Oncology Exam Preparation PDF

Mul$ple Choice Ques$ons for Oncology Exam Prepara$on Course 1: Introduc$on to Oncology Q1. What is the primary characteris.c of cancer? A) Controlled division of cells B) Forma.on of benign masses C) Uncontrolled division of cells in specific.ssues or organs D) None of the above A...

Mul$ple Choice Ques$ons for Oncology Exam Prepara$on Course 1: Introduc$on to Oncology Q1. What is the primary characteris.c of cancer? A) Controlled division of cells B) Forma.on of benign masses C) Uncontrolled division of cells in specific.ssues or organs D) None of the above Answer: C Q2. Which of the following are examples of biological carcinogens? A) Tobacco and UV rays B) Viruses, bacteria, and parasites C) Benzene and ionizing radia.on D) Sedentary lifestyle and obesity Answer: B Q3. During the G1/S checkpoint, which of the following processes occurs? A) Centrosome duplica.on B) DNA polymerase ac.va.on C) Check for sufficient nutrients and DNA damage D) Mismatch repair Answer: C Q4. Which mechanism is considered error-prone in DNA repair? A) Homologous recombina.on (HR) B) Mismatch repair (MMR) C) Non-homologous end joining (NHEJ) D) Base excision repair Answer: C Q5. Which statement is true regarding tumor suppressor genes in cancer? A) They are hypoac.vated in cancer. B) They contribute to ac.va.ng cell growth and differen.a.on. C) They are responsible for autosomal recessive inheritance. D) None of the above Answer: B Q6. Which phase of the cell cycle involves DNA replica.on? A) G1 phase B) S phase C) G2 phase D) M phase Answer: B Q7. What is the role of Rb protein in the cell cycle? A) Ac.vates DNA replica.on B) Prevents the progression from G1 to S phase un.l condi.ons are met C) Ini.ates mitosis D) Repairs DNA damage Answer: B Q8. Which DNA repair mechanism uses a complementary strand as a template? A) Non-homologous end joining B) Homologous recombina.on  C) Base excision repair D) Mismatch repair Answer: B Q9. What happens during the M phase of the cell cycle? A) DNA is replicated. B) Chromosomes are segregated into daughter cells. C) Nutrient levels are checked. D) DNA damage is repaired. Answer: B Q10. Which checkpoint ensures that all chromosomes are properly aligned before separa.on? A) G1/S checkpoint B) G2/M checkpoint C) Metaphase to anaphase checkpoint D) DNA damage checkpoint Answer: C... [Ques.ons from Q11-Q32 are unchanged] Q33. What type of cancer is most likely to have a BRCA1 or BRCA2 muta.on? A) Colorectal cancer B) Breast and ovarian cancer C) Lung cancer D) Skin cancer Answer: B Q34. What key feature defines a malignant tumor? A) Limited growth B) Metasta.c poten.al C) Large size D) Benign appearance Answer: B Q35. Which type of therapy uses small molecules or an.bodies to target cancer? A) Chemotherapy B) Targeted therapy C) Hormonal therapy D) Immunotherapy Answer: B Q36. Which cell cycle checkpoint prevents mitosis if DNA is damaged? A) G1/S checkpoint B) G2/M checkpoint C) M checkpoint D) None of the above Answer: B Q37. What characteris.c allows tumors to evade apoptosis? A) Overexpression of Bcl-2 B) Downregula.on of VEGF C) Increased DNA repair D) Reduced angiogenesis Answer: A Q38. Which pathway is commonly ac.vated in cancer to promote growth? A) MAPK pathway B) TGF-β pathway C) P53 pathway D) Nucleo.de synthesis pathway Answer: A Q39. What immune cell type directly kills tumor cells? A) B-cells B) CD8+ T-cells C) Dendri.c cells D) Fibroblasts Answer: B Q40. Which metabolic adapta.on is seen in cancer cells? A) Reliance on oxida.ve phosphoryla.on B) Aerobic glycolysis (Warburg effect) C) Reduc.on in glucose uptake D) Increased reliance on lipids Answer: B Course 1: Introduc$on to Oncology Q1. What is the primary characteris.c of cancer? A) Controlled division of cells