Colorectal cancer refers to colon or rectal cancer. Most colorectal cancers are of glandular origin and hence can be classified as adenocarcinomas. It can also be called bowel cancer and is the third most common type of cancer in the world with 45 out of 100,000 people suffering from the same according to The National Institute of Cancer statistics as of 2013. These two types of cancers are significantly similar in their genomic mutations and also bear symptomatic semblance [1]. Colorectal cancer is characterized by tumors that form in the tissues of the colon or the rectum. Like tumors in general, these too are a formed as a result of abnormal and uncontrolled division of cells. The causes of colorectal cancer are mostly unknown although it may be inherited or genetically unrelated [2].
Cancer occurs when mutations in the DNA cause uncontrolled cell proliferation and hence tumor formation. Cancer causing genes can be divided into two classes: 1.) Tumor suppressor genes 2.) Oncogenes. Tumor suppressors if underexpressed are unable to check cell proliferation, resulting in tumor formation. On the other hand, the same results if proto-oncogenes (the precursors of oncogenes) are overexpressed or activated. Isolating the causal genes in colorectal cancer, we identified 54 genes that in various capacities play an important role in the same. On screening on the basis of target site mutations we narrowed this down to 34 major genes. Around 40% of these genes show tumor suppressor properties and apart from them, others point to a number of biological processes and molecular functions such as phosphorylation, regulation and modification of proteins, binding and signaling.
With disease genetics becoming an increasingly investigated field, ...
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...e proved to meddle with immunotherapy by lowering responsiveness to it[13,14]. Another very important gene, TP53 has also been found to be overexpressed due to TS mutations. This gene plays a pivotal role in cell cycle arrest due to its function of binding to DNA to form the p21 protein that ultimately acts as a stop signal in the cell cycle [15].
Thus with the help of a systematic computational protocol of analysis and filtering we were able to isolate certain genes that can considerably alter correct genetic functioning due to predicted mutations in their nucleotide sequences. Given the functions of the above described genes, it can be said that their under or overexpression is crucial to the manifestation of cancer. The analysis of microRNA Target Site SNPs corroborating these facts say that they also might have a determining role to play in the cause of disease.
...ozzi E, Biffoni M, Todaro M, Peschle C, et al. Identification and expansion of human colon-cancer-initiating cells. Nature. 2007;445(7123):111-5.
Colorectal cancer, or CRC, affects African American men and women more than Caucasians, at a rate 20% higher. This is concerning when faced with the mortality rates among African Americans, 28% higher for women and 14% higher for men than for Whites. African Americans are also more likely to be in later stages of the disease when diagnosed. There is a need to study and evaluate why these factors exist, as proper screening and early diagnosis can severely impact survival rates for CRC. One study attempts to find the solution through testing, however, this study slightly discredits itself along the way.
The underlying purpose of the experiments performed in the study, Promoter Hypermethylation of KLF4 Inactivates its Tumor Suppressor Function in Cervical Carcinogenesis, is to investigate the mechanism by which the KLF4 gene is silenced in cervical carcinomas. Cervical cancer accounts for 250,000 female deaths every year. Developing therapies for cervical cancer has been limited due to the lack of genetic and epigenetic data of the mechanism causing the cancer. The KLF4 gene is a transcriptional regulator of cell growth and differentiation. It functions as a tumor suppressor in cervical cancer, but is found to be inactivated in cervical cancer. The overexpression of KLF4 protein is known to inhibit cervical cancer cell growth and tumor formation by activating a cell cycle suppressor. Promoter CpG island hypermethylation can result in transcriptional silencing of many tumor suppressing genes. Two CpG regions, BSQ1 and BSQ3, were examined in this experiment.
Breast cancer has always been a common thread among the women of my family; especially on my mother’s side, including my Grandmother whom passed away due to this disease before I could ever meet her. More so, my mother was gravely affected by this disease early in my life. Thankfully, she was able to stop the cancer from spreading; the doctors were able to find the cancerous cells and remove them. Due to this grave, but powerful impact on my life, I have been determined to becoming a biomedical scientist to assist on the research and treatment of this deadly disease. Although this acts as my principal driver, to study in this field, I have also been intrigued and driven by the idea that I could aid lower setting regions to receive health benefits using studies in translational medicine and
Irregular bowel movements or constipation is quite a major and common concern in adults and babies as well. The condition becomes more challenging when it comes to babies. Parents of infants worry when their infant’s bowel movement is not regular and clear as that causes formation of gas and stomach pain.
Hypermethylation of CpG islands at tumor suppressor genes turns them off, while hypomethylation leads to the instability and inappropriate activation of oncogenes and transposable elements. Methylation can be directly related to genetic mutations, an example of this case is methylated cytosine. Methylated cytosine mutates spontaneously in vivo through deamination to give thymine. According to Andy Bannister (n.d.), “37% of somatic p53 mutations and 58% of germ line mutations occur at methylated...
