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Chapter 16: Cancer Genetics

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Alison Jenkins

on 4 March 2013

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Transcript of Chapter 16: Cancer Genetics

Section 16.5: Colorectal Cancer Arises Through Sequential Mutation of a number of Genes The correlation of chromosome number and structure and their inherent cancerous repercussions. Over the years of genetic advance, it has been argued whether or not it is in fact chromosomes and their abnormalities that cause cancer. Although this is the case with regard to some cancers, we now know that the majority of cancers come from mutations at specific individual gene locations. It is the general instability of chromosomes that cause a build up of these mutations which lead to the production of mass cancer cells. So basically put is that chromosome mutations can be both the beginning factor of cancer and also a result of cancer. Section 16.4: Viruses are associated with Some Cancers Chapter 16: Cancer Genetics Section 16. 2: Mutations in a Number of Different Types of Genes Contribute to Cancer Section 16.1: Cancer Is a Group of Diseases Characterized by Cell Proliferation Cancer is not a single disease, rather a heterogeneous group of disorders characterized by the presence of cells that do not respond to the normal controls on division END Introduction Pancreatic cancer is among the most serious of all cancers. In 2006, a key gene was discovered that contributes to the development of pancreatic cancer. Palladin gene thought to contribute to pancreatic cancer- all members of a family had an identical mutation in exon 2 of the palladin gene. One in every five people in the United States will die from cancer; cancer treatments cost billions of dollars per year. Most common cancers in the United States are those of the prostate gland, breast, lung, colon, rectum, and blood Figure 16.1: Pancreatic cancer is inherited as an autosomal dominant trait in a family that possesses a mutant palladin gene Tumor Formation A normal cell's growth and division are regulated. In a cancer cell, one or more of the signals has been disrupted which causes the cell to proliferate at an abnormally high rate. The cells lose their regular shape and boundaries and eventually form a tumor. A benign tumor is localized, whereas a malignant tumor is cancer cells that invade other tissues. Cancer As a Genetic Disease Cancer arises as a result of fundamental defect in the regulation of cell division Cancer cells that spread typically have poor cytoskeleton architecture which allows them to detach from a primary tumor easily and migrate to other tissues. Cells with mutated palladin were 33% more efficient at migrating This example shows a chromosome mutation resulting in chronic myelogenous leukemia which is, as mentioned before, a chromosomal reciprocal translocation between chromosomes 9 and 22. Another example of a chromosomal reciprocal translocation occurs between chromosomes 8 and 14 which results in Berkitt lymphoma. This is cancer of the B cells, which are part of our lymphatic system and more specifically they are the lymphocytes that produce our antibodies Note: Chromosome 22 is known as the Philadelphia chromosome...know why? As I eluded to before, some cancers are caused by chromosomal abnormalities. These anomalies range from extra chromosomes to missing chromosomes to chromosomal rearrangement. It is a heterogenous group of disorders characterized by the presence of cell that do not have normal cell division Tumors formed from cancer cells crowd out normal cells and rob healthy tissues of nutrients Types of tumors Benign tumor: a tumor that lacks the ability to metastasize (spread from one area of the body to another and establish a secondary tumor) Malignant tumor: a tumor able to undergo metastasis. They are characterized by fast, uncontrolled growth and invasion of surrounding parts of the body some benign tumors may still cause adverse health effects, but the majority are not harmful to human health These tumors are not cancerous, because their cells remain localized these tumors are cancerous, if they establish tumors in other areas of the body they have undergone metastasis These most often cause adverse health conditions in those affected Genetic Evidence for Cancer 1. Many agents that cause mutations also cause cancer (carcinogens) ex, ionizing radiation, chemicals 2. Some cancers are consistently associated with particular chromosome abnormalities ex. 90% of people that have chronic myeloid leukemia also have a reciprocal translocation between chromosome 22 and chromosome 9 3. Some specific types of cancers run in families ex. Retinoblastoma is an inherited childhood cancer of the retina that appears with high frequency within a few families. It is inherited as an autosomal dominant trait, suggesting a single gene is responsible for this disease Knudson's multistep model of cancer In 1971, Alfred Knusdon created a model to explain the effects of mutation on carcinogenesis he studied retinoblastoma, which usually appears in one eye but occasionally in both eyes. In both eyes it presents early in life and affected children often have close relatives who are affected Knudson proposed that retinoblastoma results from two separate genetic defects, and that both are required for development of cancer when cancer affects just one eye, a single cell in one eye undergoes two successive mutations when cancer affects two eyes, the child must have inherited one of the two mutations required to cause cancer, so every cell in the body already contains the initial mutation Knudson's Genetic Theory Continued Most cancers result from multiple mutations This theory has been confirmed by identifying genes that cause cancer when mutated Cancer is fundamentally a genetic disease, but few cancers are actually inherited The majority of tumors arise from accumulated somatic muations (either spontaneous or in response to mutagens) Alfred Wagner Proposed that retinoblastoma results from two separate genetic