Biology
12th Edition
ISBN: 9781260494570
Author: Raven, Peter
Publisher: MCGRAW-HILL HIGHER EDUCATION
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Textbook Question
Chapter 10, Problem 3A
Genetically, proto-oncogenes act in a dominant fashion. This is because
a. there is only one copy of each proto-oncogene in the genome.
b. they act in a gain-of-function fashion to turn on the cell cycle.
c. they act in a loss-of-function fashion to turn off the cell cycle.
d. they require that both genomic copies are altered to affect function.
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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.
With regard to human cancer cells, which of the following statements is true?
A. Cancer cells within one tumor usually do not share common mutations
B. Cancer cells generally have lost the ability to divide
C. Oncogenes are non-human genes not related to normal genes in the human genome
D. Mutations in DNA repair genes result in an increased chance of getting cancer.
Which of the following statements
concerning p53 is NOT correct?
O a. p53-dependent transcription of target genes leads
to cell cycle arrest or cell death (apoptosis).
O b.
O C.
Loss of p53 function results in loss of checkpoint
controls.
Loss of p53 function creates an environment that
is permissive for genome instability--that is, more
damaged cells with chromosome aberrations and
mutations survive and propagate.
d. p53 is a tumor suppressor protein which is largely
responsible for protecting cells from cancer-
causing DNA-damaging agents.
Chapter 10 Solutions
Biology
Ch. 10.1 - Prob. 1LOCh. 10.2 - Prob. 1LOCh. 10.2 - Distinguish between homologues and sister...Ch. 10.2 - Prob. 3LOCh. 10.3 - Describe the eukaryotic cell cycle.Ch. 10.4 - Prob. 1LOCh. 10.4 - Prob. 2LOCh. 10.5 - Describe the phases of mitosis.Ch. 10.5 - Explain the importance of metaphase.Ch. 10.5 - Compare cytokinesis in plants and animals.
Ch. 10.6 - Prob. 1LOCh. 10.6 - Prob. 2LOCh. 10.7 - Prob. 1LOCh. 10.7 - Prob. 2LOCh. 10 - Binary fission in prokaryotes does not require the...Ch. 10 - Chromatin is composed of a. RNA and protein. b....Ch. 10 - What is a nucleosome? a. A region in the cells...Ch. 10 - What is the role of cohesin proteins in cell...Ch. 10 - The kinetochore is a structure that functions to...Ch. 10 - Separation of the sister chromatids occurs during...Ch. 10 - Why is cytokinesis an important part of cell...Ch. 10 - What steps in the cell cycle represent...Ch. 10 - Cyclin-dependent kinases (Cdks) are regulated by...Ch. 10 - Prob. 2ACh. 10 - Genetically, proto-oncogenes act in a dominant...Ch. 10 - The metaphase to anaphase transition involves a....Ch. 10 - The main difference between bacterial cell...Ch. 10 - In animal cells, cytokinesis is accomplished by a...Ch. 10 - Regulation of the cell cycle is very complex and...Ch. 10 - Review you knowledge of signaling pathways...Ch. 10 - Compare and contrast how mutations in cellular...
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- Mutations in the ras gene family induce normal cells to proceed into the replication cycle. This converts the ras gene from a ________ gene to a ________ gene. a. proto-oncogene; oncogene b. oncogene; proto-oncogene c. mutant; oncogene d. tumor suppressor; proto-oncogenearrow_forwardWhat is the difference between a proto-oncogene and an oncogene? a. oncogenes cause benign tumors (polyps), proto-oncogenes cause malignant tumors b. oncogenes transform cells to hyperproliferation, proto-oncogenes have a normal cellular role c. oncogenes have undergone post-translational modification, proto-oncogenes have not d. oncogenes have undergone intron splicing, proto-oncogenes have notarrow_forwardThe role of p53 in normal cells is toa. create cancer-blocking mutations.b. trigger unrestrained cell division.c. detect damaged DNA.d. splice exons together in the correct sequence.arrow_forward
- Which of the following is NOT a description of an epigenetic modification? A. regulatory patterns that persisis in the absence of the original signal B. stable alterations in gene expression without changes to the underlying DNA sequence C. the persistence of gene expression patterns through cell division D. an intrinsic signal that triggers cell differentiationarrow_forwardEpigenesis relating to genetics refers to which of the following A. Genetic information is limited to what we inherit only from our biological parents. B. Genes are not influenced by environmental factors. C. Genes we inherit are fully expressed at birth. D. Genes are turned on or off as needed, by the developing body or environmental triggers, across the life-spanarrow_forwardWhich of the following statements about cancer is correct? A. Cancer stem cells can make tumors resistant to chemotherapy. B. Intra-tumoral heterogeneity makes it easier to treat cancer. C. Mutation in p53 is a type of passenger mutation. D. One driver mutation is more than sufficient for the production of a cancer phenotype.arrow_forward
- Can you please answer questions 13,14, and 15 pleasearrow_forwardA cell inherits a mutation in a gene that results in a transcription factor, called NF-kB, constantly being in its active conformation. When active, NF-kB stimulates the expression of cyclins that promote progression of the cell cycle, regardless of other conditions. As a result of this mutation, how would this cell's phenotype be affected by this mutation? A) This cell would have a cancer phenotype B) This cell would grow larger in size, but would never divide C) This cell would likely undergo apoptosis D) This cell would not duplicate its chromosomes .arrow_forward1arrow_forward
- D) 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_forwardWhich of the following is MOST likely true of aggressively dividing cancer cells (select one)? A. They do not express telomerase B. They do not express hTERT C. They are in a state of cell crisis D. Their telomeres are stabilized (not shortening with each cellular division) E. None of Abovearrow_forwardThe 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.arrow_forward
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