B) Forma.on of benign masses C) Uncontrolled division of cells in specific.ssues or organs D) None of the above Answer: C Q2. Which of the following are examples of biological carcinogens? A) Tobacco and UV rays B) Viruses, bacteria, and parasites C) Benzene and ionizing radia.on D) Sedentary lifestyle and obesity Answer: B Q3. During the G1/S checkpoint, which of the following processes occurs? A) Centrosome duplica.on B) DNA polymerase ac.va.on C) Check for sufficient nutrients and DNA damage D) Mismatch repair Answer: C Q4. Which mechanism is considered error-prone in DNA repair? A) Homologous recombina.on (HR) B) Mismatch repair (MMR) C) Non-homologous end joining (NHEJ) D) Base excision repair Answer: C... [Con.nuing un.l Q60] Q61. What is the role of tumor microenvironment in cancer progression? A) Supports immune system ac.va.on B) Provides nutrients and growth signals to tumor cells  C) Eliminates tumor cells via apoptosis D) Reduces angiogenesis Answer: B Q62. Which checkpoint protein is directly involved in preven.ng cell cycle progression with DNA damage? A) Cyclin D B) ATM C) Rb D) p53 Answer: D Q63. What feature allows cancer cells to grow uncontrollably? A) Ac.va.on of p53 B) Loss of contact inhibi.on C) Downregula.on of VEGF D) Overexpression of cytokines Answer: B Q64. How does radia.on therapy work to treat cancer? A) Inhibits angiogenesis B) Induces DNA damage in cancer cells C) Ac.vates immune checkpoints D) Suppresses VEGF secre.on Answer: B Q65. Which of the following is an example of a tumor suppressor gene? A) Ras B) Myc C) p53 D) HER2 Answer: C Q66. What hallmark of cancer involves avoiding immune destruc.on? A) Sustaining prolifera.ve signaling B) Evading growth suppressors C) Ac.va.ng invasion and metastasis D) Evading immune system responses Answer: D Q67. What is the primary purpose of a PET scan in oncology? A) Measure glucose uptake in.ssues B) Assess bone density C) Evaluate cardiac output D) Examine angiogenesis Answer: A Q68. Which type of immunotherapy uses checkpoint inhibitors? A) Monoclonal an.bodies B) CAR-T cell therapy C) Cancer vaccines D) An.-PD-1/PD-L1 therapy Answer: D Q69. What does "angiogenesis" refer to?  A) Forma.on of new blood vessels B) Programmed cell death C) DNA repair mechanisms D) Cell cycle regula.on Answer: A Q70. Which of these cells is part of the adap.ve immune system? A) Macrophages B) Natural killer cells C) B-cells D) Neutrophils Answer: C Q71. Which stage of the immunoedi.ng theory allows tumors to avoid immune destruc.on? A) Elimina.on B) Equilibrium C) Escape D) Dormancy Answer: C Q72. What protein is involved in homologous recombina.on repair? A) Ku proteins B) Cyclin E C) BRCA1 D) ATM Answer: C Q73. What effect does IL-10 have in the tumor microenvironment? A) S.mulates T-cell ac.va.on B) Enhances pro-inflammatory signaling C) Suppresses immune responses D) Induces apoptosis Answer: C Q74. What role do tumor-associated macrophages (TAMs) play in cancer? A) Induce DNA repair B) Promote tumor growth and suppress immune ac.vity C) Facilitate chemotherapy effects D) Increase cytotoxic T-cell ac.vity Answer: B Q75. Which hallmark of cancer is addressed by an.-VEGF therapy? A) Evading growth suppressors B) Sustaining prolifera.ve signaling C) Inducing angiogenesis D) Resis.ng cell death Answer: C Q76. What is a key role of dendri.c cells in cancer immunity? A) Directly killing tumor cells B) Presen.ng an.gens to T-cells C) Producing VEGF D) Inhibi.ng angiogenesis Answer: B Q77. Which cancer treatment uses radia.on to precisely target tumors? A) Hormonal therapy B) Proton therapy C) Immunotherapy D) Chemotherapy Answer: B Q78. Which enzyme unwinds DNA for replica.on? A) DNA polymerase B) Helicase C) Topoisomerase D) Ligase Answer: B Q79. Which process is primarily disrupted in cancers with mismatch repair deficiency? A) DNA transcrip.on B) Double-strand break repair C) Replica.on fidelity D) Chromosome segrega.on Answer: C Q80. What is the mechanism of ac.on of an.