ONCOPATHOLOGY - SHORT ANSWER QUESTIONS OmpathStudy

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 (4 Questions) 53. What is genomic instability and how does it enable malignancy? Give examples of syndromes. 54. Explain tumor-promoting inflammation in two different settings. 55. Describe the link between chronic inflammation and cancer development. 56. What is the clinical significance of COX-2 in cancer? --- SECTION I: MULTISTEP CARCINOGENESIS