MCQ Oncology Exam Preparation PDF

MCQ Oncology Exam Prepara4on 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 Q2. Which of the following are examples of biological carcinogens?...

MCQ Oncology Exam Prepara4on 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 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 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 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 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 Q6. Which phase of the cell cycle involves DNA replica.on? A. G1 phase B. S phase C. G2 phase D. M phase Q7. What is the role of Rb protein in the cell cycle? A. Prevents the progression from G1 to S phase un.l condi.ons are met B. Ac.vates DNA replica.on C. Ini.ates mitosis D. Repairs DNA damage Q8. Which DNA repair mechanism uses a complementary strand as a template? A. Non-homologous end joining B. Base excision repair C. Mismatch repair D. Homologous recombina.on 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. 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 Q11. What type of cancer is most likely to have a BRCA1 or BRCA2 muta.on? A. Breast and ovarian cancer B. Colorectal cancer C. Lung cancer D. Skin cancer Q12. What key feature defines a malignant tumor? A. Metasta.c poten.al B. Limited growth C. Large size D. Benign appearance Q13. Which type of therapy uses small molecules or an.bodies to target cancer? A. Chemotherapy B. Targeted therapy C. Hormonal therapy D. Immunotherapy Q14. Which cell cycle checkpoint prevents mitosis if DNA is damaged? A. G1/S checkpoint B. M checkpoint C. G2/M checkpoint D. None of the above Q15. 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 Q16. 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 Q17. What immune cell type directly kills tumor cells? A. B-cells B. CD8+ T-cells C. Dendri.c cells D. Fibroblasts Q18. Which metabolic adapta.on is seen in cancer cells?  A. Reliance on oxida.ve phosphoryla.on B. Reduc.on in glucose uptake C. Increased reliance on lipids D. Aerobic glycolysis (Warburg effect) Q19. 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 Q20. Which checkpoint protein is directly involved in preven.ng cell cycle progression with DNA damage? A. Cyclin D B. ATM C. Rb D. p53 Q21. 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 Q22. How does radia.on therapy work to treat cancer? A. Induces DNA damage in cancer cells B. Inhibits angiogenesis C. Ac.vates immune checkpoints D. Suppresses VEGF secre.on Q23. Which of the following is an example of a tumor suppressor gene? A. Ras B. Myc C. p53 D. HER2 Q24. 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 Q25. 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 Q26. 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 Q27. 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 Q28. Which of these cells is part of the adap.ve immune system? A. Macrophages B. Natural killer cells C. Neutrophils D. B-cells Q29. Which stage of the immunoedi.ng theory allows tumors to avoid immune destruc.on? A. Elimina.on B. Equilibrium C. Escape D. Dormancy Q30. What protein is involved in homologous recombina.on repair? A. Ku proteins B. Cyclin E C. BRCA1 D. ATM Q31. 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 Q32. What role do tumor-associated macrophages (TAMs) play in cancer? A. Promote tumor growth and suppress immune ac.vity B. Induce DNA repair C. Facilitate chemotherapy effects D. Increase cytotoxic T-cell ac.vity Q33. 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 Q34. 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 Q35. Which cancer treatment uses radia.on to precisely target tumors? A. Hormonal therapy B. Proton therapy C. Immunotherapy D. Chemotherapy Q36. Which enzyme unwinds DNA for replica.on?  A. DNA polymerase B. Helicase C. Topoisomerase D. Ligase Q37. 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 Q38. 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 Q39. 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 Q40. 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 Q41. What protein complex regulates the G2/M checkpoint? A. Cdk1/Cyclin B B. Rb/E2F C. ATM/ATR D. Cyclin D/Cdk4 Q42. 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 Q43. Which therapy directly involves engineered immune cells? A. Chemotherapy B. Radia.on therapy C. CAR-T cell therapy D. Hormonal therapy Q44. 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 Q45. 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 aler 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 Q46. 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 Q47. Who first proposed the immunosurveillance theory? A. Edward Jenner B. William Coley C. F.M. Burnet D. P. Ehrlich Q48. 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 Q49. 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. Dendri.c cells and macrophages C. Natural killer cells and T-cells D. Fibroblasts and endothelial cells Q50. What is TRUE about neoan.gens? 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. Q51. 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 Q52. What occurs during the escape phase of immunoedi.ng? A. The immune system eradicates all cancer cells. B. Cancer cells acquire resistance to immune amacks and grow uncontrollably. C. Immune cells enter a dormant state. D. Tumor cells are eliminated through apoptosis. Q53. 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 Q54. 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 Q55. 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 Q56. 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 amract immune cells C. Promote tumor growth D. Inhibit an.gen presenta.on Q57. Why is the equilibrium phase olen silent in terms of clinical symptoms? A. Tumors are completely eradicated. B. Tumor cells are inac.ve. C. The immune system is suppressed. D. Immune cells maintain a balance with tumor cells, preven.ng significant growth. Q58. 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 Q59. 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. Q60. What is the primary danger signal released by cells to amract immune responses to early tumor growth? A. Heat shock proteins and IFN-γ B. TGF-β C. VEGF D. MHC molecules Q61. What does Coley’s toxin demonstrate about cancer treatment? A. Surgery is the only effec.ve cancer treatment. B. Infec.ons can boost immune responses against tumors. C. Tumors are resistant to immune-based therapies. D. Toxins inhibit an.gen presenta.on. Q62. 