low socioeconomic status, characterized by poor housing, poor hygiene and poor diet among other things. High level of infectious agents and their spread are experienced among population living in poverty. This has increased their chances of acquiring cancer caused by infectious agents. To address this situation, preventive measures employed should focus on fighting health disparities among the American population. According to the research, the American government both at the state and local levels has been passing policies and employing other strategic measures to uplift life of low income earners in the country. Although the level of success is considerably low, the success in the applied and intended measures can play a great role in eliminating preventable cancer caused by infectious agents and other behavioral issues associated with individual of low social status. Another approach that is advocated and has been employed in fighting health disparity is developing health literacy among the disadvantaged people in the society. This is being done by providing basic education on causes of infectious cancer and how they can be prevented. The information in most cases also covers other causes of cancer, especially, preventable causes that involve poor health behaviors and benefits of early regular screening procedures in enhancing early intervention. The approach to fight health disparities in most cases also focus on enhancing individual access to health care facilities for regular screening.  Measures such as Medicare and Medicaid have played a great role in enhancing minorities’ access to a healthy care including for cancer screening. Another measures employed to prevent cancer related to health disparity is educating the minority groups on importance of vaccine and encouraging them to consider these vaccines. Embracing vaccines such as Hepatitis B and HPV vaccines can play a great role in preventing a number of infectious agent related cancer cases in the population.

Cancer Prevention by Targeting of People Health Behaviors

The Health People 2020 cancer prevention goal focused on identifying preventable risk factors and avoiding them to reduce individual risk of developing cancer. According to research, chronic non-communicable diseases (NCDs) are the major cause of health care expenditure, disability and death in the United States. Six greatly modifiable risk factors and behaviors account for over 50% of premature death and significantly more disability and morbidity. These factors and behaviors include poor mental health, tobacco use, drug abuse, poor nutrition, alcohol abuse and physical inactivity. It is thus estimated that about 50% of NCDs can be prevent by changing the major risk behavior and an extra 20 to 30% by addressing environmental and social determinant of health. As a result, enhancing population health will comprehensively need implementing effectual evidence-based policies and programs that target these health determinants and can be sustained by the private-public partnership.

Read also The Environment and Cancer – My Biomedical Perspective – Descriptive Essay

 Cancer is among the NCD that can be prevented by behavior modification. According to research investing behavior changes especially among youths in colleges involved in drug, tobacco and alcohol abuse, using both secondary intervention methods, which include provision of internet based education, can play a great role in cancer prevention. Primary behavior intervention method also plays a great role in cancer prevention. Preventive strategies such as changing physical activity and food policies in early childhood education and schools programs to embrace physical activity and healthy eating from a young age, would be of great importance to the American population and cancer preventive measures. For instance, cancer primary intervention that influence children eating habits and physical activities engagement can instill a healthy culture which can be of great important to them even when they are older. This will happen when children embrace good diet and physical activities as life tradition.

Diet management is said to play a great role, specifically in preventing colorectal cancer and enhancing healthy life among colorectal cancer survivors. A research conducted to determine the role of diet in colorectal cancer demonstrated that diet which include alcohol intake is highly related to the colorectal cancer (CRC). Diet is also said to continue impacting the health of patients long after diagnosis based on the disease molarity, physical functioning and recurrence. High processed and red meat intake among CRC survivors have been associated with poorer health results, similar to the “Western dietary pattern” characterized by reliance on sweetened desserts, dairy, refined grains, and processed and red meat. Diet is in addition indirectly involved in the relation between cancer risks and excess body weight. The developing research body has integrated diet into extensive behavioral interventions especially among CRC survivors, demonstrating health benefits and well-being form boosting regular exercise and healthier eating habits. However, irrespective of reports of successes on the use of diet to prevent CRC, there has been limited reach of these efforts and there is still a great need for extensive approaches for CRC survivors’ education, regarding the role played by alcohol and diet in health. The research demonstrates lack of information on CRC survivors’ beliefs and awareness regarding dietary recommendations. Restricted information from a few international studies proposes that there is poor comprehension of nutrition recommendation among CRC survivors, and majority of those survivors do not regard diet as a significant factor in lasting health. The research recommend more information regarding what CRC survivors in the US know regarding dietary recommendations, their believe on the healthy drinking and drinking habits benefits, and the support they get for these practices, and barriers encountered in following and understanding dietary recommendations. This information according to the researchers will effectively enlighten public health effort and guide in disseminating and developing information regarding cancer survivors’ diet. 

Importance of Health Literacy in Cancer Prevention

Health literacy refers to the level to which persons have the aptitude to understand, process, and obtain basic health services and information required to make suitable health decisions. A number of studies have shown that low health literacy is playing a great role in promoting poor health outcomes and status, higher premature rate of mortality, lack of medical recommendations adherence, and higher indirect and direct health costs. The significance of health literacy is emphasized in various national guidelines and plans including the Health People 2020. These guidelines which are supported by peer-reviewed literature, define various interventions centered on enhancing customer comprehension of informed decision making regarding treatment, early screening, and prevention to enhance quality of life and health results, and to lower cost across various forms of cancer. 

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Recent researches have assessed the relation of health literacy with cancer-associated behavior, knowledge and attitudes to educate, and enhance patient involvement in decision making, self-efficacy, and trust. Systematic literature review on health literacy in early adults without and with chronic illnesses ascertains the relationship of reduced health literacy with adverse health results and more poor health behaviors. In addition, results of different research studies endorse that low health literacy is among the social determinants of health related to cancer-associated disparities. Research findings have also demonstrated that advancing partnerships with consumers and community-founded organizations handles unmet needs related to cancer disparities. In these partnerships, community is offered cancer educational materials and training. The health literacy in most cases is addressed to transverse cancer spectrum from survivorship, treatment, and prevention. The healthcare organizations focusing on cancer literacy ensure to conduct organization assessment to be able to identify literacy champions, who can be trained to work with community in providing literacy. A standing committee is also established to assess patient education materials and resources, and guide in the development of the most suitable technical resources for an extensive community. The materials developers ensure to use plain language that is easy to understand. Research has established a connection between cancer treatment, screening and prevention and health literacy and hence, improving community health literacy in cancer through plain language text messages, reading materials and teach-back can play a great role in enhancing cancer control through prevention, survivorship and treatment.

Improving Cancer Prevention by Targeting Young Adults

According to the research, early adulthood has been identified as an opportunity window for early intervention in cancer, based on various significant contextual aspects. For instance, early adulthood is the period of life transitions for many, where people get to be more independent and live life by their own terms and means. At this age, majority get to leave their homes, become patents, enter the workforce, and experience new stressors and challenges in life for the first time. In addition, young adults have been found to experience a number of health challenges including high levels of specific chronic health conditions, for instance obesity, though they tend to contain low application of preventive care services.  Young adults have also been found to be involved in various environmental, behavioral and social factors that can influence their cancer risk, especially among young adults in the United States. Although there is a variation in the strength of the association between cancer development and exposure, factors known to contribute to various forms of cancer include infectious agents such as helicobacter pylori, viral hepatitis, and human papillomavirus (HPV), medical conditions such as diabetes and obesity, alcohol, tobacco, dietary, exposed to occupational carcinogenic which include ultraviolent radiation, and chemicals used in the industries and other many environmental carcinogens. Breastfeeding and vigorous physical activities are some of the factors related to lower risks for particular forms of cancer. Dietary is another major factor, where food such as processed and red meat are said to increase the cancer risk while plant-based diet and sugar avoidance especially in drinks, serve a great purpose in cancer prevention.

In addition to the above factors, young adults are said to be involved in routines that are likely to disrupt their circadian rhythm which is influenced by generation of the melatonin hormone in the pineal gland. This hormone is said to regulate circadian rhythm, with evidence proposing that the melatonin hinders the growth of a tumor. However, melatonin production is said to be suppressed by night light, and this can distract the circadian natural rhythm. This implies that reducing circulating melatonin might increase risk of cancer by impacting other hormonal system. Routines such as insufficient sleep can add to disruption of circadian rhythm, a habit that is usual among young adults, especially those who take night shifts. Shiftwork engaging circadian disruption has been classified as possible carcinogenic to people, and it is related to endometrial, breast, colorectal, and prostate cancers, by the International Agency for Research on Cancer. Lowering exposure of night light which include urban environment light and electronic device use might lower cancer risk.

