ONCOPATHOLOGY MCQ EXAMINATION HAllmarks of Cancer 1,2 &3 – 67 MCQs | Kenya MBChB

67 Year 3: General Pathology exam questions on ONCOPATHOLOGY MCQ EXAMINATION HAllmarks of Cancer 1,2 &3 for medical students. Includes MCQs, answers, explan

This MCQ set contains 67 questions on ONCOPATHOLOGY MCQ EXAMINATION HAllmarks of Cancer 1,2 &3 in the Year 3: General Pathology unit. Each question includes the correct answer and a detailed explanation for active recall and exam preparation.

Q1: A patient with familial retinoblastoma develops bilateral tumors at age 3. According to Knudson's hypothesis, what distinguishes this presentation from sporadic cases?

  1. A. Both hits occur simultaneously in germline cells
  2. B. The first mutation is inherited, requiring only one somatic hit
  3. C. Three hits are required instead of two
  4. D. The RB gene is located on a different chromosome
  5. E. , so only one additional somatic mutation is neede

Correct answer: B – The first mutation is inherited, requiring only one somatic hit

In familial retinoblastoma, one mutation is inherited (germline), so only one additional somatic mutation is needed. Sporadic cases require both mutations to occur somatically in the same cell.

Q2: Which event would MOST effectively prevent E2F-mediated transcription of S-phase genes?

  1. A. Activation of CDK2-cyclin E complex
  2. B. Hyperphosphorylation of RB protein
  3. C. Hypophosphorylation of RB protein
  4. D. Degradation of p21 protein
  5. E.

Correct answer: C – Hypophosphorylation of RB protein

Hypophosphorylated RB binds to and sequesters E2F, preventing transcription. Hyperphosphorylation releases E2F, allowing transcription to proceed.

Q3: A tumor shows constitutive activation of growth signaling despite absence of growth factors. Which mechanism is LEAST likely responsible?

  1. A. Loss of p53 function
  2. B. Receptor dimerization without ligand binding
  3. C. Autocrine production of growth factors
  4. D. Activating RAS mutations

Correct answer: A – Loss of p53 function

Loss of p53 primarily affects cell cycle checkpoints and apoptosis, not growth factor signaling. The other options directly cause self-sufficiency in growth signals.

Q4: In chronic myeloid leukemia, the BCR-ABL fusion protein drives malignancy primarily by

  1. A. Enhancing DNA repair mechanisms
  2. B. Increasing p53-mediated apoptosis
  3. C. Constitutive tyrosine kinase activity without regulation
  4. D. Blocking cyclin D synthesis

Correct answer: C – Constitutive tyrosine kinase activity without regulation

The BCR-ABL fusion results from t(9;22) translocation and causes loss of the regulatory region controlling tyrosine kinase activity, leading to continuous mitogenic signaling.

Q5: A researcher observes that tumor cells continue dividing despite contact with neighboring cells. Which protein's function is most likely compromised?

  1. A. VEGF
  2. B. E-cadherin
  3. C. β-catenin
  4. D. MYC oncogene

Correct answer: B – E-cadherin

E-cadherin mediates contact inhibition. Its loss allows cancer cells to pile on top of each other and continue dividing despite cell-cell contact.

Q6: Why must BOTH copies of a tumor suppressor gene be lost for tumor development, unlike oncogenes which require mutation of only one allele?

  1. A. Tumor suppressors are always X-linked
  2. B. The remaining normal allele can still produce functional protein
  3. C. Oncogenes have higher mutation rates
  4. D. Tumor suppressors require post-translational modification

Correct answer: B – The remaining normal allele can still produce functional protein

This follows Knudson's two-hit hypothesis. One functional copy of a tumor suppressor gene is sufficient for normal function, so both must be lost. Oncogenes are gain-of-function mutations where one mutant copy is sufficient.

Q7: Which statement BEST explains why p53 is called the 'guardian of the genome'?

  1. A. It directly repairs DNA damage
  2. B. It only functions in DNA synthesis phase
  3. C. It monitors cellular stress and coordinates cell cycle arrest or apoptosis
  4. D. It prevents all mutations from occurring
  5. E. It doesn't repair DNA directly but coordinates the response.

Correct answer: C – It monitors cellular stress and coordinates cell cycle arrest or apoptosis

p53 acts as a central stress monitor that can activate pathways for DNA repair, cell cycle arrest, senescence, or apoptosis depending on the severity of damage. It doesn't repair DNA directly but coordinates the response.

