Robbins Basic Pathology
10th Edition
Author(s)Vinay Kumar; Abul K. Abbas;
Jon C. Aster
TEST BANK
Reference
Ch. 1 — The Genome
Question Stem
A 48-year-old man’s tumor is found to have a loss-of-
function mutation in TP53. Which cellular consequence
best explains the tumor’s increased genomic instability?
Options
A. Failure of mismatch repair leading to microsatellite
instability
B. Loss of p53-mediated cell-cycle arrest and DNA repair
,after damage
C. Increased activity of telomerase permitting limitless
replication
D. Constitutive activation of receptor tyrosine kinases
driving proliferation
Correct Answer
B
Rationales
Correct (B): p53 normally induces cell-cycle arrest and DNA
repair (or apoptosis) in response to DNA damage. Loss of
p53 removes this checkpoint, allowing cells with damaged
DNA to continue dividing, increasing genomic instability.
Incorrect (A): Mismatch repair defects cause microsatellite
instability but are due to MMR gene loss, not directly TP53
mutation.
Incorrect (C): Telomerase activation maintains telomeres
and supports immortality, but does not explain increased
immediate genomic instability from loss of DNA-damage
checkpoints.
Incorrect (D): Constitutive RTK activation drives
proliferation but is a growth-signal mechanism distinct
from defective DNA damage response caused by TP53 loss.
Teaching Point
p53 enforces DNA-damage checkpoints; its loss permits
replication of damaged genomes.
,Citation (simplified APA)
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.).
Ch. 1.
2
Reference
Ch. 1 — The Genome
Question Stem
A colon cancer specimen shows numerous short repetitive
sequence length changes on PCR of microsatellite loci.
Which defect most likely produced this molecular pattern?
Options
A. Mutation of BRCA1 causing homologous recombination
failure
B. Deficiency of DNA mismatch repair proteins (e.g., MLH1,
MSH2)
C. Overexpression of cyclin D1 causing uncontrolled S-
phase entry
D. Point mutations in TP53 leading to loss of apoptosis
Correct Answer
B
Rationales
Correct (B): Microsatellite instability results from defective
mismatch repair proteins, causing insertion/deletion errors
at repetitive sequences.
, Incorrect (A): BRCA1 defects cause problems with double-
strand break repair (homologous recombination) and
chromosomal instability, not microsatellite instability.
Incorrect (C): Cyclin D1 overexpression affects cell-cycle
regulation but does not produce the specific microsatellite
length changes.
Incorrect (D): TP53 mutations impair DNA-damage
responses, but microsatellite instability is characteristic of
mismatch repair loss.
Teaching Point
MMR deficiency → microsatellite instability (MSI) due to
replication slippage errors.
Citation (simplified APA)
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.).
Ch. 1.
3
Reference
Ch. 1 — Cellular Housekeeping
Question Stem
A patient with α1-antitrypsin (A1AT) deficiency
accumulates misfolded A1AT in hepatocyte ER. Which
intracellular pathway is most responsible for degrading
soluble misfolded proteins and preventing their
accumulation?
10th Edition
Author(s)Vinay Kumar; Abul K. Abbas;
Jon C. Aster
TEST BANK
Reference
Ch. 1 — The Genome
Question Stem
A 48-year-old man’s tumor is found to have a loss-of-
function mutation in TP53. Which cellular consequence
best explains the tumor’s increased genomic instability?
Options
A. Failure of mismatch repair leading to microsatellite
instability
B. Loss of p53-mediated cell-cycle arrest and DNA repair
,after damage
C. Increased activity of telomerase permitting limitless
replication
D. Constitutive activation of receptor tyrosine kinases
driving proliferation
Correct Answer
B
Rationales
Correct (B): p53 normally induces cell-cycle arrest and DNA
repair (or apoptosis) in response to DNA damage. Loss of
p53 removes this checkpoint, allowing cells with damaged
DNA to continue dividing, increasing genomic instability.
Incorrect (A): Mismatch repair defects cause microsatellite
instability but are due to MMR gene loss, not directly TP53
mutation.
Incorrect (C): Telomerase activation maintains telomeres
and supports immortality, but does not explain increased
immediate genomic instability from loss of DNA-damage
checkpoints.
Incorrect (D): Constitutive RTK activation drives
proliferation but is a growth-signal mechanism distinct
from defective DNA damage response caused by TP53 loss.
Teaching Point
p53 enforces DNA-damage checkpoints; its loss permits
replication of damaged genomes.
,Citation (simplified APA)
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.).
Ch. 1.
2
Reference
Ch. 1 — The Genome
Question Stem
A colon cancer specimen shows numerous short repetitive
sequence length changes on PCR of microsatellite loci.
Which defect most likely produced this molecular pattern?
Options
A. Mutation of BRCA1 causing homologous recombination
failure
B. Deficiency of DNA mismatch repair proteins (e.g., MLH1,
MSH2)
C. Overexpression of cyclin D1 causing uncontrolled S-
phase entry
D. Point mutations in TP53 leading to loss of apoptosis
Correct Answer
B
Rationales
Correct (B): Microsatellite instability results from defective
mismatch repair proteins, causing insertion/deletion errors
at repetitive sequences.
, Incorrect (A): BRCA1 defects cause problems with double-
strand break repair (homologous recombination) and
chromosomal instability, not microsatellite instability.
Incorrect (C): Cyclin D1 overexpression affects cell-cycle
regulation but does not produce the specific microsatellite
length changes.
Incorrect (D): TP53 mutations impair DNA-damage
responses, but microsatellite instability is characteristic of
mismatch repair loss.
Teaching Point
MMR deficiency → microsatellite instability (MSI) due to
replication slippage errors.
Citation (simplified APA)
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.).
Ch. 1.
3
Reference
Ch. 1 — Cellular Housekeeping
Question Stem
A patient with α1-antitrypsin (A1AT) deficiency
accumulates misfolded A1AT in hepatocyte ER. Which
intracellular pathway is most responsible for degrading
soluble misfolded proteins and preventing their
accumulation?