Another possible aspect contributing to high cancer risk is based on emerging evidence is chronic stress. Stress in America survey data demonstrate that young adults are inclined into reporting higher level of average stress compared to older adults. Chronic stress is said to impact progression of cancer via underlying molecular and cellular processes that drive growth of tumor and influence cancer biology. Stress-associated psychosocial aspects have been demonstrated to influence incidence of cancer in some researches and survival of patient in numerous studies, with the highest effects recorded in breast, liver, lung, head and neck, and ovarian hemotopoietic and lymphoid cancers. Activated pathways in reaction to chronic stress have been connected to tumor angiogenesis, inflammation, cancer cells protection from programmed cell death (anoikis), increased density of nerve, and changed microenvironment of tumor. Chronic inflammation might mediate the apparent association between stressors that include social isolation and outcomes of cancer. Research backs the idea that the social links safeguard young adults over risks of cancer and associated mortality, by lowering the response to physiologic stress. The chronic stress effect in young adulthood on lasting cancer risk might be reduced through behavioral interventions, to increase social support or reduce stress. Moreover, pharmacologic intervention to lower stress might contain the ability to lower risk of cancer.

Based on the above analysis, it is evident that young adults are at a higher risk of developing cancer based on their lifestyle, life routines, and life challenges encountered during this period of human transition and development. The changing risk factors and rates of cancer in the U.S can guide the prevention efforts targeting young adults. According to research, efforts to develop safer and healthier community environment contain the ability to reduce or modify risk factors for cancer development. Promotion of physical exercises in the community and work environment can play a great role in reducing risk of various forms of cancer among other chronic diseases. Addressing individual and community barriers to physical activity for instance physical and time limitations can be of great use in cancer prevention10. According to research, walking has been found to be an effective physical exercise with reduced injuries and without skills requirements. This should be encouraged by designing streets to encourage walking and changing local transportation practices and policies to offer access to attractive and safe areas to walk. For instance, transportation practice should include pedestrian crosswalks, well-maintained sidewalks, and parks. In addition, collaboration across various community sectors that include law enforcement, local government, schools and workplaces can enhance community-based strategies to enhance physical activity.

There are many other efforts that can be done to reduce cancer risks among young adults. For instance young adults are the main target of marketing in the country, especially for products that include alcohol, tobacco and sugar sweetened processed beverages. The government should add control to the marketing of these product that will inform the public that the products are highly carcinogenic. These advertisements should stop being misleading and give clear information that demonstrate the danger they can cause to human health. Public health should also consider taking counter-marketing effort to inform the public of the danger some of these products can cause to their health. Focusing on behavioral change measures such as discouraging unhealthy behaviors such as binge drinking, use of tobacco, poor nutrition, and lack of regular physical exercise can play a great role in reducing cancer among young adults. Other clinical measures can include encouraging people to take immunization especially among Asian Americans and other minorities and American immigrants who have high prevalence for infectious agents related to cancer. Young adults should consider taking available vaccine such as HPV vaccine and hepatitis B vaccine, and early diagnosis and treatment of hepatitis C virus infection.

Challenges Faced Addressing Cancer Prevention and Early Intervention

There are various causes of cancers identified today through research. Among the leading cancer causes are a number of which evidence-based among other interventions can lower the occurrence and alleviate the burden both at community and individual levels. Well recognized examples of such strategies based on the US preventive Service Task Force recommendations and guidelines include screening for revealing in lung, breast, colorectal, and cervical cancer, counseling for heavy consumption of alcohol and tobacco use, and education on other behavioral and lifestyle practice modification, especially in physical activity and diet. Regardless of there being evidence that supports application of these measures, their application has been ineffective in general subspecialty and primary care settings. One of the main reasons for this is the shortage of oncologists to handle emerging cancer cases. There has been documentation of oncologists shortage by the American Society of Clinical Oncology, which is modeled to go through 2020. The shortage is said make it hard for available oncologists to meet the developing need in the market. Despite of this documentation, only a small number of professionals have been able to center their attention on growing the physician workforce trained in control and prevention of cancer. In this regard, physicians contain restricted time with their patients and offering preventive services is normally less prioritized compared to addressing the most immediate medical needs of a patient. Due to the complexity of this challenge, some American Cancer Society developed guidelines for making informed decision on tests or screening for early cancer detection can vary from those provided by the US Preventive Services Task Force among other organizations. Consequently, physicians might struggle to settle the differences and establish the best intervention measure for their patients. Moreover, in various primary care settings, decision and organizational support constraints that include lack of care reminder at non-preventive visits, act as barrier to clinical services delivery for preventing cancer. The current situation act as a great barrier to realizing Healthy People 2020 cancer objective that focused on reducing the cases of cancer in the country by promoting cancer prevention, early diagnosis and treatment and high rate of cancer survivors. There is thus a great need to address the current deficiency of number of physicians trained and practicing in cancer control and prevention. Chances for increasing physician competencies and knowledge in cancer control and prevention span in the range of medical training and education, which include fellowship training, post-graduate residency, undergraduate medical education and ongoing medical and continuing experiential.

Another major challenge facing cancer prevention among other chronic non-communicable diseases in the United States is funding. According to research, directing the NIH funding in the right channels that create a great impact in the NCD disease prevention would make a significant difference in fighting NCD in the country. A research on NIH funding usage advocated for proper investigation on the funded intervention measures, to ensure that they create a great impact to the society, which is comparable to the amount of investment. According to research analysis, prevention has been receiving 18 to 20% of the NIH funds, which is the main funder in the health sector, accounting for 90% of health related funds. In most cases, this amount is directed to both NCD and infectious diseases prevention. Generally, there is underfunding for non-communicable diseases prevention in the United States. This has resulted to persistent negative view and historical trend of prevention value and historical trends.  Structural disadvantages in US prevention and public health is noted compared to healthcare services that include delayed and dispersed prevention benefits. To improve on preventive measures, strategic national priority should focus on investing on prevention to assist in enhancing the health of lagging US population when contrasted to other countries in industrialized regions.  

Conclusion The development of new cases of cancer and its spread across the US population is highly worrying. The statistics demonstrates the tendency of continuous growth of cancer, despite various measures put in place both at national and local level to fight the spread of cancer.  The analysis demonstrates that cancer is one of the most chronic preventable diseases that can be controlled or prevented by change of unhealthy behaviors and dangerous life routines. Simple chances such as regular physical exercises, change of diet, ensuring enough sleep, avoiding alcohol, tobacco and drugs, vaccination to various infectious agents, and avoiding identified carcinogenic food can play a great role in reducing risks of developing cancer in the population. However, the American population is experiencing a number of challenges which makes it hard to implement these preventive measures effectively. One of the main challenges is lack of healthy literacy among the American population, and high cost associated to development of cancer prevention literacy. In addition, the country experiences low level of experts with enough knowledge for cancer prevention and control. In addition to this, the available fund assigned to enhance cancer prevention among other non-communicable diseases is considerably low. In this has made it considerably hard for the country to manage employing all available ideas and strategies in promoting cancer prevention. Although measures such as recommended regular screening with cost covered by medical insurance, majority of beneficiary find it hard to sacrifice their time to partake these screenings. This makes it harder to enhance early intervention measures and increase the rate of cancer survivors in the country. Generally, a lot may need to be done especially in developing cancer literacy among the population to be able to meet the Health People 2020 cancer prevention and management objectives

The Molecular Basis of Cancer

Introduction

Cancer refers to a group of diseases typified by unregulated growth of cell and the spread and invasion of cells from the primary site or site of origin to other parts of the body. Cancer development involves a multistep process which needs the multiple genetic mutations accumulation in a single cell which presents neoplastic cell typical features. Tumor cells are characteristically different from normal cell since they demonstrate uncontrolled growth.

