Page 1 of 109
TEST BANK FOR ROBBINS BASIC PATHOLOGY EXAM WITH
VERIFIED ANSWERS DETAILED RATIONALES GRADED A+
Test Bank for Robbins Basic Pathology
SECTION 1: THE CELL AS A UNIT OF HEALTH AND DISEASE (Questions 1–25)
1. A 6-year-old child has extreme freckling and multiple early-onset basal cell carcinomas on
sun-exposed skin. Genetic testing shows defective removal of thymine dimers. Which DNA
repair mechanism is most likely defective?
A) Base excision repair
B) Mismatch repair
C) Nucleotide excision repair
D) Nonhomologous end-joining
Answer: C) Nucleotide excision repair
Rationale: Nucleotide excision repair removes bulky helix-distorting lesions such as UV-induced
thymine dimers; failure leads to mutation accumulation and sunlight-induced skin cancers
(classic xeroderma pigmentosum mechanism). Base excision repair corrects small, non-helix
distortions. Mismatch repair corrects replication base-base mismatches. Nonhomologous end-
joining repairs double-strand breaks.
1|Page
,Page 2 of 109
2. A patient with chronic myeloid leukemia (CML) has a BCR-ABL fusion arising from a
reciprocal translocation. Which mechanism best explains how this translocation drives
malignancy?
A) Loss of a tumor suppressor gene
B) Constitutive activation of a tyrosine kinase
C) Defective DNA mismatch repair
D) Increased mitochondrial ROS production
Answer: B) Constitutive activation of a tyrosine kinase
Rationale: The Philadelphia chromosome t(9;22) creates the BCR-ABL fusion gene, which
encodes a constitutively active tyrosine kinase that drives uncontrolled proliferation. This is a
classic example of an oncogene activated by chromosomal translocation.
3. A 2-year-old boy has recurrent infections and failure to thrive. Genetic testing shows a loss-
of-function mutation in a gene required for DNA repair. Which cellular consequence best
explains increased cancer risk in this patient?
A) Increased mitochondrial ROS production leading to apoptosis
B) Accumulation of mutations from defective DNA repair leading to genomic instability
C) Loss of extracellular matrix proteins causing tissue barrier failure
D) Persistent activation of growth factor receptors causing hypertrophy
Answer: B) Accumulation of mutations from defective DNA repair leading to genomic
instability
Rationale: Defective DNA repair allows mutations to accumulate over time, producing genomic
instability and increasing malignant transformation risk. Robbins emphasizes that accurate
maintenance of the genome prevents mutation accumulation and cancer.
2|Page
,Page 3 of 109
4. A researcher studies long noncoding RNAs (lncRNAs) and finds altered expression in a
tumor. Which functional effect of lncRNA dysregulation is most consistent with tumor
development?
A) Direct coding for oncoproteins
B) Epigenetic regulation of gene expression leading to altered transcriptional programs
C) Increasing mitochondrial ATP production
D) Serving as a structural component of collagen fibers
Answer: B) Epigenetic regulation of gene expression leading to altered transcriptional
programs
Rationale: lncRNAs commonly regulate chromatin state and gene transcription; dysregulation
can change expression of tumor suppressors or oncogenes. lncRNAs do not code for proteins;
they function as regulators rather than direct protein coding sequences.
5. Which of the following best describes the role of the ubiquitin-proteasome system in
cellular function?
A) It synthesizes new proteins
B) It degrades misfolded or damaged proteins
C) It transports proteins across membranes
D) It replicates DNA
Answer: B) It degrades misfolded or damaged proteins
Rationale: The ubiquitin-proteasome system tags misfolded or damaged proteins with ubiquitin
for degradation by the proteasome. This is essential for protein quality control and cellular
homeostasis.
3|Page
, Page 4 of 109
6. A patient with α1-antitrypsin deficiency has a mutation that causes the protein to
accumulate in the endoplasmic reticulum of hepatocytes. Which mechanism best explains the
resulting cell injury?
A) Increased proteasomal degradation
B) Overactive autophagy
C) ER stress from retention of misfolded proteins
D) Increased mitochondrial ATP production
Answer: C) ER stress from retention of misfolded proteins
Rationale: RER retention of misfolded proteins triggers ER stress and cell injury. The Z variant of
α1-antitrypsin accumulates in the ER rather than being secreted, leading to hepatocyte injury
and cirrhosis.
7. Which of the following is a function of the extracellular matrix?
A) Synthesizing proteins
B) Providing structural support and regulating cell behavior
C) Replicating DNA
D) Producing ATP
Answer: B) Providing structural support and regulating cell behavior
Rationale: The extracellular matrix provides mechanical support to tissues, regulates cell
growth, migration, and differentiation, and sequesters growth factors and signaling molecules.
