A) observation that certain tumor-suppressor genes and oncogenes are involved in a sequential manner in the development of colon cancer
B) fact that proto-oncogenes are widely conserved in evolution
C) usual occurrence of retinoblastoma at a young age
D) development of a cancer as a result of activation of a single oncogene by any of a variety of mechanisms
E) fact that there are many genetic and epigenetic mechanisms that lead to inactivation of the same tumor-suppressor gene
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A) They make products that act as signals to initiate cellular apoptosis.
B) Their products are components of cell growth pathways.
C) Proto-oncogenes make products that act as cell checkpoint regulators.
D) Proto-oncogenes make products that scan the genome for DNA damage.
E) Proto-oncogenes make products that repair DNA at sites of lesions.
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A) papilloma viruses
B) Epstein-Barr viruses
C) retroviruses
D) hepatitis B viruses
E) None of the answers is correct.
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A) All members of the family carry one mutant version of the kid gene, but those with cancer gained a second mutation of the kid gene. Therefore, it is highly likely that she will develop the kidney cancer.
B) While it is unlikely that she will develop the form of kidney cancer seen in her family, the mutant form of the kid gene she carries puts her at an increased risk of all types of cancer.
C) Because her parents did not develop kidney cancer, it is highly unlikely that they had a mutant form of the kid gene, and thus it is highly unlikely that she has a mutant kid gene. Therefore, she is not at risk of developing this form of kidney cancer.
D) While she carries a mutant copy of the kid gene, it is highly unlikely that she will develop kidney cancer because two mutant copies are required to be affected with the cancer.
E) Her father was a carrier of the mutant kid gene, and thus she is also a carrier of the mutant kid gene. She will likely not be affected, but her children will be at a high risk of developing the cancer.
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A) abnormally high levels of telomerase expression.
B) abnormally high levels of tumor-suppressor gene expression.
C) translocations that move a tumor-suppressor gene to a new location that increases its normal expression.
D) deletions that remove an oncogene from the genome.
E) DNA replication that is inhibited when it would normally occur.
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A) The p53 gene can act in a haploinsufficient manner.
B) The p53 gene is not a tumor-suppressor gene in these patients but rather an oncogene.
C) The mutant p53 gene most likely is involved in DNA-repair pathways.
D) The mutant p53 gene is having epigenetic effects in these patients.
E) The mutant p53 gene is being overexpressed in these patients.
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A) Inject extremely high levels of growth factor into the cell.
B) Inject normal levels of nonmutated growth factor into the cell.
C) Inject only the growth factor binding domain of the transmembrane receptor into the cell.
D) Inject the activated form of Ras into the cell.
E) Inject nonmutated tumor-suppressor genes into the cell.
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A) a chromosomal translocation resulting in the bringing together of two different genes that make a fusion protein
B) a chromosomal translocation resulting in enhanced regulation of the proto-oncogene
C) complete deletion of the proto-oncogene
D) a point mutation in the proto-oncogene
E) All of these are mechanisms of converting proto-oncogenes to oncogenes.
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A) primary tumors
B) secondary tumors
C) tumor vascularization
D) decreased DNA repair
E) increased apoptosis
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A) deletions; duplications
B) recessive; dominant
C) duplications; deletions
D) dominant; recessive
E) deletions; base-pair substitutions
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A) MPF would remain in its active state.
B) The cell would not be able to transition into mitosis.
C) Cyclin B levels would not be able to increase.
D) The cell would not be able to progress through the G1/S checkpoint.
E) Cyclin D could no longer be activated.
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A) a deletion
B) an inversion
C) a duplication
D) a reciprocal translocation
E) an aneuploidy involving one of the shorter autosomal chromosomes
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A) DNA sequence undergoes hypermethylation
B) DNA sequence is nearly intact but is inverted in the new position
C) gene is released from inhibition by miRNAs
D) gene is placed under the control of B-cell-specific gene regulatory sequences and is highly expressed
E) DNA sequence undergoes several point mutations
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Multiple Choice
A) They result from the activation of one critical tumor-suppressor gene.
B) They result when the transition from G2 to M in the cell cycle is inhibited.
C) They result when DNA replication during the S period of the cell cycle is inhibited.
D) They result from a series of sequential mutations in a number of genes.
E) They result from decreased expression in a series of cellular oncogenes.
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