Hi, can you explain this concept: cell cycle progression can be halted at several points by the tumor suppressor gene product p53, activated in response to checkpoints sensing DNA and possibly also chromosome damage; loss of p53 would remove this brake to cycling. How these events can lead to cancer progression?

Hi, can you explain this concept: cell cycle progression can be halted at several points by the tumor suppressor gene product p53, activated in response to checkpoints sensing DNA and possibly also chromosome damage; loss of p53 would remove this brake to cycling. How these events can lead to cancer progression?

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter10: Cell Reproduction

Section: Chapter Questions

Problem 2VCQ: Figure 10.13 Rb and other proteins that negatively regulate the cell cycle are sometimes called...

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In your own words, explain how cancer cells differ from normal cells in regard to the following: Molecular controls of the cell cycle (include Cdk and Cdk/cyclin complexes, p53 gene/protein, Rb gene/protein in response)
Discuss the complete cell cycle in a human cell, mitosis and meiosis, and the regulatory components (i.e. the proteins associated with cellular checkpoints) of the cell cycle. Tumor growth results when the cell cycle checkpoints are ignored. Give an example of how tumor growth could result from either a loss-of-function or a gain-of-function mutation.
In your own words: Describe the molecular mechanisms involved in P53’s role as a tumor repressor protein.
Cancer cells typically lose cell cycle entry control. Explain how the following mutations, which are found in some cancer cells, lead to a bypass of these controls: (a) overexpression of cyclin D, (b) loss of Rb function, (c) loss of p16 function, (d) hyperactive E2F.
Protein N, normally inactivates a tumor suppressor protein. Consider a cell with a mutation in one allele such that protein N is nonfunctional, while the other allele of gene N is wild-type. Which of the following is true for this cell? Gene N is a tumor suppressor gene, and the phenotype of the cell is not transformed. Gene N is a proto-oncogene, and the phenotype of the cell is transformed. Gene N is a tumor suppressor gene, and the phenotype of the cell is transformed. Gene N is a proto-oncogene, and the phenotype of the cell is not transformed.
The normal function of one tumor-suppressor gene acting at the G1 checkpoint is to prevent cells with damaged chromosomes and DNA from “progressing from G1 to S.” Another tumor-suppressor gene, acting at the G2/M checkpoint, prevents “passage from G2 to M.” When these tumor-suppressor genes fail to work, cancer can result. Explain what the phrases in quotations mean.
p53 gene, as is the Rb gene, is a tumor suppressor gene. p53 protein binds to DNA leading to the simulation of p21 that work together with cdk2. When p21 is defective and cannot joined to cdk2 the cell cannot pass through to the next stage of cell division. Mutated p53 cannot bind to DNA in an effective way, and therefore the p21 protein is not available to act as the 'stop signal' for cell division. Thus cells divide uncontrollably, and form tumors. Hi, can you please elaborate on this: based on the info above, what is the relationship between genetics and environment in the development of these type of cancer. Which factor (genetics or environment) is playing a larger role in the generation of these types of cancers?
1. Based on their descriptions, classify each gene as a tumor suppressor or a proto- oncogene: Tumor suppressor or proto-oncogene? Gene Protein product activity A transcription factor that turns many genes on or off. Normally, p53 is produced at high levels only when DNA damage is detected. Controls the G1/S cell cycle checkpoint. When it's present, it makes sure E2F is neutralized until it's time to proceed with DNA synthesis. A transcription factor that turns on genes needed for cell cycle progression. Binds and destroys TCF before it can enter the nucleus. р53 RB1 Мус АРС TCF A transcription factor that turns on the Myc gene. 2. Choose one of the genes from the above table and do some research. Which cancers usually have mutations in this gene?
#1) Hyperplastic growth are not cancerous yet but show a higher than normal proliferation rate. True False #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 situ #9) Cancer cells generally have missense mutations in p53 gene, resulting in truncated p53 normally active p53 dominant negative p53 inactive p53 #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
Describe the steps by which the TP53 gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?
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?
What is the most likely outcome is we lose the tumor suppressor proteins, cyclin- dependent kinase inhibitors. Select one: o a. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will not proceed. o b. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will not proceed. o c. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will proceed. o d. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will proceed.