-PD-1 an.bodies? A) Block tumor-induced immune suppression B) Induce apoptosis in tumor cells C) Prevent DNA damage D) Promote angiogenesis Answer: A Q81. How do CAR-T cells differ from natural T-cells? A) They require MHC-I for ac.va.on B) They are gene.cally engineered to target specific an.gens C) They are part of the innate immune system D) They inhibit angiogenesis Answer: B Q82. What effect does hypoxia have on the tumor microenvironment? A) Enhances immune cell ac.vity B) Suppresses tumor growth C) Promotes angiogenesis D) Reduces VEGF secre.on Answer: C Q83. What protein complex regulates the G2/M checkpoint? A) Cdk1/Cyclin B B) Rb/E2F C) ATM/ATR D) Cyclin D/Cdk4 Answer: A Q84. What is the significance of neoan.gens in cancer? A) They enhance DNA repair B) They are novel targets for immune recogni.on C) They reduce tumor growth D) They prevent angiogenesis Answer: B Q85. Which therapy directly involves engineered immune cells? A) Chemotherapy B) Radia.on therapy C) CAR-T cell therapy D) Hormonal therapy Answer: C Mul$ple Choice Ques$ons: Course 3 - Introduc$on to Immuno-Oncology Q1. What was the first documented instance of immuniza.on? A) Vaccina.on campaigns by Edward Jenner in 1789 B) Variola.on in 16th century China C) Louis Pasteur’s Germ Theory D) Coley’s toxin Answer: B Q2. What observa.on led William Coley to hypothesize the use of infec.ons to treat cancer? A) Spontaneous tumor remission in an osteosarcoma pa.ent aoer erysipelas infec.on B) Effec.veness of variola.on in China C) Vaccine development by Louis Pasteur D) Improved pa.ent outcomes with an.bio.cs Answer: A Q3. Which theory explains the ability of the immune system to detect and prevent cancerous cells from forming tumors? A) Germ Theory B) Immunosurveillance Theory C) Darwinian Evolu.on D) Immunoedi.ng Theory Answer: B Q4. Who first proposed the immunosurveillance theory? A) Edward Jenner B) William Coley C) P. Ehrlich D) F.M. Burnet Answer: C Q5. Which phase of the immunoedi.ng theory involves the immune system exer.ng selec.ve pressure, leading to tumor dormancy? A) Elimina.on B) Equilibrium C) Escape D) Ini.a.on Answer: B Q6. During the elimina.on phase of immunoedi.ng, which immune system components are primarily involved in eradica.ng tumor cells? A) B-cells and cytokines B) Natural killer cells and T-cells  C) Dendri.c cells and macrophages D) Fibroblasts and endothelial cells Answer: B Q7. What is the significance of neoan.gens in cancer immunity? A) They are derived from normal cell proteins. B) They are unique to tumor cells and help immune cells recognize cancer. C) They suppress T-cell ac.vity. D) They prevent tumor growth. Answer: B Q8. Which immune system reac.on could be a result of misrecogni.on of harmless compounds? A) Autoimmune diseases B) Cytokine storms C) Allergies D) Cancer Answer: C Q9. What occurs during the escape phase of immunoedi.ng? A) The immune system eradicates all cancer cells. B) Cancer cells acquire resistance to immune apacks and grow uncontrollably. C) Immune cells enter a dormant state. D) Tumor cells are eliminated through apoptosis. Answer: B Q10. Which type of immune cells are responsible for presen.ng an.gens to T-cells? A) Dendri.c cells B) Natural killer cells C) B-cells D) Fibroblasts Answer: A Q11. What is a major limita.on of the immunosurveillance theory? A) Lack of evidence for immune cells recognizing tumors B) Difficulty explaining tumor progression in immunocompetent individuals C) Focus on innate immunity over adap.ve immunity D) Inability to explain tumor elimina.on Answer: B Q12. What molecule on tumor cells is essen.al for T-cell recogni.on via TCR? A) Neoan.gen-MHC complex B) Cytokines C) VEGF D) Fas ligand Answer: A Q13. Which of the following is a primary func.on of IFN-γ in tumor immunity? A) Suppress T-cell ac.vity B) Induce tumor cell apoptosis and apract immune cells C) Promote tumor growth D) Inhibit an.gen presenta.on Answer: B Q14. Why is the equilibrium phase ooen silent in terms of clinical symptoms?  