What protein or gene mutations are typically studied when studying tumor apoptosis?

Answer]: A Tumor associated with a mutation in the DNA repair Zixin regulatory gene is hereditary non-polyposis colorectal cancer. In patients with hereditary non-polyposis colorectal cancer, due to the loss of DNA mismatch repair genes, the mismatch of bases in a single-stranded DNA during replication (such as mismatching A and T to G and T) cannot be repaired, resulting in mutations in oncogenes or tumor suppressor genes, and defeating colorectal cancer.

According to different functions, apoptosis-related genes can be divided into three categories, namely:

1) Inhibition of apoptosis genes such as: EIB, IAP, BC1-2.

2) Promote the disadvantages of hypocrisy and highlight the apoptotic genes, such as: FAS, BAX, ICE, p53, etc.

3) Bidirectional regulatory genes such as poor family C, MyC, BCLX, etc.

a. The root cause of cell carcinogenesis is the genetic mutation of proto-oncogenes and tumor suppressor genes, and a is wrong;

b. The increase in the incidence of lung cancer is related to smoking, air pollution, etc., b is correct;

c. The early stage of cancer is generally not easy to find, c wrong;

d. Somatic mutations are generally not inherited to offspring, and D is wrong

Therefore, b

Because the formation of tumors is the result of the gradual accumulation of genetic mutations. Tumorigenesis requires: Polygenic mutations accumulate over a long period of time.

According to a large number of case analysis, the occurrence of cancer is generally not a single gene mutation, but at least 5-6 gene mutations in a cell can give cancer cells all the characteristics: that is, cancer cells not only proliferate quickly, but also their progeny cells can escape the fate of cell senescence, replace the position of adjacent normal cells, continuously obtain nutrients from the blood, and then cross the basal membrane and blood vessel wall to place, survive and grow in new tissue sites. Thus, mutations in the cell genome that produce a proto-oncogene associated with tumorigenesis do not form cancer immediately, but continue to grow until a new episporadic mutation is created in the cell population.

Certain cells that have a competitive advantage in natural selection go through a similar process to gradually form malignant tumors with all the characteristics of cancer cells. For example, the mutation that begins in the course of rectal cancer only forms multiple benign tumors (polyps) in the intestinal wall, and further mutations develop into malignant tumors, and the whole process takes 10-20 years or more. Therefore, cancer is a typical senile disease, which involves the accumulation of a series of oncogenic mutations of proto-oncogenes and tumor suppressor genes.

In some cases of cancer, oncogenic mutations occur in proto-oncogenes or tumor suppressors in germ cells, resulting in mutations in the corresponding genes in all somatic cells in the body. In this case, the number of genetic mutations required for cancer to occur accumulates less time, and family members who carry this gene mutation are more susceptible to cancer.

There are many external factors that cause gene mutations, such as physical factors such as radiation, chemical factors such as nitrite, etc., and biological factors such as certain viruses, these factors can only increase the frequency of gene mutations, and the root cause of gene mutations is the change of the base pairs that make up genes.

As for the more complicated results, in layman's terms: if the changed base is just the right to control the trait, it can cause the trait to change, and if it does not contain the segment that controls the expression of the trait, it may not affect the lesion.