Read also Cancer Diagnosis and Staging, Complications And Treatment Side Effects

About 85% of cancers happen in epithelial cells and are grouped as carcinomas. However, cancer can occur in other cells including mesoderm cells, and glandular tissues. Cancers can be of distinct features and origin. In addition, the main factor which causes cancer in every target tissues varies extensively. Moreover, there are variations in the molecular mechanisms engaged in carcinogenesis in each type of cell and the cells spread pattern from the primary site. Hence different treatment may be needed for different cases. This paper focuses on summarizing the cancer biology.

Mutation

Cancer results from DNA sequence alterations. A large quantity of evidence demonstrates that the tumor cells DNA has a number of alterations ranging from large chromosomal aberrations that include chromosomal translocations and deletions to subtle point mutation. The cell mutations accumulation over time stands for a multi-step process which inspires carcinogenesis.

Read also Mutations in Muscular Dystrophy

The requirement for mutations accumulation over time explicates why there is increased cancer risk with age. About all tumor cells identified mutations are somatic mutations where in the somatic cell DNA has been damaged. The mutations however are not inherited by next generation of offspring, though after cell division, they are passed to daughter cells. Inheritable chromatin and genome structure modifications also play a part in carcinogenesis. Therefore at cellular level, cancer is regarded to be a genome disease, and thus only egg or sperm cells DNA alterations will be inherited by offspring.

Loss of genes Functions

There are three essential processes which contribute to the general net number of cells in an individual. These processes include cell proliferation which involves division of cells to create two daughter cells. This is followed by cells elimination through programmed death of cell which also affects net number of cells. The finally, the inactive phase which cells enter during cells differentiation process which can as well impact the net number of cells. The DNA mutation which can change the normal function of genes involved in differentiation, apoptosis, or growth can affect the cell numbers balance in the body and result to unregulated growth (). Cancer originates from a cell which has obtained genetic mutations in main genes regulating DNA repair, cell death pathways, and cell cycle. Consequently, tumors will progress to have cytogenetically diverse clones due to genetic instability initiated by the first mutations. It has been demonstrated that instability of chromosomes is an essential feature of a various kinds of cancer. It has been clear in the recent past that double stranded break of DNA and abnormalities of enzyme repair can enhance carcinogenesis. Actually, there is evidence demonstrating that deregulation of enzymes liable for DNA breaks repair can introduce lesions that might result to extensive genomic instability, resulting to cancer. This might happen when breakage of DNA strand happens and repair is bypassed and not done, if the cycle of the cell progresses either because of P53 signaling pathway abnormalities. The yielding cell clones are destined to have inherited some kinds of genomic perturbations.  

Oncogenes

Most of solid and haematological tumors are initiated by specific gene which enhances carcinogenesis usually regarded as oncogenes. These oncogenes are liable for production of genes, transcription factors, receptors, and growth factors engaged in apoptosis regulatory and chromatin remodeling factors. It is usually accepted that oncogenes are the main genes causing cancer. A study involving single cultured cells mined from non-transgenic mammary gland of mice and that assessed the oncogenes role in carcinogenesis and suppression of cancer in primary cancer cells was conducted with intention of determining the role of oncogenes in cancer development. 

Read also The Role of Infectious Agents in Oncogenesis

The study established that cells of mammary gland from mice expressing doxycycline controlled oncogenes kras and myc, lost their acini divisions and had augmented rate of cell proliferation, filling up the glands lumen, proposing cell cycle control loss and augmented cell proliferation. Moreover, when oncogenes are eliminated, the cells demonstrated a substantial decline in cell proliferation and the cells which filled up the lumen earlier went through programmed death of cell, with exception of cells located at the edge of the tumor. The study evidently illustrated that oncogenes play a great role in tumor regression and carcinogenesis. The study in addition demonstrates that cells at the tumor edge might survive the oncogene withdrawal effects by remaining in dormancy state till further events have taken place before another growth episode can happen. This mostly contributes in relapse of the tumor.

Tumor Suppressor

Tumor suppressor refers to molecules that are normally engaged in blocking tumor triggering signals. Various tumor suppressor genes have been evaluated for an obligation in cancer etiology for instance loss of mutation function in gene NF1 tumor suppressor that encodes neurofibromin has been said to initiate inherited cancer regarded as neurofibromatosis type 1. NF1 is also related to glioma development3. NFI has also been demonstrated to be created during progression cell cycle and degraded by Ras prompted during protein Kinase C (PKC) activation and hence PKC inhibition result to stabilization and accumulation of NF1 in various glioblatoma human cells in vitro.

Read also The Tumor Microenvironment – A Scientific Brief

Tumor suppressor genes that are thought to be engaged in normal cellular proliferation suppression and employ a negative cell cycle regulation are usually inactivated in tumors. This function loss is either as a result of mutations, epigenetic changes or/and deletions. Mutations of tumor suppressor gene are recessive to usual allele therefore, imposing the second eilde-type allele inactivation for tumor formation. The determinants of germline of about all familial cancers are established to be mutant tumor suppressor genes alleles. Since there are safeguards created into the system, two or more mutations have to take place before formation of cancer.  

Apoptosis

The molecular basis of cancer also involves understanding apoptosis. Apoptosis refers to a programed death of cell that is usually involved in the maintenance and development of an organism. Apoptosis might be induced after a cell turns to be abnormal particularly during tumor and maybe during malignancy thus causing the death of abnormal cell. Nevertheless, the abnormal cell may fail to as a result of mutation which results to either malfunction of this kind of tumor gene suppressor as p53 gene, which is a gene which initiates apoptosis or excessive expression of this kind of proto-oncogene such as bcl-2 that generate large volumes of bcl-2 protein that deactivate apoptotic program. Lymphomas malignant originating from changed b-lymphocyte is initiated by bcl-2 gene mutation. 

Telomerase Activities

Molecular basis of cancer can also be explained in telomerase activities. Telomerase refers to RNA-related enzyme which synthesis telomeres, specific DNA sequences found at the chromosome tip that prevent the continuous DNA loss during the cell replication process. A norm cell contains replication period, and only stop diving when it ages. Tolemeres partially regulate the cell dying and aging process as they shorten each time cell divides and chromosomes replicate6. Once telomeres are shortened to a specific size, the cell attains a crisis point where it is prohibited from dividing anymore and hence it dies, thus working as tumor suppressor by initiating cell death. Equally, the telomeres shorting in a cell going through replication can be prohibited either through expression of oncogenic or tumor suppression activity inactivation. Telomeres in the transformed cell do shorten, though as the crisis point becomes closer, a telomerase enzyme which was previously inactive is activated and therefore stopping telomeres from further shortening thus prolonging the cell life. Actually activity of telomerase has been identified in over 90% of human cancer tumors that include ovarian, breast, prostrate, and colon cancers. Telomerase might in addition act to enhance tumor genesis through mechanisms which do not rely on telomere length. Therefore, tolemere length maintenance and telomerase activity are important replicative ability maintenance in cancer cells.  Once the telomeres are reduced past a specific point in normal cells, the telomere function loss results to activation of cell-cycle checkpoints which are dependent on p53, resulting to apoptosis or proliferative arrest. Transformed cells might however contain defects in checkpoints of cell-cycle, permitting critical shortening of telomere in dividing cells. These cells might survive with defects of chromosome that result to instability of genomic or die through apoptosis. Telomerase reactivation in cells containing abnormal genomes deliberates unlimited proliferative cells capacity which contains tumouri-genic ability. 

Epigenetic Perturbation

Epigenetic perturbation is another molecular basis process of cancer where expression of gene can be changed without altering the DNA sequence. It has more recently become clear that changes of epigenetic in the CpG islands close to the tumor suppressor genes promoter areas might as well add to genetic instability. Most of the researches have demonstrated that loci epigenetic changes that control various unique factors of transcription might yield to miss-interpretation of various histone codes and generate aspects that can dysregulate control machinery of cell cycle resulting to cancer. The research on the subject demonstrated that instability of chromosomes as a result of translocations might result to factors promotion which can disrupt methylation-readout or methylation status of some essential loci in the DNA resulting to cancer. Therefore, epigenetic perturbation might contain some significant implications in initiation of cancer.

