suppose a person developed a mutation in a somatic cell diminishes the performance of the body's natural cell cycle control proteins. this mutation resulted in cancer, but was effectively treated with cocktail of cancer-fighting techniques. is it possible for this person's future children to inherit this cancer-causing mutation? Be specific when you are explain why or why not.

suppose a person developed a mutation in a somatic cell diminishes the performance of the body's natural cell cycle control proteins. this mutation resulted in cancer, but was effectively treated with cocktail of cancer-fighting techniques. is it possible for this person's future children to inherit this cancer-causing mutation? Be specific when you are explain why or why not.

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter28: Dna Metabolism: Replication, Recombination, And Repair

Section: Chapter Questions

Problem 19P: Figure 28.11 depicts the eukaryotic cell cycle. Many cell types â€œexitâ€� the cell cycle and...

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Suppose a person developed a mutation in a somatic cell that diminishes the performance of the body’s natural cell cycle control proteins. This mutation resulted in cancer, but was effectively treated with a cocktail of cancer-fighting techniques. Is it possible for this person’s future children to inherit this cancer-causing mutation? Be specific when you explain why or why not.
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)
One approach to studying the regulation of cell cycle progression (particularly in an era when genetic and molecular biology manipulations were less readily accomplished in mammalian cells) was to use treatments that induced cells to fuse and then monitor the behavior of the two nuclei in the resulting cell. The figure below depicts data from one such study. The investigators did preliminary work to produce populations of cells that were synchronized in various stages of the cell cycle (G1, S, or G2 in the examples shown below). They then fused the cells in different combinations and monitored subsequent events in each of the nuclei. For purposes of this question, we will pay particular attention to what occurred in the nucleus that came from the cell in G1. In one experiment (I), cells in the G1 and S phases were fused. That event caused the nucleus from the G1 cell to very quickly enter the S phase (sooner than it would otherwise have done so). In contrast, in a second experiment…
One approach to studying the regulation of cell cycle progression (particularly in an era when genetic and molecular biology manipulations were less readily accomplished in mammalian cells) was to use treatments that induced cells to fuse and then monitor the behavior of the two nuclei in the resulting cell. The figure below depicts data from one such study. The investigators did preliminary work to produce populations of cells that were synchronized in various stages of the cell cycle (G1, S, or G2 in the examples shown below). They then fused the cells in different combinations and monitored subsequent events in each of the nuclei. For purposes of this question, we will pay particular attention to what occurred in the nucleus that came from the cell in G1. In one experiment (I), cells in the G1 and S phases were fused. That event caused the nucleus from the G1 cell to very quickly enter the S phase (sooner than it would otherwise have done so). In contrast, in a second experiment…
Relate histopath criteria of cancer to H nana cell cycle & chromosomal instability. Analyze the image attached and discuss how many of the mutations in cancer affect the normal regulation of the cell cycle, particularly the G2 checkpoint where mutations are supposed to be caught and not passed on. If there's a mutation in this checkpoint - notably p53 - then mutations are passed on and accumulate and we see bizarre chromosomes in cancer. Refer to original question to discuss how the histopathy criteria of cancer (unifrom population of pleimorphic cells, variable cytoplasmic nuclear ratio, multiple/bizarre nucleoli and frequent/bizarre mitotic figures) these relate to H nana cell cycle and chromosomal instability.
Suppose a person developed a mutation in a somatic cell which diminishes the performance of the body’s natural cell cycle control proteins. This mutation resulted in cancer but was effectively treated with a cocktail of cancer-fighting drugs. Is it possible for this person’s future children to inherit this cancer-causing mutation? Be specific when you explain why or why not.
"Agent V" is the name of an anticancer (chemotherapy) drug. This drug works against cancer cells by inhibiting the formation of microtubules in sensitive cells. Consider a cell that is sensitive to agent V (in other words, agent V is effective at stopping growth of this cell). Based on this information, agent V would cause the cell to be frozen at which of the major cell cycle checkpoints (G1, G2 or M checkpoint)? Explain
BPA is a chemical compound that has historically been used in themanufacture of plastic products. However, cells often mistake BPAcompounds for hormones that accelerate the cell cycle. Because ofthis, BPA is associated with an increased risk of certain cancers. Question: How might BPA interact with the cell cycle and its checkpoints?
BPA is a chemical compound that has historically been used in the manufacture of plastic products. However, cells often mistake BPA molecules for hormones that accelerate the cell cycle. Because of this, BPA is associated with an increased risk of certain cancers.a. How might BPA interact with the cell cycle and its checkpoints?b. Why do you think that very small concentrations of BPA might have a large effect on a cell?
Scientists are able to isolate cells in various phases of the cell cycle. During an experiment in which Dr. Patrick McGroyn is causing cultured tumor cells to go through mitotic cell division, he isolates a group of cells that contain one and a half times more DNA than cells isolated in the G1 phase have. What phase must these cells be in? How do you know?
Passage of cells from G1 through R to S depends on the interaction of various signal molecules, proteins and enzymes which regulate the cell cycle. Imagine I have just induced a mutation in a cell line which prevents the breakdown of the cyclin molecule we discussed. Which of the following events do you predict will happen? circle all that apply Select one or more: a. Uncontrolled cell replication may result b. Retinoblastoma protein will be continuously active c. The cells will be stuck in G1 phase d. The cells will begin to replicate their DNA e. Cyclin dependent kinase (Cdk) will be continuously active
In your own words, briefly explain the different phases of the cell cycle. Explain what events take place at each phase