A) Tumors are completely eradicated. B) Immune cells maintain a balance with tumor cells, preven.ng significant growth. C) Tumor cells are inac.ve. D) The immune system is suppressed. Answer: B Q15. What feature dis.nguishes adap.ve immunity from innate immunity? A) Rapid response B) Non-specific ac.on C) Memory and specificity for an.gens D) Lack of an.gen presenta.on Answer: C Q16. What role does Darwinian microevolu.on play in cancer progression during the equilibrium phase? A) Tumor cells evolve new mechanisms to evade immune detec.on. B) Tumor cells reduce muta.ons to stabilize growth. C) Immune cells become more aggressive. D) Cancer cells become more suscep.ble to apoptosis. Answer: A Q17. What is the primary danger signal released by cells to apract immune responses to early tumor growth? A) Heat shock proteins and IFN-γ B) TGF-β C) VEGF D) MHC molecules Answer: A Q18. What does Coley’s toxin demonstrate about cancer treatment? A) Infec.ons can boost immune responses against tumors. B) Surgery is the only effec.ve cancer treatment. C) Tumors are resistant to immune-based therapies. D) Toxins inhibit an.gen presenta.on. Answer: A Q19. What is the primary role of the thymus in T-cell development? A) Eliminate self-reac.ve T-cells B) Promote an.gen presenta.on C) Enhance cytokine produc.on D) Suppress immune responses Answer: A Q20. What dis.nguishes innate immunity from adap.ve immunity? A) Involves an.gen presenta.on B) Is slow to respond C) Is immediate and non-specific D) Relies on memory of past infec.ons Answer: C Q1. Which mechanism allows tumors to avoid recogni.on by T-cells? A) Upregula.on of MHC-I molecules B) Downregula.on of MHC-I molecules C) Increased expression of cytokines D) Ac.va.on of Fas receptor Answer: B Q2. How do cancer-associated fibroblasts (CAFs) contribute to immune evasion? A) By producing VEGF B) By secre.ng lactate C) By forming a collagen barrier around the tumor D) By inhibi.ng FasL expression Answer: C Q3. What is the role of VEGF in tumor immune escape? A) Promotes aerobic metabolism B) Enhances T-cell ac.va.on C) Induces angiogenesis and reduces adherence factors on endothelial cells D) Converts M1 macrophages to M2 macrophages Answer: C Q4. How do tumors resist apoptosis mediated by T-cells? A) Downregula.ng Fas and upregula.ng FasL B) Producing VEGF C) Increasing glucose availability D) Inducing NK cell ac.va.on Answer: A Q5. What is a key characteris.c of the Warburg effect in tumors? A) Tumors rely on aerobic metabolism B) Tumors switch to glycolysis even in the presence of oxygen C) Tumors produce excess glucose D) Tumors avoid lactate produc.on Answer: B Q6. Why do immune cells become anergic in the tumor microenvironment? A) Excess glucose availability B) Lack of oxygen and glucose C) Increased VEGF levels D) High FasL expression Answer: B Q7. What is the effect of lactate produc.on by tumors? A) Enhances immune cell ac.vity B) Lowers the pH of the tumor microenvironment, inhibi.ng immune cell func.on C) Promotes T-cell ac.va.on D) Increases oxygen availability Answer: B Q8. How does hypoxia in the tumor microenvironment affect immune cells? A) S.mulates T-cell prolifera.on B) Suppresses immune cell ac.vity C) Enhances an.gen presenta.on D) Increases cytokine produc.on Answer: B Q9. Which cytokine is involved in increasing T-cell sensi.vity