Agiogenesis

Agiogenesis is another aspect involved in molecular basis of cancer. Based on research the survival and function of cell depend on nutrients and oxygen offered by the surrounding vasculature. This is factual not just for normal cells but their malignant counterparts too. Agiogenesis is said to play a vital role for tumor explants explosive growth. In addition, the research has also demonstrated that anti-VEGF antibody do impair neovascularization and growth of mice subcutaneous tumors. The angiogenic-switch, which refers to aptitude to sustain and induce angiogenesis appear to be a discrete step in development of tumor, resulting to an alteration in the inducers balance and angiogenesis inhibitor.

Read also Tumor Angiogenesis

Most tumors have been demonstrated to have an increased FGF or/and VEGF expression, which are both strong angiogenesis stimulators, comparative to their non-malignant equivalents, while others show a decreased angiogenesis inhibits expressions that include interferon β2 and thrombospondin- 1. The mechanisms fundamental to these shifts in expression of gene are not effectively understood. However, since tumor angiogenesis might play part in majority of solid tumors, it provides an attractive therapeutic objective and the anti-angiogenic strategies research has already resulted to multiple clinical trials.

Metastasis and Invasion

Metastatic disease represents 90% of adults’ cancer deaths. Although this might not be the case with children who the main malignancies are brain tumors and leukemia, it still shows the situation among children established to have solid tumors. To fruitfully produce a metastatic tumor, beyond the already discussed characteristic of cancerous tumor, the malignant cell requires the aptitude to leave the basic tumor, drift into blood circulation, live there, exit the blood circulation system and proliferate and settle in a new microenvironment. Although the extra cellular integrins, cadherins, and pro-invasion is being invested intensively, the molecular mechanism and regulatory circuits controlling this process persist to be elusive. 

Targeted Molecular Therapy

Agents utilized in targeted cancer therapy inhibit specific signaling pathways and receptors which enhance growth of tumor cells. These agents comprise of tyrosine kinase inhibitors (TKIs) small molecule and monoclonal antibodies. The tyrosine kinase family receptor includes families of platelet-derived growth factor receptor (PDGFR), epidermal growth factor (EGF), vascular endothelial growth factor receptor (VEGFR) and epidermal growth factor receptor (EGFR). These therapeutic agents obstruct signaling of receptor tyrosine kinase by binding to the growth receptors extracellular component. The agents can bind the ligand which initiates the bind or receptor intracellular sites which interfere with downstream events of signaling. The targeted agents’ toxicity profiles differ considerably from those of standard chemotherapy since they do not obstruct DNA replication.

Breast Cancer – Detailed Research Paper

Introduction

Breast cancer is among the most common causes of cancer among women and among the main cause of cancer related death in the world. Breast cancer is named after the organ where cancer originated, though it may spread to other parts of the body surrounding the breast. Breast cancer affects both men and women, though it is more common to women than men. Women can get breast cancer at any age, though it is more common among older women from age 50 to 74. Women of this age are thus needed to take breast screen after every two years to enhance its early diagnosis and effective treatment.

Read also Human Breast Anatomy – Detailed Research Paper

Breast Cancer Types/ Forms

Breast cancers can be groups as non-invasive and invasive. Non-invasive breast cancer refers to a form of cancer where the cancer cells are limited to the ducts and hence they do not invade surrounding breast connective and fatty tissues. There are two main forms of non-invasive breast cancers which include ductal carcinoma in situ (DCIS) which is the most popular form of non-invasive breast cancer, accounting for about 90% of non-invasive cancer cases in the world. The other form is lobular carcinoma in situ (LCIS).  Invasive breast cancer cells on the other hand break through the lobular wall and duct and attack the surrounding breast connective and fatty tissues.

Read also Inflammatory Pathology of the Human Breast

The most common form of invasive cancer is infiltrating ductal carcinoma (IDC) that starts in breast milk ducts and penetrates the duct walls invading breast fatty tissues and other probable areas of the body. This cancer accounts for 80% all cases of diagnosed breast cancer. Another form of invasive breast cancer is infiltrating lobular carcinoma which starts at the milk glands and metastasizes to other body areas. This accounts to 10-15% of all cases of breast cancer.  The least frequently occurring forms of breast cancers include medullary carcinoma which is a form of invasive cancer, mutinous carcinoma which a rare kind of breast cancer created by mucus-producing cancer cell, and tubular carcinoma which is an invasive breast cancer. Others include inflammatory breast cancer which starts as inflamed breast with thick ridges or dimples initiated by cancer cells blocking lymph channels or vessels over the breast skin. There is also the nipple paget’s disease which is a rear kind of breast cancer that starts at the milk duct and spreads to areola and nipple skin, and finally phylloides tumor that can be either malignant or benign. Phylloides tumors generate in the breast connective tissues and might be treated through surgical removal. This form of cancer is quite rare.  

Epidemiology

Breast cancer affects both men and women, though the cancer is more common to women and quite rare in men. Breast cancer is the most popular reason of cancer death among women in about 140 out of 184 countries in the world. Breast cancer is the most often diagnosed form of cancer among women, and it currently represents a quarter of all cancers in women. Breast cancer is the main reason for women death in ages 40 to 59. Cases of breast cancer are high in developing countries compared to developed countries, but still remain the leading cause of women death in both situations. The women lifetime risk of getting invasive breast cancer is 12.6%, and one out of eight women in the United States will develop breast cancer at a certain stage in her lifetime.

Risk Factors

The risk factors for breast cancer include environmental factors which include being exposed to ionizing radiation as a result of therapeutic procedures, medical diagnostic procedures, gadgets use or nuclear war increase breast cancer development risks. Another risk factor is sociobiological factors that include age and gender. Breast cancer is more common to women aged 50 and above. Thus being a female and at older age increases risk of developing breast cancer. Nutrition is another factor where by high fats, red meat and caffeine intake increases breast cancer developing risks, while high consumption of vegetables and fruits might reduce breast cancer development risks. Other factors include physiological factors where moderate physical exercise or activities reduce breast cancer risks. Genetic factor where 5 of  6% of occurring cases of cancers are regarded to be hereditary and also family risk factor where cancer history in the family create a possibility of cancer development among other family members. Alcohol is also said to increase breast cancer risks. Individual history of breast cancer increase risks of developing second case of breast cancer. Hormonal history of a woman is also a risk factor where risk increase with number of individual menstrual cycle in a lifetime2. Other risk factors include poor immune system, use of oral contraceptives and hormone replacement therapy, exposure to carcinogens, use of tobacco, the breast pathogenic diseases, chronic breast inflammation, conducting induced abortion, not breastfeeding or breastfeeding for a shorter period, and number of life birth where the more the life birth are the lower the risk of developing breast cancer.   

Pathobiology

Breast cancer pathobiology is complex compared to other cancers. Mammary disseminated tumor cells have the ability to remain dormant for a number of years. Nevertheless, the systematic growth of tumor resumes eventually, resulting to clinically recurrent disease. Breast cancer possibly includes over 20 subsets of tumor that affect the disease course. Such subsets of tumor are typified by specific immunological, hormonal and biochemical features.  Subclinical metastasis exists already in most patients during diagnosis time. Cancer cells hematogenous dissemination probably starts after doubling of 20 tumors. 

Molecular Basis of the Cancer

The molecular mechanisms fundamental to the breast cancer development in general and associated breast carcinogenesis in specific are not well understood. It breast cancer initiation is generally believed to emanate from aberrant programmed apoptosis or death of cell or/and uncontrolled proliferation of cell due to collective genetic damages which result to changes of genetics that yield to proto activation which implies inactivation and oncogenes of tumor suppressor genes. Genetic changes in turn can be attained as somatic mutations or be inherited as mutation of gremlin. The somatic mutations may happen due to exposure to biological, chemical or physical environmental carcinogens.

