QCM TME Quiz PDF

**1. Characteristics of Cancer Cells (10 Questions)** **1. What enables cancer cells to be self-sufficient in growth signals?**\ a. Ability to synthesize their own growth factors.\ b. Increased apoptosis.\ c. Upregulation of anti-apoptotic mediators.\ d. Activation of caspases.\ **Answer:** a **2....

**1. Characteristics of Cancer Cells (10 Questions)** **1. What enables cancer cells to be self-sufficient in growth signals?**\ a. Ability to synthesize their own growth factors.\ b. Increased apoptosis.\ c. Upregulation of anti-apoptotic mediators.\ d. Activation of caspases.\ **Answer:** a **2. What molecule is downregulated in cancer cells, reducing contact inhibition?**\ a. TGF-β\ b. E-cadherin\ c. Cyclin D\ d. VEGF\ **Answer:** b **3. How do cancer cells evade apoptosis?**\ a. Upregulation of BH3-only proteins.\ b. Overexpression of Bcl-2 and downregulation of Bax and Bak.\ c. Increased sensitivity to FasL/FasR signaling.\ d. Activation of caspases.\ **Answer:** b **4. Which mutation is commonly found in cancer cells to prevent apoptosis?**\ a. p53 mutation\ b. MYC mutation\ c. BRCA mutation\ d. Telomerase mutation\ **Answer:** a **5. What process enables cancer cells to have limitless replicative potential?**\ a. Enhanced caspase activity\ b. Overactivation of telomerase reverse transcriptase (TERT)\ c. Increased E2F activity\ d. Loss of VEGF signaling\ **Answer:** b **6. What is the role of VEGF in cancer?**\ a. Apoptosis regulation\ b. Angiogenesis\ c. Immune suppression\ d. Cellular differentiation\ **Answer:** b **7. Which feature distinguishes cancer cells as \"immortal\"?**\ a. Reduced metabolic activity\ b. Overactivation of telomerase\ c. Upregulation of Fas receptors\ d. Increased integrin signaling\ **Answer:** b **8. How do cancer cells promote tissue invasion?**\ a. Through secretion of matrix metalloproteinases (MMPs).\ b. By activating TERT.\ c. By enhancing contact inhibition.\ d. By reducing oxidative stress.\ **Answer:** a **9. What happens when TGF-β signaling is lost in cancer cells?**\ a. Cells become sensitive to anti-growth signals.\ b. E-cadherin levels increase.\ c. Cells lose their sensitivity to anti-growth signals.\ d. Caspase activity increases.\ **Answer:** c **10. What pathway is altered in cancer to promote growth signal transduction?**\ a. Caspase pathway\ b. MAPK pathway\ c. Non-homologous end joining\ d. DNA mismatch repair\ **Answer:** b **2. Deregulation of Cellular Energetics (10 Questions)** **11. What is the primary metabolic feature of cancer cells?**\ a. Warburg effect\ b. Increased OXPHOS activity\ 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 conditions.\ b. Cancer cells rely entirely on OXPHOS for energy production.\ 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 oxidation\ c. Apoptosis\ d. Nucleotide degradation\ **Answer:** a **14. Why is the Warburg effect advantageous to cancer cells?**\ a. It is more energy-efficient.\ b. It supports rapid energy generation despite lower efficiency.\ c. It prevents lactate production.\ d. It allows for less nutrient uptake.\ **Answer:** b **15. What is the major byproduct of cancer cell metabolism under aerobic conditions?**\ 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 activity of cancer cells?**\ a. Reduced mitochondrial activity\ b. Increased biosynthetic pathways (e.g., nucleotide synthesis)\ c. Elevated p53 levels\ d. Reduced oxidative stress\ **Answer:** b **18. Which of the following is NOT a hallmark of cancer cell metabolism?**\ a. Increased anabolic processes\ b. Preferential use of glycolysis\ c. Decreased ATP demand\ d. High nutrient uptake\ **Answer:** c **19. What adaptation allows cancer cells to tolerate high ROS levels?**\ a. Elevated HIF-1 signaling\ b. Enhanced antioxidant systems\ c. Suppressed mitochondrial function\ d. Reduced metabolic activity\ **Answer:** b **20. Which transcription factor is activated in cancer cells under hypoxia?**\ a. E2F\ b. HIF-1\ c. p53\ d. TERT\ **Answer:** b **3. Inflammation Promoting Tumor Growth (10 Questions)** **21. What is a major consequence of chronic inflammation in cancer?**\ a. Reduced DNA damage\ b. Stimulated angiogenesis\ c. Reduced metastasis potential\ d. Increased p53 activity\ **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 constitutively activated in hypoxic cancer environments?