to apoptosis? A) IFN-γ B) IL-10 C) TNF-α D) IL-2 Answer: B Q10. What transforma.on occurs in macrophages under tumor-induced condi.ons? A) M2 macrophages become M1 macrophages B) M1 macrophages become M2 macrophages C) T-cells are converted into macrophages D) Natural killer cells are converted into macrophages Answer: B Q11. How do tumors interfere with immune cell naviga.on? A) By secre.ng func.onal chemokine ligands B) By producing nonfunc.onal ligands that block CXCR3 C) By enhancing T-cell receptor ac.vity D) By inhibi.ng an.gen presenta.on Answer: B Q12. What role do regulatory T-cells (Tregs) play in the tumor microenvironment? A) Enhance immune cell ac.vity B) Promote tumor immune suppression C) Inhibit VEGF produc.on D) Convert fibroblasts into CAFs Answer: B Q13. What is the effect of fibroblast conversion into CAFs? A) Enhances an.gen presenta.on B) Inhibits angiogenesis C) Builds a protec.ve barrier around the tumor D) Reduces glucose uptake by tumor cells Answer: C Q14. What happens when CD4 T-cells are converted in the tumor microenvironment? A) They become cytotoxic T-cells B) They transform into regulatory T-cells (Tregs) C) They increase NK cell ac.vity D) They promote VEGF secre.on Answer: B Q15. What mechanism allows tumors to suppress NK cell ac.vity? A) Downregula.on of MHC-I B) Upregula.on of soluble ligands C) Increased Fas expression D) Reduced VEGF levels Answer: B Q16. How do tumors promote the metabolic inhibitory mechanism? A) By ac.va.ng FasL expression B) By increasing lactate produc.on and reducing oxygen availability C) By suppressing VEGF secre.on  D) By enhancing an.gen presenta.on Answer: B Q17. Which immune cells are most affected by glucose deple.on in the tumor microenvironment? A) B-cells B) T-cells C) Natural killer cells D) Macrophages Answer: B Q18. What dual role does the immune system play in cancer development? A) Acts as a suppressor and inducer of tumorigenesis B) Only promotes tumor elimina.on C) Facilitates angiogenesis and metastasis D) Inhibits both angiogenesis and metastasis Answer: A Q19. How do tumors induce apoptosis in immune cells at a distance? A) By downregula.ng MHC-I B) By producing exosomes carrying FasL C) By enhancing an.gen presenta.on D) By increasing glucose levels Answer: B Q20. What is the role of hypoxia in tumor progression? A) Promotes aerobic metabolism B) Suppresses immune cells and enhances angiogenesis C) Reduces VEGF expression D) Increases T-cell ac.vity Answer: B Mul$ple Choice Ques$ons: Course 5 - Studying CAR Ac$vatory Signaling Pathways Q1. What is the primary goal of immunotherapy in cancer treatment? A) Directly kill cancer cells B) Boost the immune system to apack its own cancer cells C) Inhibit angiogenesis D) Prevent metastasis Answer: B Q2. Which type of immunotherapy involves gene.cally engineered T-cells? A) Non-specific immunotherapy B) Cancer vaccines C) Cellular immunotherapy D) Hormonal therapy Answer: C Q3. How do CAR-T cells bypass the issue of tumor MHC-I downregula.on? A) By ac.va.ng NK cells B) By recognizing en.re proteins on tumor cell surfaces C) By inhibi.ng VEGF produc.on D) By increasing cytokine release Answer: B Q4. What was the main limita.on of 1st genera.on CAR-T cells? A) Lack of CD3ζ chains B) Inability to induce cytokine produc.on C) No co-s.mulatory signaling domains D) High persistence in the body Answer: C Q5. What improvement was introduced in 2nd genera.on CAR-T cells? A) Addi.on of CD28 co-s.mulatory domain B) Use of monoclonal an.bodies C) Elimina.on of CD3ζ chains D) Enhanced glycolysis in T-cells Answer: A Q6. Which signaling pathway step is cri.cal for T-cell ac.va.on? A) MHC-I engagement with TCR B) CD3 phosphoryla.on and ZAP70 recruitment C) VEGF secre.on by tumor cells D) Cytokine suppression