Robbins & Cotran 10th Ed. Pathology Test Bank | Chapter-
by-Chapter Questions & Verified Solutions
Robbins & Cotran Pathologic Basis of Disease
10th Edition
• Author(s)Vinay Kumar; Abul K. Abbas; Jon C. Aster
Chapter 1 — The Genome
Question: A 28-year-old woman planning pregnancy asks about
how environmental mutagens could affect her future child.
Which mechanism best explains how a mutagen in her somatic
tissues could not directly cause a heritable change in the
embryo?
A. Mutations in somatic cells are not transmitted through the
germline.
B. DNA repair mechanisms in zygotes correct all parental
mutations.
C. Mitochondrial DNA from the father prevents transmission of
maternal genomic mutations.
D. Somatic mutations are always dominant and lethal before
reproduction.
,Correct Answer: A
Rationales:
• A (Correct): Robbins states that only mutations in germ
cells (sperm or ova) can be inherited; somatic cell
mutations affect only the individual and are not passed to
offspring.
• B: Zygotes have repair systems but they do not guarantee
correction of all parental mutations; some inherited
mutations persist.
• C: Mitochondrial DNA is maternally inherited and does not
prevent transmission of nuclear genomic mutations;
paternal mitochondria are usually not transmitted.
• D: Somatic mutations vary widely; many are neutral or
sublethal and do not prevent reproduction.
Teaching Point: Only germline (not somatic) mutations are
heritable.
Citation: Robbins 10th Ed., Chapter 1 — The Genome
2. Chapter 1 — The Genome
Question: A patient’s tumor genomic analysis shows
widespread cytosine methylation at promoter CpG islands of a
tumor-suppressor gene. Which consequence best explains how
this epigenetic change promotes tumorigenesis?
A. Increased DNA replication fidelity of the gene
,B. Transcriptional silencing of the tumor-suppressor gene
C. Conversion of cytosine to thymine increasing mutation rate
D. Enhanced degradation of the gene’s mRNA transcripts
Correct Answer: B
Rationales:
• B (Correct): Robbins explains promoter CpG island
hypermethylation leads to chromatin condensation and
transcriptional silencing of tumor-suppressor genes,
contributing to cancer.
• A: Methylation does not increase replication fidelity; it
alters transcriptional activity.
• C: Spontaneous deamination of methyl-cytosine can
increase mutation risk but methylation’s principal
tumorigenic effect is silencing, not direct C→T conversion.
• D: Methylation primarily affects transcription initiation
rather than post-transcriptional mRNA degradation.
Teaching Point: Promoter hypermethylation silences tumor-
suppressor genes and can drive cancer.
Citation: Robbins 10th Ed., Chapter 1 — The Genome
(epigenetic regulation)
3. Chapter 1 — Cellular Housekeeping
Question: A 55-year-old man with chronic alcohol use develops
macrocytosis and elevated hepatic lipids. Dysfunction in which
, intracellular system most likely accounts for accumulation of
misfolded proteins and lipid droplets in hepatocytes?
A. Ubiquitin–proteasome pathway
B. Lysosomal hydrolases via autophagy
C. Endoplasmic reticulum–associated degradation (ERAD) and
unfolded protein response
D. Mitochondrial fusion–fission dynamics
Correct Answer: C
Rationales:
• C (Correct): Robbins describes ER stress and impaired
ERAD/unfolded protein response causing accumulation of
misfolded proteins and contributing to steatosis in
hepatocytes under toxic stress (e.g., alcohol).
• A: The ubiquitin–proteasome pathway degrades many
proteins, but ERAD is the specific mechanism for proteins
misfolded in the ER.
• B: Lysosomal autophagy removes organelles and proteins,
but accumulation from ER stress implicates ERAD/UPR
pathways first.
• D: Mitochondrial dynamics affect energy and apoptosis,
not primarily ER protein folding and lipid droplet
formation.