Q8: In pancreatic cancer, TGF-β pathway mutations are found in 100% of cases. However, in late-stage tumors, intact TGF-β signaling promotes metastasis. This apparent contradiction occurs because

  1. A. TGF-β always promotes tumor growth
  2. B. TGF-β switches from growth inhibition to promoting EMT and invasion
  3. C. Late-stage tumors revert their mutations
  4. D. Early and late-stage tumors are genetically unrelated

Correct answer: B – TGF-β switches from growth inhibition to promoting EMT and invasion

TGF-β has dual roles: in normal/early cancer cells it inhibits growth, but in late-stage tumors it can activate epithelial-to-mesenchymal transition (EMT), promoting migration and metastasis.

Q9: A patient with Li-Fraumeni syndrome develops multiple tumors at young age. The inherited defect most likely involves

  1. A. Both alleles of RB gene
  2. B. One allele of TP53 gene
  3. C. Activation of RAS oncogene
  4. D. Loss of E-cadherin expression
  5. E. The second hit occurs somatically, leading to multiple tumor types at young age due to loss of this critical tumor suppressor.

Correct answer: B – One allele of TP53 gene

Li-Fraumeni syndrome involves germline mutation of one TP53 allele. The second hit occurs somatically, leading to multiple tumor types at young age due to loss of this critical tumor suppressor.

Q10: During mitosis, which cyclin-CDK complex is responsible for nuclear membrane breakdown?

  1. A. Cyclin D-CDK4
  2. B. Cyclin A-CDK2
  3. C. Cyclin B-CDK1
  4. D. Cyclin E-CDK2

Correct answer: C – Cyclin B-CDK1

Cyclin B-CDK1 complex is activated by protein phosphatase at the G2/M transition and causes nuclear membrane breakdown, initiating mitosis.

Q11: Which scenario would MOST likely result in failed DNA damage repair followed by apoptosis?

  1. A. Normal p53 with minor DNA damage
  2. B. Mutated p53 with extensive DNA damage
  3. C. Normal p53 with irreparable DNA damage
  4. D. Overexpression of BCL2 with DNA damage
  5. E. Mutated p53 fails to trigger apoptosis even with extensive damag

Correct answer: C – Normal p53 with irreparable DNA damage

Normal p53 can induce apoptosis when DNA damage is irreparable. Mutated p53 fails to trigger apoptosis even with extensive damage. BCL2 overexpression blocks apoptosis.

Q12: A tumor shows loss of APC function. What is the immediate downstream effect?

  1. A. Increased p53 activation
  2. B. Nuclear accumulation of β-catenin acting as transcription factor
  3. C. Enhanced E-cadherin expression
  4. D. Decreased cyclin D levels

Correct answer: B – Nuclear accumulation of β-catenin acting as transcription factor

APC normally promotes β-catenin degradation. Loss of APC leads to β-catenin accumulation and nuclear translocation, where it acts as a growth-promoting transcription factor.

Q13: Why do HPV oncoproteins preferentially target both RB and p53 proteins?

  1. A. These are the only tumor suppressors in cells
  2. B. Inactivating both allows bypass of major cell cycle checkpoints
  3. C. They are structurally similar proteins
  4. D. This occurs accidentally without selective advantage

Correct answer: B – Inactivating both allows bypass of major cell cycle checkpoints

RB controls the G1/S checkpoint while p53 controls multiple checkpoints and apoptosis. Inactivating both allows the virus to drive cell proliferation while evading protective mechanisms.

Q14: A researcher finds that tumor cells produce the same growth factor for which they express receptors. This exemplifies which hallmark of cancer?

  1. A. Insensitivity to growth inhibitory signals
  2. B. Evasion of apoptosis
  3. C. Self-sufficiency in growth signals
  4. D. Limitless replicative potential

Correct answer: C – Self-sufficiency in growth signals

Autocrine signaling (producing growth factors for one's own receptors) is a classic mechanism of self-sufficiency in growth signals, eliminating dependence on external growth factors.

Q15: What is the functional significance of cyclin D appearing in mid-G1 phase?

  1. A. It terminates the cell cycle
  2. B. It initiates RB phosphorylation to progress toward S phase
  3. C. It directly synthesizes DNA
  4. D. It prevents mitosis
  5. E. This is the first critical step in committing the cell to proceed through the restriction point toward S phase.

Correct answer: B – It initiates RB phosphorylation to progress toward S phase

Cyclin D binds CDK4 to form a complex that phosphorylates RB. This is the first critical step in committing the cell to proceed through the restriction point toward S phase.

Q16: Which mechanism does NOT contribute to the 'angiogenic switch' in tumors?

  1. A. Hypoxia-induced HIF-1α stabilization
  2. B. Loss of p53 reducing TSP-1 production
  3. C. Enhanced E-cadherin expression
  4. D. Increased VEGF production

Correct answer: C – Enhanced E-cadherin expression

E-cadherin is involved in cell-cell adhesion and contact inhibition, not angiogenesis. The other options all promote the angiogenic switch by increasing pro-angiogenic factors or decreasing inhibitors.