defects, both of which are necessary for cancer to develop. Additional information on retinoblastoma rare cancerous tumor in the retina caused by a mutation in a gene controlling cell division, causing cells to grow out of control and become cancerous. about half of all cases develop in a child who has no family history of eye cancer If the mutation runs in the family, there is a 50% chance the child will also have the mutation mostly affects children under the age of 6, commonly diagnosed in children ages 1-2 treatments include laser surgery, radiation, chemotherapy, or enucleation (removal of the eye) Retinoblastoma with infiltrative growth pattern and optic nerve invasion The Clonal Evolution of tumors Cancer begins from a single cell that has undergone a mutation which causes it to divide abnormally The cell proliferates and creates a clone of cells, all with the same mutation Due to rapid growth, the cloned cells soon outgrow other cells In some clones an additional mutation occurs that further enhances proliferation, and soon the cells carrying both mutations are the most common This process is called clonal evolution, and it is how tumor cells acquire the mutations that allow them to continuously proliferate 16.4: Through clonal evolution, tumor cells acquire multiple mutations that allow them to become increasingly aggressive and proliferative. The rate of clonal evolution depends on the frequency with which new mutations arise DNA repair mechanisms usually eliminate mutations that occur, therefore cells of advanced cancers often have silenced DNA repair genes These cells are more likely to retain the mutations than are normal cells (including mutations in cell division genes) Ex. Xeroderma pigmentosum results in higher incidences of skin cancer when exposed to UV radiation. This disorder is caused by defect in DNA repair Ex. Breast Cancer can be cause by mutations in BRCA1 and BRCA2. These genes function in DNA repair Mutations in genes that affect chromosome segregation can also contribute to clonal evolution of tumors Cancer cells can be aneuploid, which means containing extra or missing copies of chromosomes Chromosome mutations contribute to cancer progression by duplicating some genes and eliminating others defects that interfere with chromosome separation affect aneuploidy and accelerates cancer progression Environmental Factors many cancers affected by environmental factors Suggested by differences in incidence of specific cancers around the world migrant populations take on the cancer of incidence of their host country, due to the fact that they are exposed to the same environmental factors examples of environmental factors include: smoking, chemicals (benzene, benzopyrene, polychlorinated biphenyls), UV light, ionizing radiation, and viruses environmental factors may interact with genetic predisposition to cancer Ex. Lung Cancer and smoking Problems with the theory if cancer is inherited, shouldn't it be inherited into every cell of the body? many cancers do not run in families, and those that do often appear in individuals with no family history of the disease If one or more of the required mutations is inherited, fewer additional mutations are needed to produce cancer and this cancer will run in families How does the multistep model of cancer explain the observation that sporadic cases of retinoblastoma usually appear in only one eye, whereas inherited forms of the cancer appear in both eyes? A. Sporadic cases appear in only one eye because two mutations are required to cause cancer. Two mutations occurring spontaneously in the same cell of one eye is more likely to occur. The inherited form is inherited through the germ line, meaning all cells of the body carry the mutation. Therefore, only one additional mutation is required to have the two required to cause cancer, and this is much more likely to occur. Knudson's multistep model of cancer In 1971, Alfred Knusdon created a model to explain the effects of mutation on carcinogenesis he studied retinoblastoma, which usually appears in one eye but occasionally in both eyes. In both eyes it presents early in life and affected children often have close relatives who are affected Knudson proposed that retinoblastoma results from two separate genetic defects, and that both are required for development of cancer when cancer affects just one eye, a single cell in one eye undergoes two successive mutations when cancer affects two eyes, the child must have inherited one of the two mutations required to cause cancer, so every cell in the body already contains the initial mutation Knudson's multistep model of cancer In 1971, Alfred Knusdon created a model to explain the effects of mutation on carcinogenesis he studied retinoblastoma, which usually appears in one eye but occasionally in both eyes. In both eyes it presents early in life and affected children often have close relatives who are affected Knudson proposed that retinoblastoma results from two separate genetic defects, and that both are required for development of cancer when cancer affects just one eye, a single cell in one eye undergoes two successive mutations when cancer affects two eyes, the child must have inherited one of the two mutations required to cause cancer, so every cell in the body already contains the initial mutation Knudson's multistep model of cancer In 1971, Alfred Knusdon created a model to explain the effects of mutation on carcinogenesis he studied retinoblastoma, which usually appears in one eye but occasionally in both eyes. In both eyes it presents early in life and affected children often have close relatives who are affected Knudson proposed that retinoblastoma results from two separate genetic defects, and that both are required for development of cancer when cancer affects just one eye, a single cell in one eye undergoes two successive mutations when cancer affects two eyes, the child must have inherited one of the two mutations required to cause cancer, so every cell in the body already contains the initial mutation
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