Oncopathology Hallmarks of Cancer MCQs | MCQ Quiz | OmpathStudy Kenya

Practice 39 MCQs on Oncopathology Hallmarks of Cancer MCQs with OmpathStudy. Built for Kenyan medical and health students to revise key concepts and prepare...

Questions, Answers & Explanations

  1. Q1. A 45-year-old woman with VHL syndrome develops multiple tumors. Which molecular mechanism explains the angiogenic phenotype in her renal cell carcinomas?

    Answer: Failure of HIF-1α ubiquitination in normoxic conditions

    Explanation: In VHL syndrome, mutated VHL protein cannot bind and ubiquitinate HIF-1α even in normoxic conditions, leading to constitutive HIF-1α stabilization and VEGF transcription, promoting angiogenesis.

  2. Q2. What is the maximum diameter a tumor can reach without developing its own vascular supply?

    Answer: 1-2 mm

    Explanation: Tumors cannot enlarge beyond 1-2 mm in diameter without angiogenesis due to the maximal diffusion distance for oxygen, nutrients, and waste from blood vessels.

  3. Q3. A researcher studying tumor angiogenesis finds that proteolytic cleavage of plasminogen produces a potent angiogenesis inhibitor. Which molecule is formed?

    Answer: Angiostatin

    Explanation: Angiostatin is produced by proteolytic cleavage of plasminogen. Endostatin comes from collagen cleavage, and vasculostatin from transthyretin cleavage.

  4. Q4. Which cell adhesion molecule acts as both an intercellular glue and transmits antigrowth signals by sequestering β-catenin?

    Answer: E-cadherin

    Explanation: E-cadherin functions as an intercellular adhesion molecule and transmits antigrowth signals by sequestering β-catenin. Its function is lost in almost all epithelial cancers.

  5. Q5. A patient with hereditary nonpolyposis colon cancer (HNPCC) develops multiple colonic carcinomas. Which genetic finding characterizes this syndrome?

    Answer: Mismatch repair defects with microsatellite instability

    Explanation: HNPCC is caused by defects in mismatch repair genes, leading to microsatellite instability (MSI) characterized by changes in length of short tandem repeating sequences throughout the genome.

  6. Q6. Normal p53 induces synthesis of which angiogenesis inhibitor?

    Answer: Thrombospondin-1 (TSP-1)

    Explanation: Normal p53 induces synthesis of TSP-1, the prototypical angiogenesis inhibitor, maintaining vascular quiescence in early tumor growth.

  7. Q7. Which enzyme is responsible for cleaving type IV collagen in basement membranes and releasing VEGF from ECM-sequestered pools?

    Answer: MMP-9

    Explanation: MMP-9 is a gelatinase that cleaves type IV collagen of epithelial and vascular basement membranes and stimulates release of VEGF from ECM-sequestered pools.

  8. Q8. A patient with xeroderma pigmentosum develops multiple skin cancers after minimal sun exposure. Which DNA repair pathway is defective?

    Answer: Nucleotide excision repair

    Explanation: Xeroderma pigmentosum involves defects in nucleotide excision repair, leading to inability to repair UV-induced pyrimidine dimers and increased risk of skin cancers.

  9. Q9. Which transcription factors suppress E-cadherin expression, promoting tumor cell invasion?

    Answer: SNAIL and TWIST

    Explanation: SNAIL and TWIST transcription factors suppress E-cadherin expression, leading to loss of intercellular adhesion and promoting tumor cell invasion and metastasis.

  10. Q10. In the Warburg effect, how many ATP molecules are produced per glucose molecule through aerobic glycolysis?

    Explanation: Aerobic glycolysis produces only 2 ATP molecules per glucose molecule, compared to 36 ATP from mitochondrial oxidative phosphorylation, yet supports rapid tumor growth.

  11. Q11. Which imaging modality exploits the Warburg effect to visualize tumors using 18F-fluorodeoxyglucose?

    Answer: PET scan

    Explanation: PET scanning uses 18F-fluorodeoxyglucose, a nonmetabolizable glucose derivative, to visualize the increased glucose uptake characteristic of tumors exhibiting the Warburg effect.

  12. Q12. What is the dual effect of neovascularization on tumor growth?

    Answer: Perfusion supplies nutrients AND newly formed endothelial cells secrete growth factors

    Explanation: Neovascularization has a dual effect: perfusion supplies oxygen and nutrients, while newly formed endothelial cells stimulate tumor growth by secreting growth factors like IGF, PDGF, and GM-CSF.

