27 of 41 Mutations in two important cancer-critical genes, encoding p53 and Rb, respectively, are commonly found in cancers. What type of mutations are these expected to be? O Gain-of-function mutation in p53 and loss-of-function mutation in Rb O Loss-of-function mutation in p53 and gain-of-function mutation in Rb O Loss-of-function mutations in both genes O Gain-of-function mutations in both genes
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- Cancer is driven by alterations in the expression of critical genes, namely tumour suppressors, which play a growth-regulatory role, and proto-oncogenes, which promote the growth and survival of the cell. For both classes of cancer-related gene, suggest a likely mechanism of alteration and sketch the consequence for the gene and protein. Tumour suppressor gene (i.e. TP53, PTEN or APC) Oncogene (i.e. RAS, MYC)In Metastatic Breast Cancer [such as in Breast Invasive Ductal Carcinoma; Breast Invasive Carcinoma, NOS; Breast Invasive Cancer, NOS; Invasive Breast Carcinoma; Breast Invasive Lobular Carcinoma; Breast Mixed Ductal and Lobular Carcinoma] what role does the genes Tp53 and Tp63 have? Would one of them affect the other (i.e. mutation, etc) or there is not relationship among the two genes at all.Which of the following mutations will result in cancer? a. homozygous recessive mutation in a tumor-suppressor gene coding for a nonfunctional protein b. dominant mutation in a tumor-suppressor gene in which the normal protein product is overexpressed c. homozygous recessive mutation in which there is a deletion in the coding region of a proto-oncogene, leaving it nonfunctional d. dominant mutation in a proto-oncogene in which the normal protein product is overexpressed
- Describe the general process of cell signalling pathways: what events take place for a signal to cause cellular changes? Provide examples and how perturbation of these events can result in “cancer pathways”. In addition, describe in detail a typical cancer pathway and its strategy to activate gene expression. What is the origin of many cancer pathways, i.e., during which stage of an organism’s live process(es) are they physiologically activated? Why is this important for cancer development?Skin cancer carries a lifetime risk nearly equal to that of allother cancers combined. Following is a graph [modified fromK. H. Kraemer (1997). Proc. Natl. Acad. Sci. (USA) 94:11–14]depicting the age of onset of skin cancers in patients with orwithout XP, where the cumulative percentage of skin cancer is plotted against age. The non-XP curve is based on 29,757 cancerssurveyed by the National Cancer Institute, and the curverepresenting those with XP is based on 63 skin cancers from theXeroderma Pigmentosum Registry.Which statements are true? Explain why or why not.1 The chemical carcinogen dimethylbenz[a]anthra-cene (DMBA) must be an extraordinarily specific mutagensince 90% of the skin tumors it causes have an A-to-T alter-ation at exactly the same site in the mutant Ras gene.2 In the cellular regulatory pathways that controlcell growth and proliferation, the products of oncogenesare stimulatory components and the products of tumorsuppressor genes are inhibitory components.3 Cancer therapies directed solely at killing the rap-idly dividing cells that make up the bulk of a tumor areunlikely to eliminate the cancer from many patients.4 The main environmental causes of cancer are theproducts of our highly industrialized way of life such aspollution and food additives.
- Describe the common signal transduction event that is perturbed by cancer-promoting mutations in the genes encoding RAS and NF-1. Why are mutations in RAS more commonly found in cancers than mutations in NF-1?Describe the effects of the mutation causing the p21 promoter to no longer bind p53 on cell signaling pathways and metabolism or cell cycle control.Lung cancer mitotic index: 0.25 Breast cancer mitotic index: 0.35 Skin cancer mitotic index: 0.4 Looking at the mitotic index for all 3 cancer types, which one is likely to be the most resistant (least affected) to the growth-inhibiting effects of traditional chemotherapy drugs that target rapidly dividing cells?
- . Mutations in an autosomal gene in humans cause aform of hemophilia called von Willebrand disease(vWD). This gene specifies a blood plasma proteincleverly called von Willebrand factor (vWF). vWFstabilizes factor VIII, a blood plasma protein specified by the wild-type hemophilia A gene. Factor VIIIis needed to form blood clots. Thus, factor VIII is rapidly destroyed in the absence of vWF.Which of the following might successfully be employed in the treatment of bleeding episodes in hemophiliac patients? Would the treatments workimmediately or only after some delay needed forprotein synthesis? Would the treatments have only ashort-term or a prolonged effect? Assume that allmutations are null (that is, the mutations result in thecomplete absence of the protein encoded by the gene)and that the plasma is cell-free.a. transfusion of plasma from normal blood into avWD patientb. transfusion of plasma from a vWD patient into adifferent vWD patientc. transfusion of plasma from a hemophilia A…Distinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.19: What are 3 phenotypes of GA, or BR, or ABA, or CK over-producing mutants. 20: Think about a hormone receptor, specifically the structure of the receptor. Describe ONE why a mutation would cause insensitivity to the hormone, AND ONE way it could cause hypersensitivity to the hormone. Explain your answer to each. 22: Not all cells in tissues are the same. They differentiate from stem cells. Describe how ONE cell type acquires cell identity. (Pick any cell in the plant)