Clinical Manifestation

The breast cancer clinical manifestation include swelling or thickening of some breast parts, new lump underarm or in the breast, and dimpling or irritation of breast skin. Others include flaky skin or redness of the breast or nipple area, pain in the area of the nipple or nipple pulling in. Other signs include other nipple discharge than milk which include blood, change in the breast shape or size or breast pain. Other than visible changes, the presence of breast cancer can be determined by conducting various tests which include mammogram screening, breast biopsy, magnetic resonance imaging (MRI), molecular breast imaging, and blood-based essay. 

Biomarkers and Cytogenetic Laboratory Features

Biomaker analysis in breast cancer is a routine practice. It initially focused on hormone receptor expression testing to guide tamoxifen therapy. It then advanced to human epidermal growth factor receptor 2 (HER 2) target treatment. Biomaker testing has also been integrated in genetic platform dsigned to hhelp prognosis and chemotherapy response prediction in patient with hormone receptors tumor but without lymph-node metastases.

Read also The Role of Biomarkers in Oncology

Other biomarker tests in breast cancer include ki-67 that determines breast cancer proliferative activity, and progesterone and estrogen receptors which predict hormone therapy response (Colomer et al., 2017). Complex karyotypes have been related with unfavorable breast cancer result. Modern methods that include relative genomic hybridization (CGH) and cDNA microarrays have additionally identified complex defects of genetics related with adverse prognosis. 

Metastasis

Metastasis is mechanically described as tumor cells migration from the primary tumor, subsequent by extravasation, survival, intravasation of circulatory system and advanced colonization of a detached site. Tumor cells thus spread extensively through the body, though only grow in supportive location. Breast cancer metastasis is also denoted by pathways redundancy that mediates its component steps or process. Genes enhancing flourishing of breast cancer metastasis include IDI, ERBB2, MET, CTNNBU, SNAI2, KRAS, SNAI1, PI3KCA, TWIST1, EGFR and MMYC. Metastasis complicates the cancer treatment process due to its innate or acquired resistance to therapies. In breast cancer metastasis occurs at the last stages of the cancer and is regarded as the leading cause of death among breast cancer patients.

Staging

Breast cancer can either be in situ or not invasive or invasive. In situ is the first stage of breast cancer and it is denoted by stage O. From there the cancer can be in stage I where the tumor diameter is about 2 cm and is confined within the breast. Stage IIA the tumor diameter is about 2cm and has spread to not more than three armpit lymph nodes. Stage IIB tumor diameter is less than 2 inches and has spread to not more than three armpit lymph nodes or the tumor diameter is more than 2 inches though still confined in the breast. Stage IIIA the tumor diameter is about 2 inches and has spread to not more than nine armpit lymph nodes. Stage IIIB the tumor has spread to the skin or chest wall or initiated breast inflammation, or has spread to 10 and above armpit lymph nodes. Stage IIIC, The tumor has reached lymph nodes above or below collar bone or it has enlarged in one lymph node  to the same size as the tumor in the breast.

Screening/ Prevention

Women at high risk of getting breast cancer who include women aged between 50 and 75 years should have mammogram screening once per every two years. Women at all ages are also encouraged to engage in physical activities, check on their weight, eat healthy by avoiding fats, caffeine and red meat and increasing vegetables and fruits in their diet. Women are also encouraged to avoid oral contraceptive and hormonal therapies, to consider breastfeeding their children for long and to minimize exposure to carcinogens.

Read also Developing a Health Advocacy Campaign – Breast Cancer

Cancer Therapy

Breast cancer can be treated using various methods based on the stage of development. Surgery may be done to remove the tumor or the entire breast and surrounding tissues based on the level of development. Radiation therapy can also be used where high X-ray energy or other forms of radiation are used to suppress the growth or kill cancer cells. Chemotherapy may also be used where drugs are used to stop cancer cells growth, either through killing them or preventing their division. Hormonal therapy may also be used to block hormones actions or remove them and stop growth of cancer cells. Target therapy may also be applied where drugs are applied to attack and identify particular cancer cells without damaging normal cells.

Prognosis

Breast cancer is the leading cause of malignancy death among women. Individual survival rate depend on the type of breast cancer on is suffering from; invasive or non-invasive, where those diagnosed with non-invasive or in situ cancer have a higher survival rate. Metastasis is the leading cause of breast cancer death, thus those diagnosed by cancer at its advance stages have lower chances of survival; mostly less than 3 years. However, some may survive with the tumor for over 10 years when in situ. The survival rate decrease with young age diagnosis; women below 40 years have higher death risk than women diagnose at older age. Early diagnosis; at early cancer stage increases chances of survival, while late diagnosis reduces survival rate. In addition, survival rate of women with BRCA2 mutation is lower compared to those without BRCA2 mutation.

Current/ Future Research

A lot has been done in trying to understand breast cancer. There has been research on the main risk factors and how to reduce them, different types of breast cancer and how they manifest themselves, best form of treatment, cancer stages and the best treatment based on the stage among other things. However, there is little understanding on the molecular basis of the breast cancer which is said to be considerably complex. Understanding this may play a great role in treating and preventing breast cancer and hence this topic needs to be given extra consideration in future research.

Cancer Threat to Liver Homeostasis and the Liver Cancer Mechanism

Liver cancer is among the most popular malignancies in the world, such that it is ranked as the third leading cause of death in the world. Liver cancer pathologically mainly involves intrahepatic cholangiocarcinoma (ICC) and hepatocellular carcinoma (HCC). The two kinds of liver cancers have comparable hepatic microenvironment though they might contain different tumor microenvironments (TMEs) due to varying tumor cells biological characteristics. For example, in a significant cases proportion, ICC nurtures isocitrate dehydrogenase (IDH)  2 and IDH1 mutations that are unusual in HCC. IDH2 and IDH1 are essential enzymes engaged in cellular metabolism. Thus, mutations of IDH1/2 can considerably impact the metabolite profile in TMEs and cells. In this situation, the TME roles in progression of liver cancer might be altered greatly .

Read also Liver Physiology And Anatomy

Hepaocellular, hepatoblastoma, hepatocellular adenoma carcinoma (HCC) are three main neoplasms of hepatocellular. HCC is the basic liver tumor which contributes for over 80 percent of all liver tumors. HCC prognosis is however still highly poor, with 5 year survival rate being less than 5 years. Among the main HCC etiological causes include hepatitis C and hepatitis B infection, nonalcoholic and alcoholic fatty liver diseases, chemical carcinogens, and a number of metabolic genetic diseases that include alpha-1-antitryspin and hemochromotasis deficiency have been related with development of liver cancer, though the actual hepatocarcinogenesis mechanism is still unclear. In addition, a recent global metabolic diseases trend that includes diabetes and obesity are said to favor increase in incidences of HCC (4).  According to research HCC development involves two stages that include promotion and initiation. Initiation happens when cells having DNA mutation in a single or a number of dominant proto-oncogenes, malignant tumor suppressor genes that include Ras, p53 and Wnt signaling pathway components are generated. In cancer promotion stage, the initiated cells clonally expand via the cell proliferation increase or/and the apoptosis suppression.  In addition, reactive oxygen species (ROS) and additional cellular mutagens created in the cancer promotion stage will progressively add to the accumulation of extra genomic instability and genetic mutations, therefore increasing quantity of initiated cells (4). HCC cancer development is also associated with physiological conditions of inflammation and infection. Inflammation is currently acknowledged as a key player in promotion of liver tumor with identification of STAT3 and NF-kB pathways as important for establishing the results of liver inflammation, injury, and the following tumorigenesis.