Teaching Point: ER stress and defective ERAD/UPR cause
accumulation of misfolded proteins and can promote steatosis.
by-Chapter Questions & Verified Solutions
Robbins & Cotran Pathologic Basis of Disease
10th Edition
• Author(s)Vinay Kumar; Abul K. Abbas; Jon C. Aster
Chapter 1 — The Genome
Question: A 28-year-old woman planning pregnancy asks about
how environmental mutagens could affect her future child.
Which mechanism best explains how a mutagen in her somatic
tissues could not directly cause a heritable change in the
embryo?
A. Mutations in somatic cells are not transmitted through the
germline.
B. DNA repair mechanisms in zygotes correct all parental
mutations.
C. Mitochondrial DNA from the father prevents transmission of
maternal genomic mutations.
D. Somatic mutations are always dominant and lethal before
reproduction.
,Correct Answer: A
Rationales:
• A (Correct): Robbins states that only mutations in germ
cells (sperm or ova) can be inherited; somatic cell
mutations affect only the individual and are not passed to
offspring.
• B: Zygotes have repair systems but they do not guarantee
correction of all parental mutations; some inherited
mutations persist.
• C: Mitochondrial DNA is maternally inherited and does not
prevent transmission of nuclear genomic mutations;
paternal mitochondria are usually not transmitted.
• D: Somatic mutations vary widely; many are neutral or
sublethal and do not prevent reproduction.
Teaching Point: Only germline (not somatic) mutations are
heritable.
Citation: Robbins 10th Ed., Chapter 1 — The Genome
2. Chapter 1 — The Genome
Question: A patient’s tumor genomic analysis shows
widespread cytosine methylation at promoter CpG islands of a
tumor-suppressor gene. Which consequence best explains how
this epigenetic change promotes tumorigenesis?
A. Increased DNA replication fidelity of the gene
,B. Transcriptional silencing of the tumor-suppressor gene
C. Conversion of cytosine to thymine increasing mutation rate
D. Enhanced degradation of the gene’s mRNA transcripts
Correct Answer: B
Rationales:
• B (Correct): Robbins explains promoter CpG island
hypermethylation leads to chromatin condensation and
transcriptional silencing of tumor-suppressor genes,
contributing to cancer.
• A: Methylation does not increase replication fidelity; it
alters transcriptional activity.
• C: Spontaneous deamination of methyl-cytosine can
increase mutation risk but methylation’s principal
tumorigenic effect is silencing, not direct C→T conversion.
• D: Methylation primarily affects transcription initiation
rather than post-transcriptional mRNA degradation.
Teaching Point: Promoter hypermethylation silences tumor-
suppressor genes and can drive cancer.
Citation: Robbins 10th Ed., Chapter 1 — The Genome
(epigenetic regulation)
3. Chapter 1 — Cellular Housekeeping
Question: A 55-year-old man with chronic alcohol use develops
macrocytosis and elevated hepatic lipids. Dysfunction in which
, intracellular system most likely accounts for accumulation of
misfolded proteins and lipid droplets in hepatocytes?
A. Ubiquitin–proteasome pathway
B. Lysosomal hydrolases via autophagy
C. Endoplasmic reticulum–associated degradation (ERAD) and
unfolded protein response
D. Mitochondrial fusion–fission dynamics
Correct Answer: C
Rationales:
• C (Correct): Robbins describes ER stress and impaired
ERAD/unfolded protein response causing accumulation of
misfolded proteins and contributing to steatosis in
hepatocytes under toxic stress (e.g., alcohol).
• A: The ubiquitin–proteasome pathway degrades many
proteins, but ERAD is the specific mechanism for proteins
misfolded in the ER.
• B: Lysosomal autophagy removes organelles and proteins,
but accumulation from ER stress implicates ERAD/UPR
pathways first.
• D: Mitochondrial dynamics affect energy and apoptosis,
not primarily ER protein folding and lipid droplet
formation.
Teaching Point: ER stress and defective ERAD/UPR cause
accumulation of misfolded proteins and can promote steatosis.
