HUMAN HEREDITY (LL)-W/MINDTAP ACCESS
HUMAN HEREDITY (LL)-W/MINDTAP ACCESS
11th Edition
ISBN: 9781305717022
Author: Cummings
Publisher: CENGAGE L
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Chapter 12, Problem 15QP

Which of the following mutations will result in cancer?

  1. a. homozygous recessive mutation in a tumor-suppressor gene coding for a nonfunctional protein
  2. b. dominant mutation in a tumor-suppressor gene in which the normal protein product is overexpressed
  3. c. homozygous recessive mutation in which there is a deletion in the coding region of a proto-oncogene, leaving it nonfunctional
  4. d. dominant mutation in a proto-oncogene in which the normal protein product is overexpressed
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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.
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 proliferation
Researchers 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?

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