NF-kB together with its upstream regulators such as IKKγ, IKKβ, and IKKα are known to be essential for liver homeostasis and hepatocyte survival. In recent times, the inflammatory and NF-κB pathways it controlled have been demonstrated to play an important roles promotion of cancer. The researchers noted that NF-κB activity inhibition in hepatocytes at HCC development later stages suppresses liver tumor development, demonstrating a NF-κB tumor-promotion impact. This might attribute to a distinguished NF-κB role in liver anti-apoptosis pathways (1). Actually, many targeted NF-κB genes that include JNK activation inhibitor (XIAP), caspase activator inhibitor (cFLIP), apoptosis inhibitor (c-IAPs) and Bel-2 family member Bcl-XL are key cell anti-apoptoss pathway components. It has also been established that IKK-β hepotocycte-specific deletion which is a kinase vital for the NF-κB activation result to stronger formation HCC, demonstrating the NF-κB tumor suppressor effect in liver. Correspondingly, IKKγ hepatocyte-specific deletion which regulates IKK complex subunit for activation of NF-κB results to death of liver cells, spontaneous and inflammation of HCC. The hepatocytes death is said to occur because in NF-κB absence, hepatocytes experiences accumulation of ROS and consequently, there is activation of JNK pathway in hepatocytes . This demonstrates that in varying types of liver cell and in HCC different stages NF-κB may influence tumor promotion differently. Based on the analysis, it is clear that chronic inflammation promotes liver carcinogenesis via a regeneration and death cell cycle, resulting to creation of cell proliferation and survival signals which enhance formation of dysplasia, regenerative nodules and cancer.

Normally, cell death induction works as a function of tumor suppression. However, in the liver, this function does not all the time works as tumor suppressor but on the contrary; it works as tumor promoter since hepatic mass loss as a result of hepatocyte death initiates the residue hepatocytes proliferation which might offer a promoting environment for the formation of the tumor. For instance, diethylnitrosamine (DEN) is a carcinogenic chemical that is normally applied to initiate HCC in rodents. DEN administration initiates acute DNA damage and liver injury in hepatocytes, and eventually resulting to neoplastic lesions, liver regeneration, and inflammation in the liver, which eventually promote tumor formation as explained above.

Liver tumors phenotype could also rely on interaction between immune microenvironment and oncogenes. Based on the recent animal research, various forms of liver tumors that include iCCAs, HCCs and HCC-iCCAs mix, arose through activation of distinctive oncology that includes CTNNB1 and AKT1 together with conditions of inflammatory microenvironment such as 4-dihydrocollidine, 3, 5-diethoxycarbonyl-1 or carbon tetrachloride. Tumors which generate through same oncogenes activation can still contain varying transcriptomes, based on the degree of inflammation and the microenvironment features . Immune system has been linked to the liver cancer development through various mechanisms. First cytokines secretion by immune cells that include interleukin (IL)-6 and factor of tumor necrosis, can initiate hepatocytes inflammatory signaling pathways through JAK-STAT and nuclear factor kB among others to enhance survival and proliferation of cells. The HCC immune microenvironment is typified by the immune responses coexistence resulting to both tolerance and immunogenicity. HCC enhances immunologic tolerance via cytokines release and transformation of beta (TGF)-β growth factor. The tumor-infiltrating and tumors immune cells also demonstrate immune regulators that include programmed cell death ligand PDL 1, cytotoxin t-lymphocyte protein 4 (CTLA4), and protein 1 (PD) that destroy the antitumor immune response, permitting progression and growth of tumor. Tumors containing immune infiltrates are said to have longer survival periods and minimized relapse rates after transplantation and resection. Factors which initiate inflammation that includes insulin receptor and nuclear factor kB, initiate carcinogenesis among patients suffering from nonalcoholic fatty liver diseases. In addition, the natural killer cells and CD4+ and CD8+ T cell are also said to enhance oncogenesis .

Liver cancer development demonstrates odd development situation. With limited supply of nutrient and rapid growth, the tumor cells survival is questionable. Nevertheless, the liver tumor demonstrates the ability of cellular metabolism reprograming for neoplastic proliferation. The cancer induced abnormal metabolism offers metabolites and energy for cell activity and also alters numerous associated pathways which influence a number of biological processes.  Metabolism is an important lifer function, and the liver metabolic disruption can result to spontaneous hepatocarcinogenesis. Profiling of the main metabolic modifications in the liver cancer through metabolomics analysis that demonstrated evaluated β-oxidation, gluconeogenesis and glycolysis with minimized activity of tricarboxylic acid cycle (TCA cycle) Aerobic glycolysis is observed frequently in different tumors . This theory designates that tumor cells mainly utilizes glycolysis, even when oxygen is enough. Glycolysis in addition plays a controlling role for liver cancer in glucose metabolism. Various researches have demonstrated the association between glycolysis and epigenetic as well as genetic changes. Mutant tumor supressors and activated oncogenes are also related with glycolysis. Lactate dehydrogenase (LDH), glucose transporters (GLUTs), pyruvate kinase M2 (PKM2) and glycolysis-associated enzyme hexokinase 2 (HK2) are in addition overexpressd in tissues of liver cancer, proposing an augmented glycolysis activity.  Oxidation of fatty β is also promoted in liver cancer to lower tumor glucose dependence and to overcome energy shortage. Metabolic modification increases glycerolipid metabolism and fatty acid biosynthesis, resulting to lipid and fatty acid accumulation. Moreover, approximately all amino acids are augmented in liver cancer as a result of reduction of catabolism of amino acid. These general changes together with various other factors might influence the metabolites levels in TME. Liver cancer is a serious health issue that is likely to result to death within 5 years after its manifestation. Early treatment is thus essential in saving the life of a patient. This cannot be done without clear diagnosis. Although most people do not demonstrate any symptom at the start, most of possible symptoms of liver cancer include chalky, white stool, jaundice, and unexplained loss of weigh, swelling of abdomen, loss of appetite, fatigue and general weakness, pain in upper abdomen, vomiting and nausea.  These symptoms can prompt to various liver cancer testes and procedures which include blood tests that is likely to demonstrate abnormalities in functions of a liver. Image testing such as magnetic resonance imaging (MRI), computerized tomography (CT) Scan, and ultrasound and liver biopsy may also assist in making more accurate diagnosis.  When diagnosis is positive more may need to be done to determine the stage of cancer development which may be done using bones scans, MRIs and CTs. Liver cancer test can also be run on individual with infectious and non-infectious diseases associated with liver cancer. These diseases include hepatitis C and B, cirrhosis, jaundice, obesity and diabetes.

Liver Cancer and its Treatment

The liver is famous for its amazing ability to regenerate following acute injury, that include loss of liver mass as experienced after partial hepatectomy (PHx)  or acetaminophen poisoning through compensatory hyperplasia , arbitrated by remaining healthy hepatocytes and just very restricted involvement of progenitor cell. However, prolonged hepatic damage as a result of constant carcinogenic, toxic, or viral injury compromises the hepatocytes negative capacity through replicative arrest induction and regeneration, depending on differentiation and activation of liver progenitor cells (LPCs). The growing international challenge of hepatocellular carcinoma and cirrhosis as a result of progressive prevalence of consumption of excessive alcohol, metabolic syndrome, obesity, and viral hepatitis has ignited interest in liver progenitor cells (LPCs) which is similar to stem cell as possible candidate for tissue engineering and cell therapy, as an alteration to organ transplantation (1). Nevertheless, LPCs normally multiply in chronic liver diseases with cancer predisposition, such that they have been proposed to play vital roles in disease progression, driving fibrosis, and might even signify tumor-initiating cells. A research conducted to enhance the understanding the LPCs role in liver cancer using a series of rodent experiment demonstrated that LPCs are just activated in hepatocyte replicative arrest or massive hepatocyte loss in humans. LPCs were found to be activated in most liver diseases, even in minimal level of liver damage. The research determining correlation of LPC proliferation in severe injured liver demonstrated minimization of tumor development with LPC inhibition, possibly connecting activation of LPC with HCC development proliferation (1). 