  13. Q13. A breast cancer patient's tumor shows high expression of CXCR4 and CCR7 receptors. To which organs is this tumor most likely to metastasize based on chemokine ligand expression?

    Answer: Organs expressing CXCL12 and CCL21

    Explanation: Breast cancer cells expressing CXCR4 and CCR7 metastasize to organs highly expressing their ligands (CXCL12 and CCL21), demonstrating organ tropism through chemokine receptor-ligand interactions.

  14. Q14. Which DNA repair genes are mutated in familial breast cancers and are involved in homologous recombination?

    Answer: BRCA1 and BRCA2

    Explanation: BRCA1 and BRCA2 are involved in DNA repair through homologous recombination and are mutated in familial breast cancers, increasing cancer susceptibility.

  15. Q15. In hypoxic conditions within a tumor, what prevents HIF-1α degradation?

    Answer: Lack of oxygen prevents VHL recognition of HIF-1α

    Explanation: In hypoxia, lack of oxygen prevents VHL from recognizing and binding HIF-1α, preventing its ubiquitination and degradation, allowing HIF-1α to translocate to the nucleus and activate VEGF transcription.

  16. Q16. Which of the following best describes the first step in ECM invasion by tumor cells?

    Answer: Loosening of tumor cell-to-cell contacts

    Explanation: The first step in the metastatic cascade is loosening of tumor cell-to-cell contacts, primarily through loss of E-cadherin function, before cells can invade the ECM.

  17. Q17. What happens to normal epithelial cells when they lose adhesion to the ECM?

    Answer: They undergo apoptosis

    Explanation: Loss of adhesion in normal cells leads to induction of apoptosis, while tumor cells are resistant to this form of cell death, allowing them to survive during metastasis.

  18. Q18. Which syndrome is characterized by hypersensitivity to ionizing radiation due to defects in homologous recombination DNA repair?

    Answer: Ataxia-telangiectasia

    Explanation: Ataxia-telangiectasia involves defects in homologous recombination DNA repair and is characterized by hypersensitivity to DNA-damaging agents like ionizing radiation.

  19. Q19. In the multistep carcinogenesis model of colon cancer, which genetic alteration typically occurs FIRST?

    Answer: Inactivation of APC

    Explanation: In colon carcinogenesis, inactivation of the APC tumor suppressor gene typically occurs first, followed by RAS activation, then loss of chromosome 18q, and finally loss of TP53.

  20. Q20. What is the primary reason skeletal muscles are rarely sites of metastasis despite being well vascularized?

    Answer: Nonpermissive microenvironment

    Explanation: Although well vascularized, skeletal muscles provide a nonpermissive microenvironment for tumor cell growth, demonstrating that vascularization alone is insufficient for metastasis.

  21. Q21. Which growth factor/cytokine is secreted by tumor cells to promote their own locomotion in an autocrine manner?

    Answer: Autocrine motility factors

    Explanation: Tumor cells secrete autocrine motility factors that act on themselves to potentiate and direct migration through degraded basement membranes and matrix zones during invasion.

  22. Q22. What is the role of tumor-associated fibroblasts in the tumor microenvironment?

    Answer: They exhibit altered gene expression that can promote tumorigenesis

    Explanation: Tumor-associated fibroblasts exhibit altered expression of genes encoding ECM molecules, proteases, protease inhibitors, and growth factors, actively participating in creating a microenvironment that can promote tumorigenesis.

  23. Q23. In normoxic conditions, what happens to HIF-1α?

    Answer: It is bound by VHL, ubiquitinated, and destroyed

    Explanation: In normoxic settings, VHL protein binds to HIF-1α, leading to its ubiquitination and subsequent destruction, preventing inappropriate angiogenesis activation.

  24. Q24. Which enzyme cleaves collagen to produce endostatin, a potent angiogenesis inhibitor?

    Answer: Proteases acting on collagen

    Explanation: Endostatin is produced by proteolytic cleavage of collagen by various proteases, serving as one of the potent angiogenesis inhibitors that balance pro-angiogenic signals.

  25. Q25. What characterizes tumor vasculature compared to normal vessels?

    Answer: Leaky, dilated with haphazard connections

    Explanation: Tumor vasculature is abnormal, characterized by leaky, dilated vessels with haphazard patterns of connection, unlike the organized structure of normal blood vessels.

