Robbins Basic Pathology
10th Edition
Author(s)Vinay Kumar; Abul K. Abbas;
Jon C. Aster
TEST BANK
1
Reference
Ch. 1 — The Genome
Question Stem
A 45-year-old patient receives ionizing radiation to the chest.
Hours later, molecular testing of irradiated cells shows
activation of p53 and increased expression of p21. Which
outcome is most consistent with this response?
Options
A. Immediate activation of telomerase and entry into S phase
,B. G1 cell-cycle arrest allowing DNA repair or triggering
apoptosis
C. Permanent inactivation of mismatch repair enzymes
D. Constitutive activation of receptor tyrosine kinases
Correct Answer
B
Rationales
• B (correct): p53 upregulates p21, which enforces G1/S
checkpoint arrest to permit DNA repair; if damage is
irreparable, p53 promotes apoptosis. This mechanism is
described in Robbins as a primary genome-protective
response.
• A: Telomerase activation is not an immediate DNA-damage
response and does not follow p53-mediated p21 induction.
• C: Mismatch repair enzyme inactivation is not a
downstream effect of acute p53/p21 activation.
• D: Receptor tyrosine kinase activation is unrelated to p53-
mediated DNA-damage checkpoints.
Teaching Point
p53 → p21 → G1 arrest: allows repair or triggers apoptosis if
damage persists.
Citation
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.). Ch. 1.
,2
Reference
Ch. 1 — The Genome
Question Stem
A colon cancer specimen displays high microsatellite instability
(MSI) with numerous insertion/deletion mutations. Which
defect best explains this molecular pattern?
Options
A. Defective nucleotide excision repair
B. Defective mismatch repair (MMR) system
C. Loss of base excision repair enzymes
D. Hyperactivation of homologous recombination
Correct Answer
B
Rationales
• B (correct): MSI with repetitive-sequence changes is
characteristic of mismatch repair deficiency, which fails to
correct replication slippage in microsatellites.
• A: Nucleotide excision repair defects produce bulky adduct
accumulation (e.g., UV damage), not MSI.
• C: Base excision repair repairs small base lesions (e.g.,
deamination), not microsatellite slippage.
• D: Homologous recombination hyperactivation would alter
double-strand break repair patterns, not produce MSI.
, Teaching Point
Mismatch repair deficiency → microsatellite instability →
accumulation of insertion/deletion mutations.
Citation
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.). Ch. 1.
3
Reference
Ch. 1 — The Genome
Question Stem
A tumor suppressor gene shows low mRNA expression despite
an intact coding sequence on genomic sequencing. Bisulfite
sequencing reveals heavy promoter CpG methylation. Which
mechanism explains the decreased expression?
Options
A. Frameshift mutation in an exon
B. Epigenetic promoter methylation causing transcriptional
silencing
C. Loss of ribosomal RNA synthesis
D. Increased ubiquitin-mediated degradation of the protein
Correct Answer
B
Rationales
10th Edition
Author(s)Vinay Kumar; Abul K. Abbas;
Jon C. Aster
TEST BANK
1
Reference
Ch. 1 — The Genome
Question Stem
A 45-year-old patient receives ionizing radiation to the chest.
Hours later, molecular testing of irradiated cells shows
activation of p53 and increased expression of p21. Which
outcome is most consistent with this response?
Options
A. Immediate activation of telomerase and entry into S phase
,B. G1 cell-cycle arrest allowing DNA repair or triggering
apoptosis
C. Permanent inactivation of mismatch repair enzymes
D. Constitutive activation of receptor tyrosine kinases
Correct Answer
B
Rationales
• B (correct): p53 upregulates p21, which enforces G1/S
checkpoint arrest to permit DNA repair; if damage is
irreparable, p53 promotes apoptosis. This mechanism is
described in Robbins as a primary genome-protective
response.
• A: Telomerase activation is not an immediate DNA-damage
response and does not follow p53-mediated p21 induction.
• C: Mismatch repair enzyme inactivation is not a
downstream effect of acute p53/p21 activation.
• D: Receptor tyrosine kinase activation is unrelated to p53-
mediated DNA-damage checkpoints.
Teaching Point
p53 → p21 → G1 arrest: allows repair or triggers apoptosis if
damage persists.
Citation
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.). Ch. 1.
,2
Reference
Ch. 1 — The Genome
Question Stem
A colon cancer specimen displays high microsatellite instability
(MSI) with numerous insertion/deletion mutations. Which
defect best explains this molecular pattern?
Options
A. Defective nucleotide excision repair
B. Defective mismatch repair (MMR) system
C. Loss of base excision repair enzymes
D. Hyperactivation of homologous recombination
Correct Answer
B
Rationales
• B (correct): MSI with repetitive-sequence changes is
characteristic of mismatch repair deficiency, which fails to
correct replication slippage in microsatellites.
• A: Nucleotide excision repair defects produce bulky adduct
accumulation (e.g., UV damage), not MSI.
• C: Base excision repair repairs small base lesions (e.g.,
deamination), not microsatellite slippage.
• D: Homologous recombination hyperactivation would alter
double-strand break repair patterns, not produce MSI.
, Teaching Point
Mismatch repair deficiency → microsatellite instability →
accumulation of insertion/deletion mutations.
Citation
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.). Ch. 1.
3
Reference
Ch. 1 — The Genome
Question Stem
A tumor suppressor gene shows low mRNA expression despite
an intact coding sequence on genomic sequencing. Bisulfite
sequencing reveals heavy promoter CpG methylation. Which
mechanism explains the decreased expression?
Options
A. Frameshift mutation in an exon
B. Epigenetic promoter methylation causing transcriptional
silencing
C. Loss of ribosomal RNA synthesis
D. Increased ubiquitin-mediated degradation of the protein
Correct Answer
B
Rationales