Mutation in PTEN can leads to cancer as it fails to down regulate PIP3 which activates AKT which up regulates cell proliferation and anti-apoptotic mechanisms.
Thought to be an oncogene, a gene that has potential in transforming normal cells into tumor cells, p53 was regarded as the most prominent tumor suppressor gene [1]. P53 is a gene which signals apoptosis (programmed cell death) if a cell cannot be repaired due to an extensive amount of damage. As stated in the textbook, p53 regulation occurs by an E3 ubiquitin-protein ligase known as MDM2 [1]. "Controlling the controller" is a statement that describes the molecular interaction where the presence of MDM2 targets the p53 for proteosome via degradation. With three main checkpoints in cell cycle, the literature states p53 functioning from G1 into S phase in a chaotic cell [2]. The normal state of cells is to keep p53 levels low in order to prevent uncontrolled apoptosis and random cell cycle arrest from occurring. In a further note, although p53 promotes apoptosis and cell cycle arrest, cancer may result from p53 unable to recognize the problematic site. In turn, a mutation in p53 may result engaging in new activities. These activities include cellular transformation, tumor metastasis,...
Colon cancer develops in the part of the gastrointestinal tract that absorbs water and minerals before waste products are disposed via the rectum. In women endometrial cancer is related to colon cancer. This type of cancer is the second leading cause of death due to cancer in the United States. Over one-hundred fifty thousand individuals will be diagnosed this year and this cancer will probably be responsible for about 47,900 deaths in 1999 (http://www.cancer.org). Most colon cancers are adenocarcinomas that develop from the glandular cells. Ninety percent of all colon cancer cases will develop in individuals after 50 years of age. Ninety percent of all tumors arise from polyps that are commonly found in people older than 50. Prevention includes regular exercise and a diet high in fiber. The most important risk factor is age. Medical screening includes a yearly blood occult test after age 50 and a colonoscopy every 3 years after age 50. Regular screening detects polyps that have become precancerous. If regular screening is not done, the cancer is not detected until blood is found in the...
The American Cancer Society publishes current advances made in cancer research on their website. Many of the exciting discoveries about how best to treat the disease focus on the genetic aspects associated with certain types of cancer. In addition, treatments aimed at genetic solutions to cancer may be more effective and may cause fewer adverse side effects than traditional cancer treatments (American Can...
Ulcerative colitis, or UC, is a chronic gastrointestinal disease that causes inflammation and ulcers in the lining of the large intestine. It causes ulcers in the colon and rectum. Ulcerative colitis is one of two forms of inflammatory bowel disease. In UC, the inflammation from the ulcers breaks down the lining of the colon and causes bleeding and discomfort in the abdomen.
I had the pleasure to interview my grandma, Olga Hernandez. She was born on November 8, 1951 in Cuba. She worked in a workshop making clocks. After she retired, she took care of me while my mom worked. I consider her to be my second mom because she lived with me for eight years. She taught me love, discipline, manners, etc. My grandma is: strong, beautiful, caring, and passionate. Most importantly, she is a breast cancer survivor. I chose to interview my grandma because October is Breast Cancer Awareness Month. I couldn’t think of a better time to do this interview. I like her story because although it’s sad, it has a happy ending. It shows you that no matter how hard things get, there’s always light at the end of the tunnel.
My grandfather on my mum’s side died of colon cancer, colon cancer is where the body extracts water and salt from solid wastes. Colon cancer happens when out of control cell growth occurs in the large intestine. Colon cancer can be caused through genetics; a genetic predisposition that can be inherited from family members, but most colon cancer occur in people without a family health history.
These oncogenes cause cancer because they do not allow the cells to self-destruct or become epistatic. There have been several research projects which have been testing epistatis. Transfecting DNA To perform the experiments for this research, the researchers had to grow certain pieces of DNA.... ... middle of paper ...
Tumors are formed by the alteration of the body’s own cells. This can be caused by environmental factors such as radiation, like UV exposure, chemicals or viruses 1. These can disrupt genes that control growth and cause an increase in cell division and proliferation. Proto-oncogenes are those genes that control normal but essential cell processes that keep cell growth and death in check. Two important categories are apoptosis genes, which regulate cell death, and tumor suppressor genes, which decrease cell propagation 1 . If these genes were mutated to the point where they cannot produce a functioning protein, cell division would continue far past what it was supposed to and unhealthy cells would be allowed to live and continue to multiply. This is what creates a malignant tumor. Certain conditions in the body can also promote the growth of cancer cells. One of these is a deficiency of natural killer (NK) cells, which are able to kill cancer cells by creating a pore in the cell membrane with perforin and releasing granzymes into the cell. Low levels of perforin allow for tumor growth 1. Chronic inflammation can also ...