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
1. Stem: A 52-year-old patient’s tumor biopsy shows
promoter hypermethylation of a DNA repair gene and loss
of its expression. Which mechanism best explains how this
epigenetic change contributes to tumorigenesis?
A. Promoter methylation increases transcription of
oncogenic microRNAs.
B. Promoter methylation suppresses gene transcription
without altering the DNA sequence.
C. Promoter methylation causes point mutations in the
coding region of the gene.
D. Promoter methylation induces histone acetylation and
chromatin opening.
Correct Answer: B
Rationales:
, • Correct (B): Promoter CpG methylation is an epigenetic
modification that represses transcription by recruiting
repressor proteins and condensing chromatin; silencing
DNA repair genes can increase mutation accumulation and
cancer risk (Robbins Ch.1).
• A: Methylation does not generally increase transcription of
oncogenic microRNAs; it typically represses transcription.
• C: Methylation alters chromatin and transcriptional
activity, not the nucleotide sequence or cause point
mutations directly.
• D: Methylation is associated with chromatin condensation;
histone acetylation instead correlates with chromatin
opening and active transcription.
Teaching Point: Promoter CpG methylation represses gene
expression without changing DNA sequence.
Citation: Robbins & Cotran, 10th Ed., Ch. 1 — The Genome
(Noncoding DNA / Epigenetic regulation).
2. Chapter 1 — The Genome
Stem: A researcher finds elevated levels of a specific
microRNA in a carcinoma; this microRNA reduces
translation of a tumor suppressor mRNA. Which statement
best describes how microRNAs (miRNAs) modulate gene
expression?
A. miRNAs typically bind promoter DNA to prevent
transcription.
, B. miRNAs are translated into small peptides that inhibit
transcription factors.
C. miRNAs base-pair with target mRNAs to inhibit
translation or accelerate degradation.
D. miRNAs permanently change the DNA sequence of
target genes.
Correct Answer: C
Rationales:
• Correct (C): miRNAs function post-transcriptionally by
imperfect base pairing with target mRNAs, leading to
translational repression or mRNA degradation;
dysregulated miRNAs can act as oncogenes or tumor
suppressors (Robbins Ch.1).
• A: miRNAs act on RNA, not by binding DNA promoters to
block transcription.
• B: miRNAs are noncoding RNAs and are not translated
into peptides.
• D: miRNAs modulate gene expression without altering
DNA sequence.
Teaching Point: miRNAs regulate gene expression post-
transcriptionally by targeting mRNAs.
Citation: Robbins & Cotran, 10th Ed., Ch. 1 — The Genome
(Micro-RNA and long noncoding RNA).
, 3. Chapter 1 — The Genome
Stem: A geneticist notes that a patient’s disease risk maps
to a region of noncoding DNA that controls a distant gene’s
transcription. Which regulatory element is most likely
involved?
A. Ribosomal RNA gene cluster
B. Promoter proximal element only
C. Enhancer sequences interacting through chromatin
looping
D. Open reading frame (ORF) of a neighboring gene
Correct Answer: C
Rationales:
• Correct (C): Enhancers are noncoding DNA elements that
can act at a distance via chromatin looping to increase
transcription of target genes; variation in enhancers can
affect disease susceptibility (Robbins Ch.1).
• A: rRNA gene clusters are structural genes for ribosomes,
not long-range regulatory elements for distant genes.
• B: Promoter-proximal elements act close to transcription
start sites, not necessarily at long distances.
• D: An ORF is coding sequence; disease-associated
noncoding regulatory variation is more commonly in
enhancers or promoters.
Teaching Point: Enhancers control distant gene expression via
chromatin looping.
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
1. Stem: A 52-year-old patient’s tumor biopsy shows
promoter hypermethylation of a DNA repair gene and loss
of its expression. Which mechanism best explains how this
epigenetic change contributes to tumorigenesis?
A. Promoter methylation increases transcription of
oncogenic microRNAs.
B. Promoter methylation suppresses gene transcription
without altering the DNA sequence.
C. Promoter methylation causes point mutations in the
coding region of the gene.
D. Promoter methylation induces histone acetylation and
chromatin opening.
Correct Answer: B
Rationales:
, • Correct (B): Promoter CpG methylation is an epigenetic
modification that represses transcription by recruiting
repressor proteins and condensing chromatin; silencing
DNA repair genes can increase mutation accumulation and
cancer risk (Robbins Ch.1).
• A: Methylation does not generally increase transcription of
oncogenic microRNAs; it typically represses transcription.
• C: Methylation alters chromatin and transcriptional
activity, not the nucleotide sequence or cause point
mutations directly.
• D: Methylation is associated with chromatin condensation;
histone acetylation instead correlates with chromatin
opening and active transcription.
Teaching Point: Promoter CpG methylation represses gene
expression without changing DNA sequence.
Citation: Robbins & Cotran, 10th Ed., Ch. 1 — The Genome
(Noncoding DNA / Epigenetic regulation).
2. Chapter 1 — The Genome
Stem: A researcher finds elevated levels of a specific
microRNA in a carcinoma; this microRNA reduces
translation of a tumor suppressor mRNA. Which statement
best describes how microRNAs (miRNAs) modulate gene
expression?
A. miRNAs typically bind promoter DNA to prevent
transcription.
, B. miRNAs are translated into small peptides that inhibit
transcription factors.
C. miRNAs base-pair with target mRNAs to inhibit
translation or accelerate degradation.
D. miRNAs permanently change the DNA sequence of
target genes.
Correct Answer: C
Rationales:
• Correct (C): miRNAs function post-transcriptionally by
imperfect base pairing with target mRNAs, leading to
translational repression or mRNA degradation;
dysregulated miRNAs can act as oncogenes or tumor
suppressors (Robbins Ch.1).
• A: miRNAs act on RNA, not by binding DNA promoters to
block transcription.
• B: miRNAs are noncoding RNAs and are not translated
into peptides.
• D: miRNAs modulate gene expression without altering
DNA sequence.
Teaching Point: miRNAs regulate gene expression post-
transcriptionally by targeting mRNAs.
Citation: Robbins & Cotran, 10th Ed., Ch. 1 — The Genome
(Micro-RNA and long noncoding RNA).
, 3. Chapter 1 — The Genome
Stem: A geneticist notes that a patient’s disease risk maps
to a region of noncoding DNA that controls a distant gene’s
transcription. Which regulatory element is most likely
involved?
A. Ribosomal RNA gene cluster
B. Promoter proximal element only
C. Enhancer sequences interacting through chromatin
looping
D. Open reading frame (ORF) of a neighboring gene
Correct Answer: C
Rationales:
• Correct (C): Enhancers are noncoding DNA elements that
can act at a distance via chromatin looping to increase
transcription of target genes; variation in enhancers can
affect disease susceptibility (Robbins Ch.1).
• A: rRNA gene clusters are structural genes for ribosomes,
not long-range regulatory elements for distant genes.
• B: Promoter-proximal elements act close to transcription
start sites, not necessarily at long distances.
• D: An ORF is coding sequence; disease-associated
noncoding regulatory variation is more commonly in
enhancers or promoters.
Teaching Point: Enhancers control distant gene expression via
chromatin looping.