Answer: B Q7. What is the primary func.on of the LAT-SLP76 signalosome in T-cells? A) Enhance glycolysis B) Suppress immune response C) Amplify T-cell signaling D) Promote angiogenesis Answer: C Q8. Which clinical issue is associated with 2nd genera.on CAR-T cells? A) High toxicity levels B) Poor persistence and sensi.vity to low an.gen levels C) Inability to target liquid tumors D) Overac.va.on of immune responses Answer: B Q9. What was the purpose of introducing the IL-2 receptor domain in 5th genera.on CAR-T cells? A) To enhance glycolysis B) To auto-produce cytokines and boost responses C) To eliminate MHC-I dependency D) To increase an.gen presenta.on Answer: B Q10. What does the term “proof of concept” refer to in 1st genera.on CAR-T cell development? A) It failed in vitro tests but succeeded in clinical trials. B) It demonstrated the poten.al to ac.vate T-cells but had limita.ons. C) It was highly effec.ve in elimina.ng tumors in humans. D) It proved CAR-T cells are more effec.ve than TCRs. Answer: B Q11. Which factor limits CAR-T cell sensi.vity in recognizing tumors with low an.gen levels? A) Absence of CD28 co-s.mula.on B) Reduced LAT signaling assembly  C) High an.gen thresholds required for ac.va.on D) Increased glycolysis by tumor cells Answer: C Q12. What is a major cause of relapse in CAR-T cell therapy? A) Lack of ini.al tumor response B) Tumor an.gen variance with reduced surface expression C) Excessive cytokine produc.on D) High persistence of CAR-T cells Answer: B Q13. Which signaling domain combina.on is found in 2nd genera.on CAR-T cells? A) CD3ζ + CD28 B) CD3ζ + IL-2 C) CD28 + LAT D) CD3ζ + VEGF Answer: A Q14. How does the CAR receptor differ from the TCR? A) CAR recognizes linear an.gens only. B) CAR recognizes en.re proteins on the tumor surface. C) CAR requires MHC-I for ac.va.on. D) CAR ac.va.on does not involve ZAP70. Answer: B Q15. What role does ZAP70 play in T-cell ac.va.on? A) Promotes glycolysis B) Phosphorylates LAT and amplifies signaling C) Inhibits an.gen presenta.on D) Suppresses cytokine release Answer: B Q16. Why did the 1st genera.on CAR-T cells fail in clinical trials? A) They lacked an.gen recogni.on ability. B) They induced excessive toxicity and failed to form memory T-cells. C) They caused rapid tumor progression. D) They targeted healthy cells instead of tumors. Answer: B Q17. What major advancement made 2nd genera.on CAR-T cells more effec.ve? A) Improved targe.ng of solid tumors B) Integra.on of co-s.mulatory signals (Signal 2) C) Elimina.on of cytokine dependence D) Enhanced reliance on VEGF Answer: B Q18. What does LAT phosphoryla.on in CAR-T cells indicate? A) Complete signaling ac.va.on B) Loss of tumor an.gen recogni.on C) Reduced CAR sensi.vity D) Increased VEGF produc.on Answer: A Q19. Why do tumors relapse aoer ini.al CAR-T therapy success? A) CAR-T cells become too persistent.  B) Tumors develop resistance via an.gen downregula.on. C) CAR-T cells induce excessive cytokine produc.on. D) An.gen-presen.ng cells are overac.vated. Answer: B Q20. What is a major challenge in crea.ng next-genera.on CAR-T cells? A) Achieving MHC-independent ac.va.on B) Balancing sensi.vity with safety C) Reducing cytokine dependence D) Elimina.ng VEGF secre.on by tumors Answer: B Q1. What are extracellular vesicles (EVs)? A) Lipid bilayer-enclosed par.cles secreted by cells B) Immune cells specialized in an.gen presenta.on C) Protein aggregates that facilitate tumor growth D) Components of the extracellular matrix Answer: A Q2. What is the primary func.on of extracellular vesicles in cancer? A) Repair DNA damage in tumor cells B) Facilitate communica.on between tumor cells and the microenvironment C) Directly kill immune cells D) Prevent tumor metastasis Answer: B Q3. Which of the following is