Q17: Patients with xeroderma pigmentosum develop skin cancers primarily because

  1. A. They have enhanced RAS signaling
  2. B. They cannot repair UV-induced pyrimidine dimers
  3. C. They have inherited activated oncogenes
  4. D. They overproduce growth factors

Correct answer: B – They cannot repair UV-induced pyrimidine dimers

Xeroderma pigmentosum involves defects in nucleotide excision repair, preventing repair of UV-induced pyrimidine dimers in DNA, leading to accumulation of mutations and skin cancer.

Q18: In von Hippel-Lindau (VHL) syndrome, loss of VHL protein function leads to cancer primarily through

  1. A. Direct activation of oncogenes
  2. B. Stabilization of HIF-1α and increased VEGF transcription
  3. C. Inhibition of DNA repair
  4. D. Enhanced p53 degradation

Correct answer: B – Stabilization of HIF-1α and increased VEGF transcription

VHL normally targets HIF-1α for degradation in normoxic conditions. Loss of VHL leads to HIF-1α accumulation, nuclear translocation, and transcription of pro-angiogenic genes like VEGF.

Q19: The "point of no return" in the cell cycle, after which cells are committed to division, occurs at

  1. A. G2/M checkpoint
  2. B. M phase
  3. C. G1/S transition
  4. D. G0 phase
  5. E.

Correct answer: C – G1/S transition

The G1/S transition (restriction point) is the critical decision point. Once cells pass this checkpoint, they are committed to completing the cell cycle.

Q20: A tumor measuring 3 mm in diameter shows areas of necrosis in its center. This observation suggests

  1. A. Enhanced apoptosis machinery
  2. B. Failure to induce angiogenesis beyond 1-2 mm diameter
  3. C. Excessive growth factor production
  4. D. Loss of cell-cell adhesion

Correct answer: B – Failure to induce angiogenesis beyond 1-2 mm diameter

Tumors cannot grow beyond 1-2 mm without angiogenesis due to the limited diffusion distance of oxygen and nutrients. Central necrosis indicates inadequate vascularization.

Q21: What distinguishes proto-oncogenes from oncogenes?

  1. A. Proto-oncogenes are viral in origin
  2. B. Proto-oncogenes are normal genes; oncogenes are mutated versions
  3. C. Proto-oncogenes suppress growth
  4. D. Oncogenes are always inherited

Correct answer: B – Proto-oncogenes are normal genes; oncogenes are mutated versions

Proto-oncogenes are normal cellular genes that regulate cell proliferation and differentiation. Oncogenes are mutated or overexpressed versions that promote uncontrolled growth.

Q22: In familial adenomatous polyposis syndrome, hundreds of colonic polyps develop due to

  1. A. Germline mutation in one APC allele plus somatic loss of the second
  2. B. Activation of RAS in every polyp
  3. C. Loss of p53 in colonic epithelium
  4. D. Inherited BCR-ABL fusion gene

Correct answer: A – Germline mutation in one APC allele plus somatic loss of the second

FAP follows the two-hit hypothesis for tumor suppressors. Patients inherit one mutant APC allele, and sporadic loss of the second allele in individual cells leads to multiple polyps.

Q23: The Warburg effect refers to cancer cells'

  1. A. Dependence on oxidative phosphorylation
  2. B. Preference for aerobic glycolysis despite oxygen availability
  3. C. Inability to use glucose
  4. D. Enhanced mitochondrial function

Correct answer: B – Preference for aerobic glycolysis despite oxygen availability

The Warburg effect (aerobic glycolysis) involves cancer cells using glycolysis even when oxygen is available, sacrificing ATP efficiency for rapid biomass production to support proliferation.

Q24: Which statement about the G2/M checkpoint is correct?

  1. A. It monitors DNA damage before S phase
  2. B. It checks completion of DNA replication before mitosis
  3. C. It is controlled exclusively by p53
  4. D. It prevents RB phosphorylation

Correct answer: B – It checks completion of DNA replication before mitosis

The G2/M checkpoint ensures DNA replication is complete and checks for DNA damage before allowing the cell to enter mitosis. Defects lead to chromosomal abnormalities.

Q25: p21, p27, and p57 belong to which family of cell cycle regulators?

  1. A. Cyclins
  2. B. CDKs
  3. C. Cip/Kip family of CDK inhibitors
  4. D. INK4/ARF family

Correct answer: C – Cip/Kip family of CDK inhibitors

p21, p27, and p57 are members of the Cip/Kip family of CDK inhibitors that bind and inactivate cyclin-CDK complexes. p21 is transcriptionally activated by p53.

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