ONCOPATHOLOGY - SHORT ANSWER QUESTIONS (SAQs)

## High-Yield Exam-Style Questions --- ## SECTION A: NORMAL CELL CYCLE (8 Questions) **1. Explain the role of RB protein as the "Governor of the Cell Cycle."** **2. Describe how p53 functions as "Guardian of the Genome" in response to DNA damage.** **3. What are the two families of CDK inhibitors and how do they act as tumor suppressors?** **4. Explain the molecular mechanism of the G1/S checkpoint and its importance in cancer prevention.** **5. Describe the sequential activation of cyclins throughout the cell cycle.** **6. How do oncogenic viruses like HPV disable cell cycle checkpoints?** **7. What is the significance of the G2/M checkpoint and what happens when it's defective?** **8. Explain Knudson's "two-hit hypothesis" using retinoblastoma as an example.** --- ## SECTION B: SELF-SUFFICIENCY IN GROWTH SIGNALS (8 Questions) **9. Distinguish between proto-oncogenes, oncogenes, and oncoproteins.** **10. Explain the RAS oncogene: its normal function, mechanism of activation, and effects on cell proliferation.** **11. Describe how cancer cells achieve growth factor independence.** **12. What is the BCR-ABL fusion protein and why is it significant in CML?** **13. Explain the role of MYC oncogene in human cancers.** **14. How do growth factor receptor mutations contribute to oncogenesis? Give examples.** **15. Describe the role of signal-transducing proteins in oncogenesis.** **16. Explain how alterations in cyclins and CDKs contribute to cancer development.** --- ## SECTION C: INSENSITIVITY TO GROWTH INHIBITORY SIGNALS (8 Questions) **17. Compare and contrast oncogenes and tumor suppressor genes.** **18. Explain how RB gene inactivation affects the cell cycle in cancer.** **19. Describe the mechanisms by which p53 prevents cancer development.** **20. What is Li-Fraumeni syndrome and what does it teach us about p53?** **21. Describe the TGF-β pathway and explain its dual role in cancer (tumor suppressor early, tumor promoter late).** **22. Explain the role of APC gene in colorectal cancer development.** **23. How does loss of contact inhibition contribute to cancer? Discuss E-cadherin and NF2.** **24. What is the significance of TP53 being mutated in 70% of cancers?** --- ## SECTION D: EVASION OF APOPTOSIS (6 Questions) **25. Compare and contrast the extrinsic and intrinsic apoptotic pathways.** **26. Explain the role of BCL2 family proteins in regulating apoptosis.** **27. How does p53 induce apoptosis in response to irreparable DNA damage?** **28. Describe the mechanisms by which cancer cells evade apoptosis.** **29. What is the significance of BCL2 translocation t(14;18) in follicular lymphoma?** **30. Explain the concept of "oncogene addiction" and its therapeutic implications.** --- ## SECTION E: LIMITLESS REPLICATIVE POTENTIAL & ANGIOGENESIS (8 Questions) **31. Explain the Hayflick limit and how cancer cells overcome it.** **32. What is telomerase, how is it reactivated in cancer, and why is this significant?** **33. Describe the process of mitotic crisis and its role in tumorigenesis.** **34. Why can't tumors grow beyond 1-2mm without angiogenesis?** **35. What is the "angiogenic switch" and what factors control it?** **36. Explain the role of hypoxia and HIF-1α in tumor angiogenesis. Include VHL in your answer.** **37. What are the characteristics of tumor vasculature and why is it abnormal?** **38. Explain the role of VEGF in tumor angiogenesis and how it's therapeutically targeted.** --- ## SECTION F: INVASION AND METASTASIS (10 Questions) **39. Outline the sequential steps of the invasion-metastasis cascade.** **40. Describe the four steps involved in invasion of the extracellular matrix.** **41. Explain the molecular mechanisms of E-cadherin loss in cancer invasion.** **42. What is epithelial-mesenchymal transition (EMT) and how does it promote metastasis?** **43. Explain the role of matrix metalloproteinases (MMPs) in cancer invasion.** **44. What determines the organ tropism of metastases? Discuss the "seed and soil" hypothesis.** **45. Explain the concept of metastatic inefficiency. Why do so few circulating tumor cells form metastases?** **46. Describe the process of colonization and why it's the rate-limiting step in metastasis.** **47. What is the role of the tumor microenvironment in invasion and metastasis?** **48. Explain how tumor cells survive in the bloodstream.** --- ## SECTION G: REPROGRAMMING ENERGY METABOLISM (4 Questions) **49. Describe the Warburg effect and explain why cancer cells use aerobic glycolysis despite its inefficiency.** **50. What are the advantages of aerobic glycolysis for rapidly proliferating cancer cells?** **51. How do oncogenes (MYC, RAS, AKT) and tumor suppressors (p53, PTEN) regulate the Warburg effect?** **52. Explain how hypoxia and HIF-1α contribute to metabolic reprogramming in cancer.** --- ## SECTION H: IMMUNE EVASION & GENOMIC INSTABILITY (