Non-alcoholic fatty liver disease (NAFLD) is identified as one of the leading cause of HCC as the secondary obesity pandemic consequence. NAFLD is identified in about 30 to 40% of the US general population, where about 95% of them have morbid obesity. Excess accumulation of fats triggers liver injury, regeneration and inflammation which advance to non-alcoholic steatohepatitis (NASH) in a percentage of patients (5). This additional stimulates cirrhosis and scar tissue (fibrosis) formation both of which are HCC predispose. The NAFLD and obesity in the society is coupled with chronic circadian epidemic disruption or social jet lag. A research was conducted to determine whether disruption of chronic circadian is enough to trigger spontaneous hepatocarcinogensis by driving persistent oncogenic activation and liver metabolic dysfunction. The research was carried out by inducing spontaneous HCC in wild-type of mice using chronic jet through mechanism that are very similar to these observed among obese humans. The process initiates NAFLD, which progresses to fibrosis and steorohepatitis before detection of HCC. This pathophysiological path is controlled by degeneration of jet-lag-trigged genome-wide gene and worldwide metabolic dysfunction of liver, with cholesterol/bile acid controlled nuclear receptor and xenobiotic metabolism amongst the deregulated top pathways. Farnesoid X receptor ablation dramatically augments levels of enterohepatic bile acid and Jet-lag-triggered HCC, while constitutive androstane receptor (CAR) loss inhibits HCC induced by NAFLD. CAR is well known promoter of liver tumor which mediates signaling of toxic bile acid. CAR is activated by circadian disruption through promoting sympathetic dysfunction, peripheral clock disruption, and promoting cholestasis (5).

Hepaticc stellate cells (HSCs) are also said to play significant role in HCC and liver fibroid. However, activation of vitamin D receptor (VDR) in HSCs suppresses liver fibrosis and inflammation. A protein p62/SQSTM2 upregulate parenchymal liver cells but downregulate in HCC-related to HSCs, controls activation of HSC negatively.  HSC-unique p62 ablation increases the effect of HSCCs and promotes HCC progression, fibrosis, and inflammation.  p62 interacts directly with RXR and VDR enhancing their heterodimerization that is vital for recruitment of target gene VDR:RXR. . P62 loss in HSCs destroys the inflammation and fibrosis repression through VDR agonists. This shows that p62 is a negative liver fibrosis and inflammation regulator, which achieves this through its aptitude to promote HSCs VDR signaling whose activation promote HCC (4).

 Chronic liver damage sets hepatocytle fibrosis, inflammation and cell death in vicious cycle motion which results in cancer and cirrhosis, where a decisive role is played by hepatic stellate cells (HSCs). Quiescent HSCs express glial fibrillar and store retinoid droplets of lipid related to protein, never receptor p75 growth factor and synaptophysin. In reaction to injury, HSCs separate into α-smooth muscle actin (αSMA)- articulating myofibroblasts. The research was conducted to demonstrate HSCs critical role in the pro-inflammatory signal generation which is significant for development of HCC (2). The previous research has demonstrated a connection between autophagy substrate p62 and signaling adapter and liver cancer. p62 is hyaline granules and Mallory-Denk bodies (MDBs) component, which are aggregates of protein which accumulate in the damaged cytoplasm liver cells in HCC, cirrhosis, and NASH. P62 is significantly upregulated in liver cancer and a number of epithelial cancers which include the prostate, kidney, glioblastoma, and lung. The results strongly proposed that p62-driven paths could be regarded as possible therapeutic targets in HCC and NASH. Nevertheless, some studies handling the p62 role in cancer have centered on its function in epithelial cells transformation. P62 was found to inhibit prostate cancer (2).

 To determine if ablation of total body p62 inhibits development of HCC in mice, 2 week old of total p62 knockout (p62KO) and wild-type (WT) mice were injected with the hepatic carcinogen diethylnitrosamine (DEN) of 25 mg/kg. The mice were then fed with high-fat diet (HFD) as promoter of tumor under obesity conditions. Surprisingly the p62 global loss did not constrain HCC and on the contrary it promoted its development. Even if the multiplicity of the tumor was not impacted, the tumor size increased and there were larger tumor in p62KO compared to WT mice. Although edenomas with inflammation and steatosis developed in both genotypes, HCC only developed in p62KO mice. Tumors in p62K demonstrated higher α-fetoprotein (Afp) expression, a common marker of HCC (2).

There has been significant progress in the HCC treatment. However, success of poor treatment and high tumor incidences continue to be great challenge. Poor therapy has made HCC one of the main causes of death among common malignancies. In an effort to determine the best HCC intervention measure proteomic analysis was conducted to evaluate protein expression in HCC after it has been successfully applied in neoplastic disease. Prolonged hepatitis B virus (HBV) infection is regarded to be engaged in HCC pathogenesis (2). To advance HCC pathogenesis knowledge and to determine the possible new mass spectrometry, anticancer therapy and isobaric tag for absolute and relative quotation (iTARQ) were used. The research studied the variations between nine adjusted non-HCC and HBV-associated HCC tissues specimens. A total of 222 proteins were evaluated for disparity expression in the two kinds of samples. Among the analyzed proteins, a number were confirmed by real time RT-PCR, immunoblotting, and immunohistochemical analysis. Interference of RNA prompted glucose-6-phospahate dehydrogenase (G6PD) downregulation and reduce replication of HBV by fivefold through the IFN pathway. Reduced expression of G6PD resulted in reduction of migration of hepatoma cell and cell culture inversion. The investigation process in general offered new HBV infection pathogenesis information and proposes G6PD as a new target for anti-HCC. The suppression of G6PD might contribute to treatment approaches for inhibiting progression of tumor. The research process used proteomic analysis which is a helpful technology for protein expression evaluation, which has been widely used to neoplastic diseases. To contrast levels of protein expression in HCC, two-dimensional electrophoresis (2-DE), basic proteomic-founded technology is used. 2-DE and MALDI-TOF/MS were used to show that tubulin alpha-6 chain is a probable biomarker for effectively differentiated HCV-related HCC.  On the foundation of adjacent non –HCC and HCC 2-DE tissues specimens, SULT1A1 was said to be helpful in early HCC discovery and helped in the clinical outcome prediction for HCC patients. Nevertheless, 2-DE contains drawbacks that include high labor costs, excessive time, low sensitivity and integral variation (2).   

Liver cancer has been associated to a number of changes in its homeostasis reaction and presence of different receptors in its surrounding. One of the receptors associated with liver cancer is CD151 receptor which is regarded as a member of the tetraspanin receptors family. CD151 is a lateral modulator and organizer of activities of various transmembrane proteins families. This receptor has been associated with the progression and development of various cancers, though its contribution to chronic inflammatory diseases remains unclear. In a research conducted to determine CD151 role in liver cancer established that CD151 is up-regulated by different   signals of microenvironment in a range of prime liver cancer and in various inflammatory liver diseases, where it supports recruitment of lymphocyte. CD151 was highly demonstrated in hepatic neovessels and sinusoids endothelial cells developing in tumor margins and fibrotic septa. Human hepatic sinusoidal endothelial cells (HSECs) primary cultures showed CD151 at the intercellular vesicles and cell membrane (3). There was upreglation of CD151 by HepG2 and VEGF conditioned media through not by proinflammatory cytokines. It was confirmed through confocal microscope that colonization of CD151 happens with superfamily member of endothelial adhesion immunoglobulin/molecule, VCAM-1. Evaluation of functional flow-founded connection with HSECs and basic human lymphocytes illustrated a 40% lymphocccyte adhesion reduction with blockade of CD151. Lymphocyte adhesion inhibition was similar between CD151/VCAM-I blockade combination and CD151 blockade, proposing a collaborative role in the two receptors. The research thus demonstrated that there is upregulation of CD151 in the liver where during prolonged inflammation, where CD151 supports recruitment of lymphocyte through live endothelium. The research thus suggests that the VCAM-1 activity is regulated by the CD151 in the recruitment of lymphocyte to human liver and this could be a new target of anti-inflammatory target in hepatocellular cancer and liver disease prevention. Chronic hepatitis which is one main cause of liver cancer is characterized accumulation of lymphocyte in liver tissues, which drives carcinogenesis and fibrosis. CD151 tetraspanin support connection of lymphocyte to liver endothelium. The research demonstrates upregulation of CD151 in hepatocellular carcinoma (HCC) and liver disease and is controlled on endothelium by procarcinogenic and tissues remodeling factors. These functional and regulatory studies identify CD151 as a possible therapeutic target for HCC and liver fibrosis treatment (3).

