Genetic Changes And Cancer Essay

Hereditary breast and ovarian cancer is mostly due to a mutation in the Breast cancer susceptibility gene 1(BRCA1) and breast cancer susceptibility gene 2 (BRCA 2) genes and is the most common cause of both forms of breast and ovarian cancers due to hereditary (Weitzel, Blazer, MacDonald, Culver, & Offit, 2011). Although the overall prevalence of the BRCA 1/2 genes is estimated 1 in 400 to 1 in 800 with a higher occurrence in the Ashkenazi Jewish population which is 1 in 40 that have the BRCA genes. According to Weitzel, Blazer, MacDonald, Culver, & Offit (2011), the likelihood of having the BRCA1 or BRCA2 mutation is dependent on one’s personal and/or family history of cancer and can be assessed by using several mutation probability models. After a BRCA1 or BRCA2 gene has been identified in the family, testing of all of at-risk relatives can identify those family members who may also have the BRCA gene and therefore will need to have an increased in following and early intervention when a cancer is diagnosed. There are several options that a person who has been diagnosed with having

All cancers arise as a result of changes that have occurred in the DNA sequence of the cell genomes, occurring through chromosome abnormalities (Stratton, Campbell, and Futreal, 2009). Chromosomes are made up of tightly wound DNA and proteins which form a highly condensed tertiary structure. Chromosomal abnormalities are a prominent characteristic of cancer cells, often resulting from nondisjunction, the failure of chromosomes to separate properly during meiosis (Peña-Diaz et al., 2012). Nondisjunction results in cells that have too many or too few chromosomes. A normal human karyotype would contain forty-four autosomes and two sex chromosomes; each chromosome has a homologous pair. Females

cell division. They can also develop in response to radiation or chemicals in the environment

Moore, S. W. (2009). Developmental genes and cancer in children. Pediatric. Blood Cancer, 52(7), 755-760. doi:10.1002/pbc.21831. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/19165888

that heredity has little to nothing to do with malignancies. Studies have demonstrated that irregularities

The testing is not a bad idea as such but it should not be done to children. This regards to personal autonomy where it would be better if the testing is delayed until an individual is old enough to make his or her own decision about the test. A person’s genetic information should be private and counselling should be done to elucidate the basis for and consequences of the test in question. Individuals should be allowed to choose when and which

The defective genes job to identify and repair somatic mutations in DNA during cell division was later referred to as microsatellite instability. It was identified in a number of genes through screenings of blood tests. This microsatellite instability lead in some cases to loss of imprinting, but further research is need to determine if this loss of imprinting in healthy people will lead to the development in cancer. A study done in 1997 revealed that the microsatellite instability in genes p53, RAS, and APC fit 85% of colon carcinomas, many of which were aneuploidy and all sequential mutations of those genes. The rest were deficient in DNA mis- match repair genes which tended to have near diploid genotypes. This study was tested with cultures, it is now being tested with clinical specimens.

Multiple evidence indicates susceptibility to cancer is mediated by genetically determined differences in the effect of detoxification of carcinogens. Susceptibility to cancer is characterized by the activation of enzymes involved in carcinogen activation or deactivation. Polymorphic variants in xenobiotic-metabolism genes, including CYP1A1 and GSTT1, may increase the risk of adult AML, particularly when present simultaneously.

An ordinary human body contains approximately one trillion cells and precisely 46 chromosomes in each cell. However, the human body can be altered by a genetic mutation. Over the course of history, genetic mutations have had a large impact on the human race. They have brought harm to numerous amounts of people. Cancer, in particular, is one of the most lethal diseases. Cancer begins when a portion of DNA inside a chromosome is damaged, causing a cell to mutate. Then, the mutated cell reproduces multiple times and creates a tumor. Afterwards, cancer cells break off of the tumor, enter the bloodstream, and disperse throughout the body. If the cells break off, the tumor is considered malignant - this type of cancer is very difficult to cure.

Cancer is beyond mutations. By definition, epigenetics is the change in gene translation that is caused by alterations not directly due to genetic mutations in the DNA sequence. The 2 main mechanisms are DNA methylation and covalent modification of histones. By methylation, certain molecular tags (methyl groups) bind to a specific sequence of a gene, that results in its disability hence incapable of being translated into its appropriate protein product. These changes affect the cell’s functions leaving its DNA unchanged. Epi is derived from Latin meaning above; hence an epigenetic configuration overlies our genetic predispositions.

Protein coding genes, which represent just 1% of the genomic sequence, contain most of the known DNA sequence variants that have been linked to disease (Kumar, Dudley, Filipski, and Liu, 2011). Many of these variants occur in non-coding sequence, but an estimated 6,000 to 10,000 variants alter protein sequence and more than a thousand have been linked to major diseases. In addition to these heritable variants, somatic and germline mutations have been found to be associated with increased cancer susceptibility and the mitochondrial genome contributes thousands of variants of its own.

The first role is that there is a predisposition to cancer development, meaning that a mutation in Mlh1 or Msh2 provide alternate causes for LS2,5. These mutations are distinguished because of the presence of CpG islands and following transcriptional loss of single genetic alleles of the affected gene, which results in the comparison of a heterozygous mutation2,10. CpG islands are clusters of the sequence CG which may be gathered near promoter regions in a gene10. Another role is when the Lynch-associated tumors developed as a result a somatic loss-of-function of the last normal allele of the mutated gene2. Somatic loss-of-function is a genetic change that takes place in a somatic cell, but the change is not aquired2,10. Finally, the last role is the role of more derived epigenetic changes that may be gained to assist the growth and advancement of associated Lynch tumors2. The studies of these roles have shown that tumor suppressor genes occur within Lynch syndrome

Since the DNA is passed down from parent to offspring, the risk of developing certain diseases, including cancer is passed down as well; the DNA is divided down into genes. Cancer cell growth is a result of abnormal cell growth after there has been an error in the cells DNA, thus causing a mutation. Cancers can be caused by DNA mutations that activate oncogenes or inactivate tumor suppressor genes. In many cases, genetic testing can be used to see if someone has one of these mutations. Most bone cancers are not caused by inherited DNA mutations. They are the result of mutations acquired during the person’s lifetime. These mutations may result from exposure to radiation or cancer-causing chemicals, but most often they occur for no apparent reason. Scientists are making progress in understanding this process but there are still some points that are not completely understood. As their knowledge increases, they hope to develop ways to better prevent and treat bone cancers (Cancer.org).

Heredity also plays a role in the development of cancer. If a person’s relatives have a history of cancer, then that person has a higher risk of developing cancer. Genetic variations, particularly those influencing how the body responds to carcinogens, may create a greater vulnerability to cancer.

They analyzed the genetic profiles of these patients to study a concept known as the “double-hit hypothesis”, which is a widely accepted theory in the field of cancer.