12.What is field of cancerization? Explain part A and B of this figure. How does it explain field of cancerization?| (A) mutation mutation mutation mutation morphologically normal morphologically abnormal, hyperplastic, dysplastic, or neoplastic (D) tumor 1 tumor 2 (8) 7,8,9 10 wild-type p53 only G-T45. wt p53 NORMAL PATCH FIELD CARCINOMA 17p 3p, 9p, 8p, 189 11g Figure 11.14 The Biology of Cancer (0 Garland Sdener 2014)

12.What is field of cancerization? Explain part A and B of this figure. How does it explain field of cancerization?| (A) mutation mutation mutation mutation morphologically normal morphologically abnormal, hyperplastic, dysplastic, or neoplastic (D) tumor 1 tumor 2 (8) 7,8,9 10 wild-type p53 only G-T45. wt p53 NORMAL PATCH FIELD CARCINOMA 17p 3p, 9p, 8p, 189 11g Figure 11.14 The Biology of Cancer (0 Garland Sdener 2014)

Biology: The Unity and Diversity of Life (MindTap Course List)

14th Edition

ISBN:9781305073951

Author:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Publisher:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Chapter42: Animal Development

Section: Chapter Questions

Problem 3CT

See similar textbooks

Similar questions

3.3. Using your knowledge of the function of p53, discuss why targeting mutant p53 is promising for cancer therapy. 3.4. Using your knowledge of the function of Rb, discuss the consequences of a dysfunctional Rb protein on cell cycle progression. 4.1. Why is glucose consumed at a high rate in the absence of oxygen and at a low rate in its presence? Explain.
D) The level of carbon dioxide increases with the level of available oxygen. 60) The TPS3 gene provides instructions for making a protein called tumor protein p53. Known as the guardlan of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing t0o fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will not…
4). p53 (sometimes called TP53 for “tumor protein 53") is a human tumor suppressor gene that is mutated in the majority of human cancers (many tumor types). a. For each of the mutations described below (i-iv): is this a mutation you would expect to find when sequencing p53 alleles from tumor cells? Why or why not? i. A missense mutation encoding a hyperactive form of the protein. ii. A deletion of the gene. iii. An insertion in the promoter that increases transcription 10-fold. iv. A nonsense mutation. b. When sequencing the p53 gene in tumor cells, would you expect to find only mutant version(s) of the gene or a mix of mutant and wild type versions? c. For any of the mutations you said you would expect to find in tumor cells, would you expect tumor cells to be homozygous (same mutation on both chromosomes)? Why or why not? d. Individuals with Li-Fraumeni syndrome have a very high risk of tumors originating in various tissues due to inheritance of a loss-of-function mutant allele of…
Loss of p53 function occurs in the majority of human tumors. Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function.
The P63 and P53 have similar functionalities in the cell, however, p53 is rarely associated directly with p63, suggesting that p63 may indirectly act as an oncogene by blocking p53 function. This hypothesis may also explain why p63 is associated with other indications of misinterpretation. I do understand the above statement, however once piece not clear – why would p63 block p53 function? Have these genes been shown to have opposing functions? From the background information provided above, it seems like they would have seminar functions. Explain.
/20. In class, we discussed diffferent types of genetic change that can cause a normal gene (proto- oncogene) to become a cancer-causing gene (oncogene), Which of the following would not be a cause? A) translocation or transposition (movement of DNA within the same genome) B) gene ampliffication (increased number of copies of a given gene) C) epigenetic change D) point mutation that changes the gene's product E) loss of telomeres during DNA replication ancer?
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)
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.
2. For a fictional human tissue, it is hypothesised that cancer stem cells have the following expression pattern of cell surface markers (CD44+/CD24+/ESA+). Flow cytometry was used to isolate this population of cells. COMM CD24 ESA 1% Tumour volume (cm³) a) In the flow cytometry experiment, explain how to determine what percentage of the total cell population are the putative cancer stem cells. Also, briefly describe two controls that should be included in the experimental design. (30%) 3.01 2.5- +602 In a follow-up experiment, sorted and unsorted cells were injected subcutaneously into immunodeficient mice. The following plot depicts the results from the experiment. 2.0- 1.5- 1.0- CD24 0.5- ESA 37% • Unsorted CD44+/CD24+/ESA+ CD44+/CD24-/ESA- Time (weeks) 10 12
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?
Describe the mutational event that produces the MYC oncogene in Burkitt’s lymphoma. Why does the particular mechanism for generating oncogenic MYC result in a lymphoma rather than another type of cancer? Describe another mechanism for generating oncogenic MYC.
#9) Cancer cells generally have missense mutations in p53 gene, resulting in truncated p53 normally active p53 dominant negative p53 inactive p53 #2) When cancer cells have not spread beyond its original site, the term used to describe it is benign growth intraepithelial neoplasia carcinoma stage 3 carcinoma in sit #10) Single or double stranded breaks in DNA activate Chk 1 and 2 kinases, which phosphorylates p53. This results in --- in the level of p53 in the cell. increase decrease please answer them all. they are very short and won't take your time. Thank you in advance.