2. Cells that accumulate mutations can become cancerous over time. Mutations that develop late in cancer often lead to an increase in microfilament polymerization. (1) How do microfilaments polymerize? (2) Give an example of a possible mutation that would lead to an increase in microfilament polymerization. (3) Why would an increase in microfilament polymerization be advantageous to a cancer cell?

answer

watching

355

views

For unlimited access to Homework Help, a Homework+ subscription is required.

You have 0 free answers left.
Get unlimited access to 3.8 million step-by-step answers.

Get unlimited access

Already have an account? Log in

Lelia LubowitzLv2

23 Jul 2018

Unlock all answers

Get 1 free homework help answer.

Already have an account? Log in

Related questions

Tumor cells often develop mutations that lead to the loss of mitochondria. However, tumor cells are still able to proliferate rapidly even in the presence of oxygen. (1) How is this possible? (2) How would a drug that inhibits hexokinase interfere with cancer growth? (3) Give 2 examples of how a drug could inhibit hexokinase. (4) How could normal cells survive?

greenguinea-pig366

As discussed in the lectures, independent mutations in 4different gene types are required for the cell to become cancerous.Assume that a hypothetical intestinal stem cell divides every 4days. The general DNA replication error is 10^-8 pernucleotide per replication, average gene length is 8000nucleotides, and the person average lifespan is 70 years. If weassume that mutations in both alleles of 4 specific genes arerequired for the cell to become cancerous, what is an averagerandom chance for that intestinal stem cell to acquire thesespecific mutations during its lifetime? After calculating thisnumber, think how it compares to the lifetime chances of a persongetting cancer, and why these numbers do not seem to match(remember that human body has 10¹³ cells).

amaranthantelope460

Read the linked blog post about a recent study of a prostate cancer drug (http://goo.gl/O2GxAG) and answer a few questions based on the reading above.

1. The researchers tried to detect AR-V7 in the blood of men with advanced prostate cancer. Could they do this by sequencing DNA? What about by sequencing RNA? What about by detecting the protein? Donât worry about technical limitations; just tell me what is theoretically possible.

2. Healthy prostate cells do not produce AR-V7. Cancer cells tend to accumulate mutations more quickly than other cells. Given these two facts, it is tempting to propose that prostate cancer cells acquire a mutation that causes the production of AR-V7. Is this theory compatible with your understanding of how splicing works? Why or why not?