  26. Q26. Which mechanism do aggregated tumor cells in the bloodstream use to avoid immune destruction?

    Answer: Adhesion to leukocytes and platelets forming emboli

    Explanation: Tumor cells form emboli by aggregating and adhering to circulating leukocytes and platelets, affording them protection from antitumor host effector cells during circulation.

  27. Q27. What is the significance of the "angiogenic switch" in tumor development?

    Answer: It terminates the stage of vascular quiescence allowing tumor progression

    Explanation: The angiogenic switch terminates the stage of vascular quiescence, allowing tumors that were small or in situ for years to progress by acquiring blood supply through increased angiogenic factors and/or loss of inhibitors.

  28. Q28. Which chronic inflammatory condition of the gastrointestinal tract increases cancer risk through persistent cell proliferation and DNA damage?

    Answer: Ulcerative colitis

    Explanation: Ulcerative colitis increases cancer risk through chronic inflammation causing compensatory proliferation and DNA damage.

  29. Q29. How do inflammatory cells like neutrophils contribute to carcinogenesis?

    Answer: By secreting reactive oxygen species causing DNA damage

    Explanation: Neutrophils and other inflammatory cells contribute to carcinogenesis by secreting reactive oxygen species (ROS), which inflict DNA damage in rapidly dividing cells during chronic inflammation.

  30. Q30. Which enzyme's increased expression in colon cancers has led to research on its inhibitors for cancer prevention?

    Answer: Cyclooxygenase-2 (COX-2)

    Explanation: COX-2 expression is increased in colon cancers and other tumors. It converts arachidonic acid to prostaglandins and is induced by inflammatory stimuli, making COX-2 inhibitors a target for cancer prevention research.

  31. Q31. What finding challenges the traditional theory that metastasis results from random mutation accumulation in tumor subclones?

    Answer: Some primary tumors have gene expression signatures similar to metastases before clinical metastasis

    Explanation: Gene profiling studies show some breast cancers have metastasis-like gene expression signatures in primary tumors before clinical metastasis, suggesting metastatic potential may be an early intrinsic property.

  32. Q32. Which paracrine factor produced by stromal cells binds to receptors on tumor cells to promote motility?

    Answer: Hepatocyte growth factor/scatter factor (HGF/SCF)

    Explanation: HGF/SCF is a paracrine effector of cell motility produced by stromal cells. It binds to receptors on tumor cells and is elevated at advancing edges of invasive tumors.

  33. Q33. Benign tumors of the breast show little activity of which enzyme compared to their malignant counterparts?

    Answer: Type IV collagenase (MMP activity)

    Explanation: Benign tumors show little type IV collagenase activity, whereas their malignant counterparts overexpress this enzyme, which is crucial for basement membrane degradation.

  34. Q34. What is the consequence of MMP-mediated cleavage of basement membrane proteins like collagen IV and laminin?

    Answer: Generation of novel binding sites that stimulate tumor cell migration

    Explanation: MMP-2 and MMP-9 cleavage of collagen IV and laminin generates novel sites that bind to receptors on tumor cells and stimulate migration.

  35. Q35. Which oncogenes and tumor suppressors stimulate glucose uptake and favor aerobic glycolysis in cancer cells?

    Answer: TP53, PTEN, and Akt

    Explanation: TP53, PTEN, and Akt stimulate glucose uptake by affecting glucose transporter proteins and favor aerobic glycolysis (the Warburg effect).

  36. Q36. In the invasion-metastasis cascade, which step must occur before intravasation?

    Answer: Local invasion

    Explanation: The invasion-metastasis cascade follows a specific sequence: local invasion must occur before tumor cells can intravasate into blood and lymph vessels.

  37. Q37. What is the primary function of integrins on normal epithelial cells in relation to the basement membrane?

    Answer: Act as polarized receptors maintaining cells in resting, differentiated state

    Explanation: Normal epithelial cells have integrins at their basal surface for basement membrane components that help maintain cells in a resting, differentiated state.

  38. Q38. Which cleavage products of matrix components have chemotactic activity for tumor cells?

    Answer: Collagen and laminin fragments

    Explanation: Cleavage products of collagen and laminin, along with certain growth factors like IGF-I and IGF-II, have chemotactic activity that directs tumor cell migration.

  39. Q39. What typically happens to the levels of metalloproteinase inhibitors in malignant tumors?

    Answer: They are reduced, tilting balance toward tissue degradation

    Explanation: In malignant tumors, levels of metalloproteinase inhibitors are typically reduced, tilting the balance toward tissue degradation and facilitating invasion.

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