Robbins Basic Pathology
10th Edition
Author(s)Vinay Kumar; Abul K. Abbas;
Jon C. Aster
TEST BANK
Reference – Ch. 1 — The Cell as a Unit of Health and Disease —
The Genome
Question Stem
A 42-year-old patient’s tumor shows loss of heterozygosity
(LOH) at a tumor suppressor locus. Which mechanism best
explains how LOH promotes neoplastic transformation?
Options
A. Increased expression of oncogenic microRNAs from the
remaining allele
,B. Complete loss of functional tumor suppressor gene product
due to deletion of the second allele
C. Activation of telomerase leading to chromosomal
stabilization
D. Enhanced DNA repair from compensatory alleles
Correct Answer
B
Rationales
Correct: LOH eliminates the remaining functional allele of a
tumor suppressor gene, producing loss of protein function and
facilitating unchecked cell growth. This is a classic two-hit
mechanism described in Robbins.
A (incorrect): Overexpression of oncogenic microRNAs can
contribute to cancer but LOH specifically denotes loss of the
remaining functional allele, not microRNA upregulation.
C (incorrect): Telomerase activation confers replicative
immortality but is not the immediate result of LOH at a tumor
suppressor locus.
D (incorrect): LOH reduces, not enhances, functional gene
products and typically impairs protective mechanisms rather
than augmenting DNA repair.
Teaching Point
LOH removes the last functional tumor suppressor allele → loss
of growth control.
Citation
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.). Ch. 1.
,2
Reference – Ch. 1 — The Cell as a Unit of Health and Disease —
Cellular Housekeeping
Question Stem
A patient’s biopsy shows accumulation of polyubiquitinated
proteins and dilated endoplasmic reticulum with increased
chaperone expression. Which cellular process is primarily
overwhelmed?
Options
A. Proteasomal degradation (ubiquitin–proteasome system)
B. Autophagy via lysosomal pathways
C. Mitochondrial oxidative phosphorylation
D. DNA mismatch repair
Correct Answer
A
Rationales
Correct: Accumulation of polyubiquitinated proteins indicates
impairment of the ubiquitin–proteasome system, the main
route for selective degradation of misfolded or short-lived
proteins.
B (incorrect): Autophagy degrades bulk cytoplasmic contents
and organelles; polyubiquitination with ER dilation more
specifically implicates proteasomal overload.
C (incorrect): Mitochondrial dysfunction causes energy failure
and ROS but does not directly produce polyubiquitinated
protein accumulation.
D (incorrect): DNA mismatch repair targets nucleotide errors in
, DNA, unrelated to cytoplasmic protein clearance.
Teaching Point
Ubiquitin–proteasome clears misfolded proteins; overload
causes protein aggregation.
Citation
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.). Ch. 1.
3
Reference – Ch. 1 — The Cell as a Unit of Health and Disease —
Cellular Metabolism and Mitochondrial Function
Question Stem
A patient with ischemia-reperfusion injury develops rapid cell
swelling and lactic acidosis. Which mitochondrial event most
directly precipitates these findings?
Options
A. Increased mitochondrial biogenesis
B. Loss of oxidative phosphorylation leading to decreased ATP
generation
C. Upregulation of electron transport chain complexes
D. Enhanced fatty acid β-oxidation
Correct Answer
B
Rationales
Correct: Ischemia impairs mitochondrial oxidative
phosphorylation, producing ATP depletion; ATP deficiency
causes Na⁺/K⁺ pump failure, cellular swelling, and anaerobic
10th Edition
Author(s)Vinay Kumar; Abul K. Abbas;
Jon C. Aster
TEST BANK
Reference – Ch. 1 — The Cell as a Unit of Health and Disease —
The Genome
Question Stem
A 42-year-old patient’s tumor shows loss of heterozygosity
(LOH) at a tumor suppressor locus. Which mechanism best
explains how LOH promotes neoplastic transformation?
Options
A. Increased expression of oncogenic microRNAs from the
remaining allele
,B. Complete loss of functional tumor suppressor gene product
due to deletion of the second allele
C. Activation of telomerase leading to chromosomal
stabilization
D. Enhanced DNA repair from compensatory alleles
Correct Answer
B
Rationales
Correct: LOH eliminates the remaining functional allele of a
tumor suppressor gene, producing loss of protein function and
facilitating unchecked cell growth. This is a classic two-hit
mechanism described in Robbins.
A (incorrect): Overexpression of oncogenic microRNAs can
contribute to cancer but LOH specifically denotes loss of the
remaining functional allele, not microRNA upregulation.
C (incorrect): Telomerase activation confers replicative
immortality but is not the immediate result of LOH at a tumor
suppressor locus.
D (incorrect): LOH reduces, not enhances, functional gene
products and typically impairs protective mechanisms rather
than augmenting DNA repair.
Teaching Point
LOH removes the last functional tumor suppressor allele → loss
of growth control.
Citation
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.). Ch. 1.
,2
Reference – Ch. 1 — The Cell as a Unit of Health and Disease —
Cellular Housekeeping
Question Stem
A patient’s biopsy shows accumulation of polyubiquitinated
proteins and dilated endoplasmic reticulum with increased
chaperone expression. Which cellular process is primarily
overwhelmed?
Options
A. Proteasomal degradation (ubiquitin–proteasome system)
B. Autophagy via lysosomal pathways
C. Mitochondrial oxidative phosphorylation
D. DNA mismatch repair
Correct Answer
A
Rationales
Correct: Accumulation of polyubiquitinated proteins indicates
impairment of the ubiquitin–proteasome system, the main
route for selective degradation of misfolded or short-lived
proteins.
B (incorrect): Autophagy degrades bulk cytoplasmic contents
and organelles; polyubiquitination with ER dilation more
specifically implicates proteasomal overload.
C (incorrect): Mitochondrial dysfunction causes energy failure
and ROS but does not directly produce polyubiquitinated
protein accumulation.
D (incorrect): DNA mismatch repair targets nucleotide errors in
, DNA, unrelated to cytoplasmic protein clearance.
Teaching Point
Ubiquitin–proteasome clears misfolded proteins; overload
causes protein aggregation.
Citation
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.). Ch. 1.
3
Reference – Ch. 1 — The Cell as a Unit of Health and Disease —
Cellular Metabolism and Mitochondrial Function
Question Stem
A patient with ischemia-reperfusion injury develops rapid cell
swelling and lactic acidosis. Which mitochondrial event most
directly precipitates these findings?
Options
A. Increased mitochondrial biogenesis
B. Loss of oxidative phosphorylation leading to decreased ATP
generation
C. Upregulation of electron transport chain complexes
D. Enhanced fatty acid β-oxidation
Correct Answer
B
Rationales
Correct: Ischemia impairs mitochondrial oxidative
phosphorylation, producing ATP depletion; ATP deficiency
causes Na⁺/K⁺ pump failure, cellular swelling, and anaerobic
