QCM Part TME PDF

1. Characteris-cs of Cancer Cells (10 Ques-ons) 1. What enables cancer cells to be self-sufficient in growth signals? a. Ability to synthesize their own growth factors. b. Increased apoptosis. c. Upregula:on of an:-apopto:c mediators. d. Ac:va:on of caspases. Answer: a 2. What molecule is downregulate...

1. Characteris-cs of Cancer Cells (10 Ques-ons) 1. What enables cancer cells to be self-sufficient in growth signals? a. Ability to synthesize their own growth factors. b. Increased apoptosis. c. Upregula:on of an:-apopto:c mediators. d. Ac:va:on of caspases. Answer: a 2. What molecule is downregulated in cancer cells, reducing contact inhibi-on? a. TGF-β b. E-cadherin c. Cyclin D d. VEGF Answer: b 3. How do cancer cells evade apoptosis? a. Upregula:on of BH3-only proteins. b. Overexpression of Bcl-2 and downregula:on of Bax and Bak. c. Increased sensi:vity to FasL/FasR signaling. d. Ac:va:on of caspases. Answer: b 4. Which muta-on is commonly found in cancer cells to prevent apoptosis? a. p53 muta:on b. MYC muta:on c. BRCA muta:on d. Telomerase muta:on Answer: a 5. What process enables cancer cells to have limitless replica-ve poten-al? a. Enhanced caspase ac:vity b. Overac:va:on of telomerase reverse transcriptase (TERT) c. Increased E2F ac:vity d. Loss of VEGF signaling Answer: b 6. What is the role of VEGF in cancer? a. Apoptosis regula:on b. Angiogenesis c. Immune suppression d. Cellular differen:a:on Answer: b 7. Which feature dis-nguishes cancer cells as "immortal"? a. Reduced metabolic ac:vity b. Overac:va:on of telomerase c. Upregula:on of Fas receptors d. Increased integrin signaling Answer: b 8. How do cancer cells promote -ssue invasion? a. Through secre:on of matrix metalloproteinases (MMPs). b. By ac:va:ng TERT. c. By enhancing contact inhibi:on. d. By reducing oxida:ve stress. Answer: a 9. What happens when TGF-β signaling is lost in cancer cells? a. Cells become sensi:ve to an:-growth signals. b. E-cadherin levels increase. c. Cells lose their sensi:vity to an:-growth signals. d. Caspase ac:vity increases. Answer: c 10. What pathway is altered in cancer to promote growth signal transduc-on? a. Caspase pathway b. MAPK pathway c. Non-homologous end joining d. DNA mismatch repair Answer: b 2. Deregula-on of Cellular Energe-cs (10 Ques-ons) 11. What is the primary metabolic feature of cancer cells? a. Warburg effect b. Increased OXPHOS ac:vity c. Decreased glycolysis d. Elevated mismatch repair Answer: a 12. What is the main metabolic difference between cancer cells and normal cells? a. Cancer cells produce ATP primarily via glycolysis, even in aerobic condi:ons. b. Cancer cells rely en:rely on OXPHOS for energy produc:on. c. Cancer cells have reduced anabolic processes. d. Cancer cells do not require glucose for survival. Answer: a 13. Which metabolic process is upregulated in cancer cells to support rapid growth? a. Protein synthesis b. Lipid oxida:on c. Apoptosis d. Nucleo:de degrada:on Answer: a 14. Why is the Warburg effect advantageous to cancer cells? a. It is more energy-efficient. b. It supports rapid energy genera:on despite lower efficiency. c. It prevents lactate produc:on. d. It allows for less nutrient uptake. Answer: b 15. What is the major byproduct of cancer cell metabolism under aerobic condi-ons? a. Pyruvate b. Lactate c. ATP d. CO2 Answer: b 16. Which protein is upregulated in cancer cells to enhance glucose uptake? a. GLUT1 b. TGF-β c. MMPs d. Caspases Answer: a 17. What drives the high anabolic ac-vity of cancer cells? a. Reduced mitochondrial ac:vity b. Increased biosynthe:c pathways (e.g., nucleo:de synthesis) c. Elevated p53 levels d. Reduced oxida:ve stress Answer: b 18. Which of the following is NOT a hallmark of cancer cell metabolism? a. Increased anabolic processes b. Preferen:al use of glycolysis c. Decreased ATP demand d. High nutrient uptake Answer: c 19. What adapta-on allows cancer cells to tolerate high ROS levels? a. Elevated HIF-1 signaling b. Enhanced an:oxidant systems c. Suppressed mitochondrial func:on d. Reduced metabolic ac:vity Answer: b 20. Which transcrip-on factor is ac-vated in cancer cells under hypoxia? a. E2F b. HIF-1 c. p53 d. TERT Answer: b 3. Inflamma-on Promo-ng Tumor Growth (10 Ques-ons) 21. What is a major consequence of chronic inflamma-on in cancer? a. Reduced DNA damage b. S:mulated angiogenesis c. Reduced metastasis poten:al d. Increased p53 ac:vity Answer: b 22. Which cells secrete matrix metalloproteinases (MMPs) in the tumor microenvironment? a. Neutrophils b. Fibroblasts c. Cancer cells and inflammatory cells d. T-cells Answer: c 23. Which factor is cons-tu-vely ac-vated in hypoxic cancer environments? a. VEGF b. HIF-1 c. FasL d. Caspases Answer: b 24. Which immune cells play