Genetics: From Genes to Genomes
6th Edition
ISBN: 9781259700903
Author: Leland Hartwell Dr., Michael L. Goldberg Professor Dr., Janice Fischer, Leroy Hood Dr.
Publisher: McGraw-Hill Education
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Chapter 20, Problem 29P
| a. | The legend to Fig. 20.29 identifies which of the analyzed genes are oncogenes and which are tumor suppressor genes. You could have made most of these assignments yourself without the legend, just by looking at the data. Explain. |
| b. | Which of the mutations in b. Fig. 20.29 are most likely to be passenger mutations? |
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4). p53 (sometimes called TP53 for “tumor protein 53") is a human tumor suppressor gene that is
mutated in the majority of human cancers (many tumor types).
a. For each of the mutations described below (i-iv): is this a mutation you would expect to find
when sequencing p53 alleles from tumor cells? Why or why not?
i. A missense mutation encoding a hyperactive form of the protein.
ii. A deletion of the gene.
iii. An insertion in the promoter that increases transcription 10-fold.
iv. A nonsense mutation.
b. When sequencing the p53 gene in tumor cells, would you expect to find only mutant version(s) of
the gene or a mix of mutant and wild type versions?
c. For any of the mutations you said you would expect to find in tumor cells, would you expect
tumor cells to be homozygous (same mutation on both chromosomes)? Why or why not?
d. Individuals with Li-Fraumeni syndrome have a very high risk of tumors originating in various
tissues due to inheritance of a loss-of-function mutant allele of…
Which of the following statements are true about the rate of mutation in tumor cells (select all that apply)?
A.
Mutation rate of tumor cells is reduced compared to normal cells of the same tissue type
B.
Mutation rate of tumor cells is unchanged compared to normal cells of the same tissue type
C.
Mutation rate in tumor cells is higher compared to normal cells of the same tissue type
D.
Affected by genome instability within the tumor cells
Describe error prone polymerases and the process of translesion synthesis (TLS). In regards to tumor biology, what is the mutator phenotype hypothesis? What are some ways in which error-prone polymerases could be targeted for potential anti-cancer treatments?
Chapter 20 Solutions
Genetics: From Genes to Genomes
Ch. 20 - For each of the terms in the left column, choose...Ch. 20 - Characterize the differences between tumor cells...Ch. 20 - Prob. 3PCh. 20 - Prob. 4PCh. 20 - A carcinogenic compound is placed on the skin of...Ch. 20 - You have decided to study genetic factors...Ch. 20 - B cells are specialized blood cells that secrete...Ch. 20 - Molecules outside and inside the cell regulate the...Ch. 20 - Put the following steps in the correct ordered...Ch. 20 - a. Would you expect a cell to continue or to stop...
Ch. 20 - Two different protein complexes called SCF and APC...Ch. 20 - One of the hallmarks of mitotic anaphase is the...Ch. 20 - Concerning the Tools of Genetics Box Analysis of...Ch. 20 - Are genome and karyotype instabilities...Ch. 20 - Prob. 15PCh. 20 - Why dont all loss-of-function mutations that are...Ch. 20 - Chromothripsis is a rare phenomenon, first...Ch. 20 - The chromosome 9/22 translocation associated with...Ch. 20 - A female patient 19 years old, whose symptoms are...Ch. 20 - Prob. 20PCh. 20 - A generic signaling cascade is shown in the...Ch. 20 - Neurofibromatosis type 1 NF1; also known as von...Ch. 20 - Families with germ-line BRCA1 or BRCA2...Ch. 20 - The text explained that retroviruses can cause...Ch. 20 - Hepatocellular carcinoma is the most frequent form...Ch. 20 - Suppose that instead of microarrays, you analyzed...Ch. 20 - Prob. 27PCh. 20 - Glioblastoma multiforme GBM is the most common and...Ch. 20 - a. The legend to Fig. 20.29 identifies which of...Ch. 20 - The website CBioPortal http://www.cbioportal.org...
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- Why is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings. Please sort as a list.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_forwardIn what category of cancer-related genes is it possible to find inherited variants that are associated with cancer? Why? Group of answer choices 1. Tumor suppressor genes, because genes in this category are very important in the process of developing cancer. 2. Proto-oncogenes, because individuals who carry only one cancer-causing allele will have a wildtype phenotype. 3. Proto-oncogenes, because there are very few genes in this category, so mutations in them are rare. 4. Tumor suppressor genes, because individuals who carry only one cancer-causing allele will have a wildtype phenotype.arrow_forward
- There are three broad categories of cancer-related genes: proto-oncogenes, tumor suppressor genes, and DNA repair/stability genes. Distinguish between these three groups, then indicate which you think RB1 belongs to.arrow_forwardThere are three broad categories of cancer-related genes: proto-oncogenes, tumor suppressor genes, and DNA stability/repair genes. Define each of these categories and indicate which one you think the RB1 gene belongs to and why.arrow_forwardTumor 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_forward
- The p53 gene was discovered in 1979, but it was not clear whether the gene functioned as an oncogene or a tumor-suppressor gene. Several years later, researchers showed that both p53 alleles are inactivated in some mouse cancers. This evidence suggests A. the p53 gene is an oncogene because inactivated alleles would produce mutated signal transduction proteins that would result in stimulating cell division. B. the p53 gene is an oncogene because the cell would overproduce transcription factors to compensate for the inactive alleles, resulting in increased cell division. C. the p53 gene is a tumor-suppressor gene because inactivated alleles indicate a loss of protein function which allowed the cancer to develop D. the p53 gene is a tumor-suppressor gene because the cell would produce too few transcription factors for gene activation, resulting in decreased cell division.arrow_forwardGenetic tests that detect mutations in the BRCA1 and BRCA2 tumor-suppressor genes are widely available. These tests reveal a number of mutations in these genes—mutations that have been linked to familial breast cancer. Assume that a young woman in a suspected breast cancer family takes the BRCA1 and BRCA2 genetic tests and receives negative results. That is, she does not test positive for the mutant alleles of BRCA1 or BRCA2. Can she consider herself free of risk for breast cancer?arrow_forwardThe p53 gene is a tumor-suppressor gene while Ras is a proto-oncogene. Mutation in either one can result in the transformation of a normal cell into a cancer cell. Explain the difference between the functions of the two proteins and how their mutation can lead to cancer development.arrow_forward
- Which of the following steps are correct about multistep tumorigenesis (select all that apply)? A. Mutations in progenitor cells are more likely to develop a neoplastic state compared to mutations in stem cells B. Driver mutations give a cell clone a proliferative advanage C. The rate of mutation /genetic change is constant during tumor progression D. Nutrition/diet may effect rate of tumorigenesis E. All cells within a tumor are biologically equivalent and equally capable of high levels proliferationarrow_forwardMany of the mutations in cancer samples are not necessarily driver mutations, but rather passenger mutations that are along for the ride. Just because the tumors with a strong environmental component possess a higher frequency of mutations does not mean more oncogenes or more failure of tumor suppressors is occurring. Hematologic childhood cancers have a lower frequency of mutations than tumors with a strong environmental component such as lung cancers and melanoma; WHY?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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