You are studying a new type of cancer and you discover that there is a mutation in a gene that encodes a histone acetylase. You hypothesize that the mechanism by which this mutation causes cancer is by altering the expression of a gene involved in the control of cell proliferation by introducing a mutation in a gene involved in the control of cell proliferation mutating DNA repair genes introducing random mutations

You are studying a new type of cancer and you discover that there is a mutation in a gene that encodes a histone acetylase. You hypothesize that the mechanism by which this mutation causes cancer is by altering the expression of a gene involved in the control of cell proliferation by introducing a mutation in a gene involved in the control of cell proliferation mutating DNA repair genes introducing random mutations

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter12: Genes And Cancer

Section: Chapter Questions

Problem 15QP: Which of the following mutations will result in cancer? a. homozygous recessive mutation in a...

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You are studying cancer progression in mice. Your results show the following pathway in which two proteins play important roles in how mouse cell division is regulated. nutrients cell division Prot 1 Prot 2 You isolate a mutant strain of mice that have a Prot 1 mutation (Prot 1-). These mutant mice frequently develop cancer as young adults. Which of the following can you conclude from these observations? Select all that apply Prot 1- mutation can be classified as dominant Prot 1 can be classified as a proto-oncogene Prot 1- mutation can be classified as recessive Prot 1 can be classified as a tumor suppressor gene
p53 iš an important tumor suppressor gene that is activated in response to a variety of stress signals. Upon activation it induces a cell cycle arrest or cell death. Hence, loss-of-function mutations in the p53 gene are found in almost every type of cancer. How do you predict loss-of-function mutations in the DNA binding domain of the p53 protein affect its function? OIt no longer will act as activator of gene expression O It no longer will act as repressor of gene expression O It no longer will act as activator or repressor of gene expression O It no longer will act as coactivator or corepressor
You are studying cancer progression in mice. Your results show the following pathway in which two proteins play important roles in how mouse cell division is regulated. nutrients cell division Prot 1 Prot 2 You isolate a mutant strain of mice that have a Prot 1 mutation (Prot 1-). These mutant mice frequently develop cancer as young adults. You isolate a mutant strain of mice that have a Prot 2 mutation (Prot 2-). These mutant mice frequently develop cancer as young adults. Which of the following can you conclude from these observations? Select all that apply O Function of wild-type Prot 2 is to promote cell division when nutrients are present Function of wild-type Prot 2 is to promote cell division when nutrients are absent Function of wild-type Prot 1 is to inhibit cell'division when nutrients are absent Function of wild-type Prot 1 is to inhibit cell division when nutrients are present
A research study indicated that an agent in cigarette smoke caused the silencing of a tumor suppressor gene called p53. However,upon sequencing, no mutation was found in the DNA sequence for this gene. Give two possible explanations for these results.
The rb gene encodes a protein that inhibits E2F, a transcriptionfactor that activates several genes involved in cell division.Mutations in rb are associated with certain forms of cancer,such as retinoblastoma. Under each of the following conditions,would you expect the cancer to occur?A. One copy of rb is defective; both copies of E2F are functional.B. Both copies of rb are defective; both copies of E2F arefunctional.C. Both copies of rb are defective; one copy of E2F is defective.D. Both copies of rb and E2F are defective.
Match each example of mutation to the correct effect on function. Hypomorphic mutation Hypermorphic mutation Antimorphic mutation Neomorphic A deletion results in the loss of part of a protein and the protein retains some of its normal activity. A mutant allele makes a protein with increased cataytic activity. A mutant form of a transcription factor binds new DNA sequences to activate different genes. A mutant from of a receptor protein interferes with the function of the wild-type receptor through heterodimerization.
Which of the following mutations will result in cancer? a. homozygous recessive mutation in a tumor-suppressor gene coding for a nonfunctional protein b. dominant mutation in a tumor-suppressor gene in which the normal protein product is overexpressed c. homozygous recessive mutation in which there is a deletion in the coding region of a proto-oncogene, leaving it nonfunctional d. dominant mutation in a proto-oncogene in which the normal protein product is overexpressed
Cancer is caused by many different types of gene mutations. Some mutations are in proto-oncogenes, which lead to overexpression of the genes, and other mutations are in tumor suppressor genes, which lead to under expression or no expression in these genes. Which kinds of gene mutations would RNA interference (RNAi) be better at treating? Explain.
The retinoblastoma tumor suppressor gene Rb (RB1) codes forthe retinoblastoma protein (pRB). pRB prevents the progression of the cell cycle through G1 if DNA has been damaged. Itdoes so in part because it binds a transcription-activatingdimer referred to as E2F-DP. The pRB-E2F/DP complex recruits a histone deacetylase to chromatin. Explain.
One major goal of modern cancer therapy is toidentify small molecules—anticancer drugs—that canbe used to inhibit the products of specific cancer-criticalgenes. If you were searching for such molecules, wouldyou design inhibitors for the products of oncogenes orthe products of tumor suppressor genes? Explain why youwould (or would not) select each type of gene.
Why is it important to model cancer through the generation of induced pluripotent stem cells ? Please list item by item. Explain in detail the main findings.
Artificially induced apoptosis (controlled cellular death) is found to be an effective treat- ment for some forms of cancer. Which of the following describes the most likely mechanism by which apoptosis might be induced? A B с D by causing ribosomes to increase the rate of protein synthesis by triggering the division of mitochondria in the cell to increase ATP production by increasing the expression of membrane-bound glucose protein channels by causing lysosomes to release digestive enzymes into the cytosol