Conclusion

Liver is one of the largest and most important human organs in enhancing effective operation of human body and human general health and safety. The organ has extensive important responsibilities that ensure effective operation of various body mechanisms that include metabolism of carbohydrates, fatty acids and proteins, bile secretion, blood storage, detoxification of blood, storage and distribution of nutrients and vitamins, and enhance immunity. It also has a complex anatomy that promotes its ability to execute its responsibilities, with its primary functional unit being lobule that has substructures which include hepatocytes plates, portal triads, liver sinusoids and bile canaliculi. However, its main role is to control safety and flow of food substances absorbed from the digestive system before they are circulated in the entire circulatory system. The liver is position in right upper abdomen where it is protected by the lib cage and the diaphragm. Its healthy operation ensures general body health, with its failure in operation increasing death risk. Liver can suffer from various health conditions which include jaundice, Hepatitis B and C, cirrhosis and cancer, which is a condition that can be initiated by the other liver diseases especially when the diseases advance to chronic cases.     

Liver cancer is ranked among the most popular solid cancers in the globe and the leading cause of cancer related death. Liver cancer cause death at a very high rate, while its disease burden and global incidences are increasing steadily. HCC symbolizes liver cancer major subtype that accounts for about 90% of all cases of liver cancers, with the main risk factors including HCV and HBV infection, NAFLD, prolonged and continuous excessive consumption of alcohol among other metabolic disorders. Studies have demonstrated various mechanisms that can influence the development of liver cancer, especially sever inflammation that results to cells mutation and extensive growth of mutated cells creating liver tumor. It has also been established that development of HCC among patients with metabolic syndrome as the main risk factor might generate from malignant alteration of preexisting adenomas liver cell in the absence of important liver cirrhosis and fibrosis. Due to the increasing prevalence of Type 2 diabetes and obesity globally, that essentially predispose patients to progression of metabolic fatty liver disorder, thus NAFLD has been of specific concern.

Today, arthotopic liver transplantation, radio-frequency ablation surgical resection, small-molecule tyrosine kinase sorafenib inhibitor and transcatheter arterial chemoebolization are the main treatment of HCC. However,, research still continue to determine other therapeutic methods that can be used to inhibit growth and development of HCC in the liver which include CD151 and glucose-6-phospahate dehydrogenase (G6PD) among other therapeutic measures that are being discovered with advanced research. The second most popular basic liver cancer is ICC which accounts for about 10% of cancer cases, with its main causes being environmental factors. However, the research development in this cancer is considerably minimal and thus, making it complex to handle. Generally, cancer is initiated by sequential mutations of genes resulting to either change in the genes epigenetic signature such as tumor genes suppressor and oncogenes, or sequence alterations. The genes that are most impacted play main roles in differentiation, self-renewal,, cell proliferation, and cell cycle control mechanisms. Both ICC and HCC develop from central precursor lesions, demonstrating the hepatic carcinogenesis multistep process.

The Environment and Cancer – My Biomedical Perspective – Descriptive Essay

Assignment Instructions

You have been invited to submit an article to the Environmental Protection Agency’s Annual journal for this year. After doing research on environmental carcinogenesis, write a descriptive essay on the topic “The Environment and Cancer – My Biomedical Perspective”. 

The Environment and Cancer – My Biomedical Perspective – Sample Essay

Environment Carcinogenesis and Cancer

Environmental carcinogens refer to substances that human are exposed to through occupation, infectious agents, lifestyle and diet. They are regarded as non-genetic factors which contribute risk of getting cancer. A subset of reasonably anticipated and known human carcinogens can be categorized as environmental carcinogens and include compounds such as pesticides components, metals, dioxins, mineral fibers that include asbestos and erionite, and the polyaromatic hydrocarbon (Sabo-Attaword 234).

Read also Best Ways to Protect Yourself From Exposure to Carcinogens

These contaminants are key constituents of outdoor and indoor air, soil and water pollution as well as food products. The principles for deciding if a substance is carcinogenic is being modified constantly as our carcinogenesis understanding and technology evolve. However, the level of exposure to environment contaminants is highly related to the chances of developing cancer. This level of exposure is determined based on exposure route, composition, duration and dosage (Parsa 2).

Environment Carcinogen Mechanisms

Cancer involves multistage process which entails initiation of tumor, tumor promotion and advancement. Environmental carcinogen can advance or initiate this process by changing activity and expression of genes vital to biological processes which uphold apoptosis, cell growth, differentiation, cell-cycle control, and DNA repair. Environmental carcinogens act via genetic mechanisms, directly interacting with DNA. Some are activated metabolically to reactive molecules which create covalent lesions with DNA initiating mutations in genes essential to process that include DNA repair and cell-cycle regulation (Sabo-Attaword 233).

Read also The Role of Infectious Agents in Oncogenesis

Environmental carcinogenic might as well act via epigenetic mechanisms such that they do not change the genome directly, but cause initiated cells mitogenic expansion by modifying genes expression which control cell death and proliferation. Alterations in DNA methylation, cellular communication, oxidative stress, and growth factor motioning pathways are said to contribute to carcinogenesis (Sabo-Attaword 234).

Examples of environmental Carcinogens

There are different environment carcinogens which contribute to development of different cancers in human. For instance, exposure to esbestos is basically linked to lung cancer while exposure to dyes chemical known as benzidine is related to development of bladder cancer (Parsa 3). In addition, exposure to tobacco is related to lungs cancer pancreas, bladder, liver, mouth, cervix, colon, stomach, kidney, lip, throat, esophagus, and voice box.

Read also Comparing and Contrasting Mutagenic and Non-Mutagenic Carcinogens

Exposure to some viral and bacterial infections is also related to development of different cancers. For instance, Human papillomaviruses is related to cervical cancer, and Helicobacter Pylori is related to stomach cancer (Parsa 4-5). Other environmental carcinogenic include ionized radiations such as UV lights which are associated with skin cancer. Obesity is also related to esophagus, colon, kidney, endometrial and breast cancer (Niehs 6-9).

Environmental Carcinogens preventive Measures

The best preventive measures to employ include knowing and being able to identify environmental carcinogens and try to avoid them where possibly. This can highly be possible especially in food carcinogens and drugs such as tobacco and alcohol. Another measure is to employ safety measures while being exposed to carcinogenic environment. For instance, one should wear recommended safety gear while handling different chemicals. Companies should always maintain the work environment in the recommendable safety level.

Read also Cancer Diagnosis and Staging, Complications And Treatment Side Effects

People should also consider substituting unsafe procedures with more safety assured operational procedures. For instance, one should consider mechanical weeding than use of pesticide or application of organic farming compared to inorganic farming. Other preventive measures include checking on body weight and checking on personal diet and lifestyles. Although no activity guarantee a cancer free life, people should try reducing the risk factors by employing preventive measures.   

Skin Cancer – Assignment Instructions

Paper instructions:

  1. Etiology & Pathophysiology: Include populations affected, risk factors, and other related factors (age, gender, etc.). Discuss method of transmission and gene (s) affected.
  2. Physical Concerns: What physical characteristics may be apparent? Is an affected patient at risk for additional complications? Is mobility affected? Nutritional status? Etc.
  3. Psychosocial & Family/Support Systems: Discuss psychosocial implications, including body image, socialization issues, and educational concerns. How might friends and family members of an affected person be impacted? Why? Is government assistance available? How would a patient access available resources?
  4. Genetic Testing: Is genetic testing available? When might it be indicated? Discuss cost/benefit ratio.
  5. Legal/Ethical Considerations: What ethical implications might arise as a result of genetic testing; of opting in/out of testing? Who can consent to testing?
  6. Cultural Considerations: Is the incidence of the disorder increased in certain cultural populations? Would members of various cultures be impacted differently based on underlying beliefs, practices, etc.?
  7. Teaching Points: At what age is the disorder typically identified? What usually leads to diagnosis? What can the patient/family expect as the person ages and the disease progresses? What are current treatment options?
  8. Scholarly Presentation: Spelling, grammar, visual interest of PowerPoint Presentation