**\ a. VEGF\ b. HIF-1\ c. FasL\ d. Caspases\ **Answer:** b **24. Which immune cells play a key role in promoting inflammation 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. Stimulates apoptosis\ **Answer:** c **4. Immune Cells (10 Questions)** **26. What type of immunity involves macrophages and neutrophils?**\ a. Innate immunity\ b. Adaptive immunity\ c. Humoral immunity\ d. Passive immunity\ **Answer:** a **27. Which immune cells are involved in antigen presentation to T cells?**\ a. Neutrophils\ b. Natural killer (NK) cells\ c. Dendritic 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 antigen presentation.\ **Answer:** b **29. How does hypoxia in the tumor microenvironment affect T cells?**\ a. Enhances T cell activation.\ b. Promotes T cell exhaustion.\ c. Increases cytotoxic activity.\ d. Reduces regulatory T cells (Tregs).\ **Answer:** b **30. What is the role of M1 macrophages in cancer?**\ a. Anti-inflammatory, supporting tumor growth.\ b. Pro-inflammatory, fighting tumor progression.\ c. Promoting 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 antibodies in the adaptive immune response?**\ a. T cells\ b. Dendritic 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 function of regulatory T cells (Tregs) in the tumor microenvironment?**\ a. Stimulate cytotoxic T cells.\ b. Suppress the immune system.\ c. Promote antigen presentation.\ d. Activate dendritic cells.\ **Answer:** b **35. What process is mediated by myeloid cells in the early tumor elimination phase?**\ a. Immune suppression\ b. Pro-tumoral response\ c. Anti-tumoral response\ d. Apoptosis inhibition\ **Answer:** c **5. Extracellular Matrix (ECM) (10 Questions)** **36. What is the primary structural protein in the ECM?**\ a. Fibronectin\ b. Elastin\ c. Collagen\ d. Perlecan\ **Answer:** c **37. What is the role of matrix metalloproteinases (MMPs) in cancer?**\ a. Repair DNA damage.\ b. Promote collagen degradation 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. Fibronectin\ d. Both b and c\ **Answer:** d **39. How does the ECM contribute to tumor progression?**\ a. Reduces angiogenesis.\ b. Prevents immune cell infiltration.\ c. Provides physical support and regulates cellular functions.\ d. Blocks MMP activity.\ **Answer:** c **40. What hallmark is associated with cancer-associated fibroblasts (CAFs)?**\ a. Reduced proliferation.\ b. Secretion of TGF-β and FGF to remodel the ECM.\ c. Suppression of matrix synthesis.\ d. Decrease in collagen deposition.\ **Answer:** b **41. What modification in the ECM prevents immune cell infiltration?**\ a. Loss of adhesive proteins.\ b. Matrix deposition and stiffening by CAFs.\ c. Upregulation of integrins.\ d. Reduced VEGF secretion.\ **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 stiffness and promotes tumor growth?**\ a. Fibronectin\ b. E-cadherin\ c. Collagen\ d. Caspase-3\ **Answer:** c **44. Which ECM component regulates cell communication?**\ a. Integrins\ b. Perlecan\ c. Laminin\ d. Glycosaminoglycans\ **Answer:** a **45. How does ECM remodeling aid metastasis?**\ a. Enhances M1 macrophage activity.\ b. Provides haptokinetic cues and creates a path for invasion.\ c. Blocks VEGF signaling.\ d. Prevents angiogenesis.\ **Answer:** b **6. EMT and Metastasis (5 Questions)** **46. What is the key feature of epithelial-to-mesenchymal transition (EMT) in cancer?**\ a. Increased E-cadherin expression.\ b. Loss of cell adhesion and increased motility.\ 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 activation\ c. GLUT1 upregulation\ d. CD8+ T cell activation\ **Answer:** a **48. What is the first step in metastasis after EMT?**\ a. Extravasion\ b. Intravasion\ c. Survival in circulation\ d. Colonization\ **Answer:** b **49. What is the predominant mode of migration in solid tumors?**\ a. Mesenchymal migration\ b. Amoeboid migration\ c. Transcoelomic migration\ d. Lymphatic migration\ **Answer:** a **50. What role do MMPs play in the EMT-to-metastasis transition?**\ a. Suppress collagen degradation.\ b. Degrade ECM components to allow tumor cell invasion.\ c. Promote apoptosis of cancer cells.\ d. Stimulate E-cadherin expression.\ **Answer:** b