NOT a subtype of extracellular vesicles? A) Exosomes B) Microvesicles C) Apopto.c bodies D) Lysosomes Answer: D Q4. What is a key role of tumor-derived EVs in cancer progression? A) Suppress tumor growth B) Deliver oncogenic molecules to recipient cells C) Decrease VEGF expression D) Promote DNA repair in immune cells Answer: B Q5. What type of molecules are typically carried by extracellular vesicles? A) Proteins, lipids, and nucleic acids B) Only proteins C) Carbohydrates and oxygen D) DNA repair enzymes Answer: A Q6. Which process is promoted by EVs in the tumor microenvironment? A) Immune cell ac.va.on B) Angiogenesis and metastasis C) Increased DNA stability D) Mitochondrial repair Answer: B Q7. How can EVs act as biomarkers in cancer? A) They reflect the gene.c and proteomic content of the tumor B) They suppress immune responses C) They directly induce apoptosis in cancer cells D) They form part of the extracellular matrix Answer: A Q8. Which technique is commonly used to isolate extracellular vesicles? A) Density gradient centrifuga.on B) Western blot C) Polymerase chain reac.on (PCR) D) CRISPR-Cas9 Answer: A Q9. What role do tumor-derived EVs play in immune modula.on? A) Ac.vate immune checkpoints B) Induce T-cell ac.va.on C) Suppress immune responses by carrying inhibitory molecules D) Enhance an.gen presenta.on Answer: C Q10. What is the size range of exosomes? A) 1-10 nm B) 30-150 nm C) 500-1000 nm D) Greater than 1 micron Answer: B Q11. Which protein marker is typically enriched in exosomes? A) CD63 B) VEGF C) PD-L1 D) Cyclin D Answer: A Q12. How do EVs contribute to the "seed and soil" hypothesis in metastasis? A) By directly ini.a.ng tumor cell death B) By modifying the microenvironment of distant organs to support tumor growth C) By increasing DNA methyla.on in tumor cells D) By enhancing immune cell ac.va.on Answer: B Q13. What dis.nguishes microvesicles from exosomes? A) Microvesicles are larger and bud directly from the plasma membrane. B) Microvesicles are smaller and originate from mul.vesicular bodies. C) Microvesicles carry only proteins, while exosomes carry nucleic acids. D) Microvesicles are secreted by immune cells only. Answer: A Q14. What is the effect of EV-mediated transfer of PD-L1 in cancer? A) Enhances immune cell ac.vity B) Promotes immune evasion by suppressing T-cell func.on C) Induces tumor cell apoptosis D) Increases DNA stability in tumor cells Answer: B Q15. What is the role of exosomal miRNAs in cancer progression? A) They directly induce apoptosis in tumor cells. B) They regulate gene expression in recipient cells to promote tumor growth. C) They prevent angiogenesis. D) They enhance tumor cell differen.a.on. Answer: B Q16. How do EVs facilitate therapy resistance in cancer? A) By carrying drug efflux pumps to tumor cells B) By delivering oncogenes to recipient cells C) By transpor.ng an.-apopto.c molecules D) All of the above Answer: D Q17. Which of the following is a method to track EV uptake in recipient cells? A) Immunohistochemistry B) Fluorescent labeling of EVs C) Mass spectrometry D) Western blot Answer: B Q18. How do tumor-derived EVs impact macrophages? A) Convert M1 macrophages to M2 macrophages B) Ac.vate macrophage cytotoxic ac.vity C) Reduce macrophage migra.on D) Suppress macrophage cytokine produc.on Answer: A Q19. What is the clinical poten.al of EVs in cancer treatment? A) Use as drug delivery vehicles B) Biomarkers for early diagnosis C) Therapeu.c targets to inhibit tumor progression D) All of the above Answer: D Q20. Why is EV heterogeneity a challenge in cancer research? A) EVs from different sources have overlapping proper.es. B) EVs cannot be isolated from tumors. C) EVs lack consistent protein markers. D) EVs cannot influence cancer progression. Answer: A