Cancer+Questions+HW6+MC

Assignment Detail Cancer Questions SCI Human Biology - 1 Assigned: 11/12 Due: 11/13 Wiki Assignment on Cancer (Answers in Book--Chapter 19)

Define: apoptosis, telomeres, metastisis, tumor, proto-oncogenes, oncogenes, growth factor, tumor suppressor gene, oncology, carcinoma, sarcoma, leukemia, lymphoma -apoptosis: is a programmed cell death involving a cascade of specific cellular events leading to death and destruction of the cell. -telomeres: the tip of the end of a chromosome. -metastasis: spread of cancer from the place of origin throughout the body; caused by the ability of cancer cells to migrate and invade tissues. -tumor: cells derived from a single mutated cell that has repeatedly undergone cell division;benign tumors remain at the site of origin, and malignant tumors metastasize. -proto-oncogenes: normal gene that can become an oncogene through mutation. -oncogenes: cancer-causing gene. -growth factor: chemical signal that regulates mitosis and differentiation of cells that have receptors for it; important in such processes as fetal development, tissue maintenance and repair, and hematopoiesis; sometimes a contributing factor in cancer. -tumor suppressor gene: gene that codes for a protein that ordinarily suppresses cell division; inactivity can lead to a tumor. -oncology: the study of cancer. -carcinoma: cancer arising in epithelial tissue. -sarcoma: cancer that arises in muscles and connective tissues. -leukemia: cancer of the blood-forming tissues leading to the overproduction of abnormal white blood cells. -lymphoma: cancer of lymphatic tissue (reticular connective tissue). 1. What do cancer cells look like? -cancer cells are nonspecialized and do not contribute to the functioning of a body part. A cancer cell does not look like a differentiated epithelial, muscle, nervous,, or connective tissue cell; instead, it looks distinctly abnormal. 2. What is unusual about the nuclei of cancer cells? -The nuclei of cancer cells are enlarged and may contain an abnormal number of chromosomes. Not only the nuclei but also chromosomes of cancerous cells are abnormal. Some portions of the chromosomes may be duplicated, and some may be deleted. Tissues that divide frequently are more likely to become cancerous. 3. Why don't cancer cells die? -The gene that codes for telomerase is turned on in cancer cells. Telomerase continuously rebuilds the telomeres in cancer cells so that the telomeres remain at a constant length, and the cell can keep dividing over and over again. 4. Describe the three phases of the development of cancer. -During Initiation a single cell undergoes a mutation that causes it to begin to divide repeatedly. In promotion, a tumor develops, and the tumor cells continue to divide. As they divide, they undergo mutations. During progression, one cell undergoes a mutation that gives is a selective advantage over the other cells. This process is repeated several times, and, eventually there is a cell that has the ability to invade surrounding tissues. 5. Mutations in what two types of genes lead to uncontrollable growth? - The two types are Angiogenesis and Metastasis. Angiogenesis is the formation of new blood vessels. The low oxygen content in the middle of a tumor may turn on genes coding for angiogenic growth factors that diffuse into the nearby tissues and cause new vessels to form. Metastasis is the spread of cancer from the place of origin throughout the body; caused by the ability of cancer cells to migrate and invade tissues. 6. What is p53? How does it cause cancer? -p53 is a protein that turns on genes that stop the cell cycle and activates repair enzymes. If repair is impossible, the p53 protein promotes apoptosis, programmed cell death. One proto-oncogene codes for a protein that functions to make p53 unavailable. When this proto-oncogene becomes an oncogene, no matter how much p53 is made, none will be available. Many tumors are lacking in p53 activity. 7. What is RB? How does it cause cancer? -RB is the retinoblastoma protein that turns on the gene for cyclin D and other genes whose products promote entry into the S phase of the cell cycle.When the tumor-supressor gene p16 mutates, the RB protein is always functional, and the result is, again, too much active cyclin D in the cell. The cell experiences repeated rounds of DNA synthesis without the occurrence of mitosis.The protein Bax promotes apoptosis. When a tumor-suppressor gene Bax mutates, the protein Bax is not present, and apoptosis is less likely to occur. The gene contains a run of eight consecutive G bases, making it subject to mutations. 8. What are the most common cancers cases for males and females? - For men, the most common cancer cases is prostate 234,460 (33%), then lungs and bronchus 92,700 (13%), then colon and rectum 72,800 (10%). For females, the most common cancer cases is breast cancer 212,900 (31%), then lung and bronchus 81,770 (12%), then colon and rectum cancer 75,810 (11%). 9. What are the most common cancer deaths for males and females? - For men, the most common cancer deaths are lung and bronchus 90,330 (31%), then colon and rectum 27,870 (10%), then prostate cancer 27,350 (9%). For women the most common cancer deaths are lung and bronchus 72,130 (26%), then breast 40,970 (15%), then colon and rectum cancer 27,300 (10%).