The Mutation of Cancer Cells Essay

Researchers have associated mutations in specific genes with more than 50 hereditary cancer syndromes, which are disorders that may predispose individuals to developing certain cancers. Genetic tests can tell whether a person

Its locus is particularly amplified in these noted tumours leading to the progression of these cancers, it can be suppressed by p53 (tumour/ proliferation suppressor) which represses the EZH2 promoter, resulting inhibition of cell proliferation and invasion (Bracken, 2003; Xiao, 2011).

level? A mutation in just one allele of proto-oncogenes can cause over production of cells tumor, and thus tumor formation, because they are dominant. Tumor suppressor genes require mutations of both alleles to inhibit function because they are recessive.

In addition to translocations and gene amplifications, deletions can occur and also result in oncogene activation. This can be by the removal of negative regulatory elements or the elimination of regulatory protein domains. However it is more common for a deletion to cause the loss of a tumor suppressor and therefore lead to a cancerous cell i.e. one which rapidly divides.

When a tumor suppressor gene is effected by a mutation, it loses its control over the cell and the cell does not stop to get inspected. When this happens, the mutation is copied, the cell divides and damage is passed down to the newly formed daughter cells. The mutation then becomes permanent and the now mutated cell will continue to divide and proliferate when it normally would not.

It was Monday March 17th, 2014 when I received a phone call from my grandma asking me to come visit her. That day is the day when I received the news that my grandma has been diagnosed with invasive lobular carcinoma breast cancer. My grandma and I are very close. Her diagnosis is what persuaded me to write my I- search paper on this specific breast cancer. One topic I am really focusing on when I write my paper is the genetic factors because its important to my family and I. Even though I began to research about the cancer when my grandma was diagnosed, there are still a lot of things I don’t know about and I’m interested to learn about within creating this paper. In this paper I will share with you the importance of invasive lobular

Imagine having an almost 100% chance of developing colon cancer. That is what people are told with Familial Adenomatous Polyposis (FAP) if they do not have their over 100 polyps, or growths, removed. FAP is a genetic disorder where normal cells that line your large intestine can grow into cancerous tumors. These tumors must be removed before they become cancerous. This disorder is passed down from parents on the APC gene which is on your fifth chromosome. If the APC gene is mutated you are more likely to develop these growths which lead to cancer in your lifetime. This disorder has an autosomal dominant inheritance pattern, which means if either parent has just one dominant mutated APC gene you have a 50% chance of inheriting it. Symptoms of FAP do not just include the growths in your colon. They can also include skin changes, osteomas or bone growths, and extra or missing teeth.

Hereditary breast and ovarian cancer syndrome (HBOC) and LS (also known as hereditary non-polyposis colorectal cancer (HNPCC) combined likely affect 1 in 250 individuals in the general population, therefore, suggests that primary care providers (PCP) actively cares for a number of these individuals and their family members (Metcalf, Tanner, Buchanan, 2010). Failure to identify and manage individuals with HBOC and LS can result in more harm and increase poor cancer prognosis (Metcalf, Tanner, Buchanan, 2010; Rosato et al., 2013). There are a number of guidelines from prominent organizations including the United States Preventive Services Task Force (USPSTF) and Evaluation of Genomic Applications in Practice and Prevention suggesting that identification of HBOC and LS patients can improve outcomes through enhanced screening and preventive measures (Metcalf, Tanner, Buchanan, 2010). Although not recognized as a universal agreement, the best approaches to high risk individuals with HBOC and Lynch syndrome is a primary care setting, until there is universal agreement with improved identification of LS risk measures (Metcalf, Tanner, Buchanan, 2010). Researchers are exploring recommendations to offer genetic testing for LS to all individuals with diagnosed CRC, with the intent of reducing morbidity and mortality in family members (Bellcross et al., 2011). Currently there are no significant efforts on a national level to facilitate widespread genetic screening to prevent LS adult onset conditions in family members of affected individuals using a public health model (Bellcross et al., 2011). The same concepts and processes used in newborn universal screening are being considered as a model for implementing universal LS screening on a population level (Bellcross et al., 2011). In recognizing universal LS

There are two important type of genes responsible for the development or cancer namely tumor suppressor because their normal function is

Cells may experience uncontrolled growth and if they are damaged or mutated in the DNA.There are four types of genes that are responsible for the cell division process. Those four types of genes are Oncogenes, Tumor Suppressor genes, Suicide genes, and DNA-Repair genes. Oncogenes tell the cells when to divide. Tumor Suppressor genes tell the cells when not to divide. Suicide genes controls apoptosis and tell the cells to kill themselves if something goes wrong. DNA-Repair informs the cells to repair damaged DNA. Cancer can occur when the cells of genes mutation are not able to correct damaged DNA and are not able to commit cell suicide. If you have some DNA mutations of the oncogenes or tumor suppressor genes that can lead to pancreatic cancer. It is a Great chance that the mutation was a result of some factors that affected the DNA after you were born rather than you inheriting it from your parents.

are able to fix the mistakes in the DNA that could potentially cause cancer. Unfortunately,

that can play a role in tumor development." These 300 altered genes could or could not change

The normal function of the p53 gene is to bind to other genes like miRNA34a (which codes for p21)(3). P21 is a protein that acts as signal for the shut of DNA replication, so mutation in P53 causes no direct signal to the p21 gene and there is uncontrolled growth and proliferation.

What might you expect to find in a cell with mutation that yielded the following organelles (1) 50% functional and (2) non-functional. Justify your answers. Mitochondria, rough ER, smooth ER, Peroxisomes, Golgi, and Chloroplasts.

Lynch syndrome, previously known as hereditary nonpolyposis colorectal cancer (HNPCC) is a parental inherited condition that exposes a person to the risks of cancers, but most commonly colon cancer1-9. It is a heterozygous autosomal dominant genetic condition, which means that if only one parent carries the gene for Lynch syndrome (LS), then a 50 percent chance of passing on the mutation will be passed to each child1-9. LS is limited to families with a known pathogenic germline mutation2. A germline mutation is when mutations occur in the germ line, which is a group of cells that contribute to the improvement of gametes2,3,10. To find out how individuals are to contract this disease, the family medical history must be taken into account. Early