a key role in promo-ng inflamma-on in tumors? a. M1 macrophages b. Regulatory T cells (Tregs) c. B cells d. Neutrophils Answer: a 25. What role does ROS play in cancer progression? a. Promotes DNA stability b. Inhibits cell division c. Causes DNA damage and supports tumor growth d. S:mulates apoptosis Answer: c 4. Immune Cells (10 Ques-ons) 26. What type of immunity involves macrophages and neutrophils? a. Innate immunity b. Adap:ve immunity c. Humoral immunity d. Passive immunity Answer: a 27. Which immune cells are involved in an-gen presenta-on to T cells? a. Neutrophils b. Natural killer (NK) cells c. Dendri:c cells d. B cells Answer: c 28. What is the role of cytotoxic CD8+ T cells in cancer? a. Promote angiogenesis. b. Directly kill tumor cells. c. Induce regulatory T cells (Tregs). d. Suppress an:gen presenta:on. Answer: b 29. How does hypoxia in the tumor microenvironment affect T cells? a. Enhances T cell ac:va:on. b. Promotes T cell exhaus:on. c. Increases cytotoxic ac:vity. d. Reduces regulatory T cells (Tregs). Answer: b 30. What is the role of M1 macrophages in cancer? a. An:-inflammatory, suppor:ng tumor growth. b. Pro-inflammatory, figh:ng tumor progression. c. Promo:ng ECM remodeling. d. Suppressing immune response. Answer: b 31. What phenotype do macrophages switch to in the immunosuppressive tumor microenvironment? a. M0 b. M1 c. M2 d. N1 Answer: c 32. Which immune cells produce specific an-bodies in the adap-ve immune response? a. T cells b. Dendri:c cells c. B cells d. Macrophages Answer: c 33. Which molecule contributes to immune suppression in the tumor microenvironment? a. Interferon-gamma (IFN-γ) b. TGF-β c. Fas ligand (FasL) d. Caspase-3 Answer: b 34. What is the func-on of regulatory T cells (Tregs) in the tumor microenvironment? a. S:mulate cytotoxic T cells. b. Suppress the immune system. c. Promote an:gen presenta:on. d. Ac:vate dendri:c cells. Answer: b 35. What process is mediated by myeloid cells in the early tumor elimina-on phase? a. Immune suppression b. Pro-tumoral response c. An:-tumoral response d. Apoptosis inhibi:on Answer: c 5. Extracellular Matrix (ECM) (10 Ques-ons) 36. What is the primary structural protein in the ECM? a. Fibronec:n b. Elas:n c. Collagen d. Perlecan Answer: c 37. What is the role of matrix metalloproteinases (MMPs) in cancer? a. Repair DNA damage. b. Promote collagen degrada:on and tumor invasion. c. Increase apoptosis. d. Suppress angiogenesis. Answer: b 38. What molecule provides adhesive support in the ECM? a. Heparan sulfate b. Laminin c. Fibronec:n d. Both b and c Answer: d 39. How does the ECM contribute to tumor progression? a. Reduces angiogenesis. b. Prevents immune cell infiltra:on. c. Provides physical support and regulates cellular func:ons. d. Blocks MMP ac:vity. Answer: c 40. What hallmark is associated with cancer-associated fibroblasts (CAFs)? a. Reduced prolifera:on. b. Secre:on of TGF-β and FGF to remodel the ECM. c. Suppression of matrix synthesis. d. Decrease in collagen deposi:on. Answer: b 41. What modifica-on in the ECM prevents immune cell infiltra-on? a. Loss of adhesive proteins. b. Matrix deposi:on and s:ffening by CAFs. c. Upregula:on of integrins. d. Reduced VEGF secre:on. Answer: b 42. Which signaling molecule polarizes fibroblasts into cancer-associated fibroblasts? a. VEGF b. TGF-β c. HIF-1 d. FasL Answer: b 43. What molecule increases ECM s-ffness and promotes tumor growth? a. Fibronec:n b. E-cadherin c. Collagen d. Caspase-3 Answer: c 44. Which ECM component regulates cell communica-on? a. Integrins b. Perlecan c. Laminin d. Glycosaminoglycans Answer: a 45. How does ECM remodeling aid metastasis? a. Enhances M1 macrophage ac:vity. b. Provides haptokine:c cues and creates a path for invasion. c. Blocks VEGF signaling. d. Prevents angiogenesis. Answer: b 6. EMT and Metastasis (5 Ques-ons) 46. What is the key feature of epithelial-to-mesenchymal transi-on (EMT) in cancer? a. Increased E-cadherin expression. b. Loss of cell adhesion and increased mo:lity. c. Reduced collagen synthesis. d. Elevated apoptosis. Answer: b 47. What is the primary driver of EMT in cancer? a. TGF-β signaling b. Caspase ac:va:on c. GLUT1 upregula:on d. CD8+ T cell ac:va:on Answer: a 48. What is the first step in metastasis ager EMT? a. Extravasion b. Intravasion c. Survival in circula:on d. Coloniza:on Answer: b 49. What is the predominant mode of migra-on in solid tumors? a. Mesenchymal migra:on b. Amoeboid migra:on c. Transcoelomic migra:on d. Lympha:c migra:on Answer: a 50. What role do MMPs play in the EMT-to-metastasis transi-on? a. Suppress collagen degrada:on. b. Degrade ECM components to allow tumor cell invasion. c. Promote apoptosis of cancer cells. d. S:mulate E-cadherin expression. Answer: b