4|Page
TEST BANK FOR ROBBINS BASIC PATHOLOGY EXAM WITH
VERIFIED ANSWERS DETAILED RATIONALES GRADED A+
Test Bank for Robbins Basic Pathology
SECTION 1: THE CELL AS A UNIT OF HEALTH AND DISEASE (Questions 1–25)
1. A 6-year-old child has extreme freckling and multiple early-onset basal cell carcinomas on
sun-exposed skin. Genetic testing shows defective removal of thymine dimers. Which DNA
repair mechanism is most likely defective?
A) Base excision repair
B) Mismatch repair
C) Nucleotide excision repair
D) Nonhomologous end-joining
Answer: C) Nucleotide excision repair
Rationale: Nucleotide excision repair removes bulky helix-distorting lesions such as UV-induced
thymine dimers; failure leads to mutation accumulation and sunlight-induced skin cancers
(classic xeroderma pigmentosum mechanism). Base excision repair corrects small, non-helix
distortions. Mismatch repair corrects replication base-base mismatches. Nonhomologous end-
joining repairs double-strand breaks.
1|Page
,Page 2 of 109
2. A patient with chronic myeloid leukemia (CML) has a BCR-ABL fusion arising from a
reciprocal translocation. Which mechanism best explains how this translocation drives
malignancy?
A) Loss of a tumor suppressor gene
B) Constitutive activation of a tyrosine kinase
C) Defective DNA mismatch repair
D) Increased mitochondrial ROS production
Answer: B) Constitutive activation of a tyrosine kinase
Rationale: The Philadelphia chromosome t(9;22) creates the BCR-ABL fusion gene, which
encodes a constitutively active tyrosine kinase that drives uncontrolled proliferation. This is a
classic example of an oncogene activated by chromosomal translocation.
3. A 2-year-old boy has recurrent infections and failure to thrive. Genetic testing shows a loss-
of-function mutation in a gene required for DNA repair. Which cellular consequence best
explains increased cancer risk in this patient?
A) Increased mitochondrial ROS production leading to apoptosis
B) Accumulation of mutations from defective DNA repair leading to genomic instability
C) Loss of extracellular matrix proteins causing tissue barrier failure
D) Persistent activation of growth factor receptors causing hypertrophy
Answer: B) Accumulation of mutations from defective DNA repair leading to genomic
instability
Rationale: Defective DNA repair allows mutations to accumulate over time, producing genomic
instability and increasing malignant transformation risk. Robbins emphasizes that accurate
maintenance of the genome prevents mutation accumulation and cancer.
2|Page
,Page 3 of 109
4. A researcher studies long noncoding RNAs (lncRNAs) and finds altered expression in a
tumor. Which functional effect of lncRNA dysregulation is most consistent with tumor
development?
A) Direct coding for oncoproteins
B) Epigenetic regulation of gene expression leading to altered transcriptional programs
C) Increasing mitochondrial ATP production
D) Serving as a structural component of collagen fibers
Answer: B) Epigenetic regulation of gene expression leading to altered transcriptional
programs
Rationale: lncRNAs commonly regulate chromatin state and gene transcription; dysregulation
can change expression of tumor suppressors or oncogenes. lncRNAs do not code for proteins;
they function as regulators rather than direct protein coding sequences.
5. Which of the following best describes the role of the ubiquitin-proteasome system in
cellular function?
A) It synthesizes new proteins
B) It degrades misfolded or damaged proteins
C) It transports proteins across membranes
D) It replicates DNA
Answer: B) It degrades misfolded or damaged proteins
Rationale: The ubiquitin-proteasome system tags misfolded or damaged proteins with ubiquitin
for degradation by the proteasome. This is essential for protein quality control and cellular
homeostasis.
3|Page
, Page 4 of 109
6. A patient with α1-antitrypsin deficiency has a mutation that causes the protein to
accumulate in the endoplasmic reticulum of hepatocytes. Which mechanism best explains the
resulting cell injury?
A) Increased proteasomal degradation
B) Overactive autophagy
C) ER stress from retention of misfolded proteins
D) Increased mitochondrial ATP production
Answer: C) ER stress from retention of misfolded proteins
Rationale: RER retention of misfolded proteins triggers ER stress and cell injury. The Z variant of
α1-antitrypsin accumulates in the ER rather than being secreted, leading to hepatocyte injury
and cirrhosis.
7. Which of the following is a function of the extracellular matrix?
A) Synthesizing proteins
B) Providing structural support and regulating cell behavior
C) Replicating DNA
D) Producing ATP
Answer: B) Providing structural support and regulating cell behavior
Rationale: The extracellular matrix provides mechanical support to tissues, regulates cell
growth, migration, and differentiation, and sequesters growth factors and signaling molecules.
4|Page
