Concept explainers
C.1Identify the normal functions of the genes whose mutations are associated with development of cancer.
RBI(retinoblastoma)
c
p
APC(familial adenomatous polyposis)
Which of these genes would you classify as a protooncogene and which as a tumor suppressor gene? Explain your categorization for each gene.
To review:
To identify normal function of the given genes, as the mutation of these genes is related to cancer development.
The normal function of
The normal function of
The normal function of
The normal function of APC is to be identified.
The proto-oncogene and tumor suppressor genes is to be classified.
Introduction:
Proto oncogenes are those which perform normal function in the cell cycle. Mutation in proto oncogenes results in over expression of proto oncogenes which leads to uncontrolled cell division, now, they are termed as oncogenes. On the other hand, genes normally faction in DNA damage repair and control the normal cell cycle. If mutation occurs in this gene, they lose their function and DNA damage cannot be repaired; in such condition, the cell is termed as transformed, and it undergoes uncontrolled cell division.
These genes prevent cell transformation and maintain a normal cell cycle and are termed as tumor suppresser genes.
Explanation of Solution
RB1 normally inhibit the
APC (Adenomatous polyposis coli) functions as a tumor suppresser gene. It is involved in proteolytic cleavage and degradation of
Proto oncogenes accelerate rate of normal cell division and are responsible for the formation of tumors. Tumor suppresser genes suppress the formation of tumor.
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Chapter C Solutions
GENETIC ANALYSIS: INTEGRATED - ACCESS
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- Tumor suppressor genes and oncogenes are implicated in carcinogenesis. However, one can predict whether a gene potentially encodes for a protein that influences carcinogenesis by examining their mutational profile. You sequence the genome of 4 cancers and identify 3 genes of interest. Which of the following genes has the best potential to an oncogene? Tumor 1 Tumor 2 Tumor 3 Tumor 4 Gene A S24F, N465T R33T T345S, G366R P367E, P368Y Gene B S34R, F360I S34R V254I S34E, T67Y Gene C S24F, I322E C255I, E344D S34E, P367Earrow_forwardThe Human papillomavirus (HPV) has been linked to an increased risk of cervical cancer. The HPV E6 and E7 proteins govern the cell via altering cellular proteins. The E6 protein interacts with the tumor suppressor protein p53 and directs its ubiquitin-mediated destruction. Can you elaborate about the P63 gene: its function and if it can be altered/mutated by HPV? If it does, what is the relationship between P53 and P63? Thank you!arrow_forwardResearchers have identified some tumors that have no recurrent mutations or deletions in known oncogenes or tumor-suppressor genes and no detectable epigenetic alterations. However, these tumors often have large chromosomal deletions. What are some possible explanations that could account for the genetic causes behind these tumors?arrow_forward
- 1) Create a graph as a better way to display the data in the table 2) Determine which mutations (5q, 18q, 17p, Ras) caused the progression to each stage of tumorigenesis.arrow_forwardHow can the role of epigenetics in cancer be reconciled with the idea that cancer is caused by the accumulation of genetic mutations in tumor-suppressor genes and proto-oncogenes?arrow_forward46. Explain why mutations in oncogenes are generally dominant while those in tumor suppressor genes are recessive.arrow_forward
- Explain Mutations in tumor-suppressor genes are recessive at the cellular level but dominant at the organismal level.arrow_forwardD) The level of carbon dioxide increases with the level of available oxygen. 60) The TP53 gene provides instructions for making a protein called tumor protein p53. Known as the guardian of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too 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. eg 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…arrow_forwardCellular levels of tumor suppressor protein p53 is maintained by a ubiquitin ligase protein, called Mdm2. Over expression of Mdm2 destabilizes p53. Another protein p19ARF inhibits the activity of Mdm2, thus stabilizing p53. Loss of p19ARF function converts normal cells into cancer cells With the above information, which of the following statements are true? Mdm2 is a tumor suppressor gene but p19ARF is an oncogene Both Mdm2 & P19ARF are oncogenes Both Mdm2 & P19ARF are tumor suppressor genes O Mdm2 is an oncogene but p19ARF is a tumor suppressor genearrow_forward
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