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 Q63. 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 Q64. 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 Q65. 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 Q66. What is the role of VEGF in tumor immune escape? A. Promotes aerobic metabolism B. Enhances T-cell ac.va.on C. Converts M1 macrophages to M2 macrophages D. Induces angiogenesis and reduces adherence factors on endothelial cells Q67. 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 Q68. 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 Q69. 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 Q70. 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 Q71. How does hypoxia in the tumor microenvironment affect immune cells? A. Suppresses immune cell ac.vity B. S.mulates T-cell prolifera.on C. Enhances an.gen presenta.on D. Increases cytokine produc.on Q72. Which cytokine is involved in increasing T-cell sensi.vity to apoptosis? A. IFN-γ B. TNF-α C. IL-2 D. IL-10 Q73. 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 Q74. How do tumors interfere with immune cell naviga.on? A. By producing nonfunc.onal ligands that block CXCR3 B. By secre.ng func.onal chemokine ligands C. By enhancing T-cell receptor ac.vity D. By inhibi.ng an.gen presenta.on Q75. 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 Q76. 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 Q77. 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 Q78. 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 Q79. How do tumors promote the metabolic inhibitory mechanism? A. By ac.va.ng FasL expression B. By suppressing VEGF secre.on C. By enhancing an.gen presenta.on D. By increasing lactate produc.on and reducing oxygen availability Q80. Which immune cells are most affected by glucose deple.on in the tumor microenvironment? A. T-cells B. B-cells C. Natural killer cells D. Macrophages Q81. 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 Q82. 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 Q83. What is the role of hypoxia in tumor progression? A. Promotes aerobic metabolism B. Reduces VEGF expression C. Suppresses immune cells and enhances angiogenesis D. Increases T-cell ac.vity Q84. What is the primary goal of immunotherapy in cancer treatment? A. Directly kill cancer cells B. Boost the immune system to amack its own cancer cells C. Inhibit angiogenesis D. Prevent metastasis Q85. Which type of immunotherapy involves gene.cally engineered T-cells? A. Non-specific immunotherapy B. Cancer vaccines C. Cellular immunotherapy D. Hormonal therapy Q86. How do CAR-T cells bypass the issue of tumor MHC-I downregula.on? A. By ac.va.ng NK cells B. By inhibi.ng VEGF produc.on C. By increasing cytokine release D. By recognizing en.re proteins on tumor cell surfaces Q87. 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 Q88. 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 Q89. 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 Q90. 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 Q91. 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 Q92. 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 Q93. 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. Q94. 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. Increased glycolysis by tumor cells D. High an.gen thresholds required for ac.va.on Q95. What is a major cause of relapse in CAR-T cell therapy? A. Tumor an.gen variance with reduced surface expression B. Lack of ini.al tumor response C. Excessive cytokine produc.on D. High persistence of CAR-T cells Q96. 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 Q97. 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. Q98. 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 Q99. Why did the 1st genera.on CAR-T cells fail in clinical trials? A. They lacked an.gen recogni.on ability. B. They caused rapid tumor progression. C. They induced excessive toxicity and failed to form memory T-cells. D. They targeted healthy cells instead of tumors. Q100. What major advancement made 2nd genera.on CAR-T cells more effec.ve? A. A) Improved targe.ng of solid tumors B. B) Integra.on of co-s.mulatory signals (Signal 2) C. C) Elimina.on of cytokine dependence D. D) Enhanced reliance on VEGF Q101. 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 Q102. Why do tumors relapse aler 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. Q103. 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 Q104. 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 Q105. 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 Q106. Which of the following is NOT a subtype of extracellular vesicles? A. Exosomes B. Microvesicles C. Apopto.c bodies D. Lysosomes Q107. 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 Q108. 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 Q109. 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 Q110. 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 Q111. 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 Q112. 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 Q113. What is the size range of exosomes? A. 1-10 nm B. 30-150 nm C. 500-1000 nm D. Greater than 1 micron Q114. Which protein marker is typically enriched in exosomes? A. CD63 B. VEGF C. PD-L1 D. Cyclin D Q115. 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 Q116. 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. Q117. What is the effect of EV-mediated transfer of PD-L1 in cancer? A. Enhances immune cell ac.vity B. Induces tumor cell apoptosis C. Increases DNA stability in tumor cells D. Promotes immune evasion by suppressing T-cell func.on Q118. 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. Q119. 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 Q120. Which of the following is a method to track EV uptake in recipient cells? A. Immunohistochemistry B. Fluorescent labeling C. Mass spectrometry D. Western blot Q121. 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 Q122. 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 Q123. 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 : 1. C 46. B 91. B 2. B 47. D 92. B 3. C 48. B 93. B 4. C 49. C 94. D 5. B 50. B 95. A 6. B 51. C 96. A 7. A 52. B 97. B 8. D 53. A 98. B 9. B 54. B 99. C 10. C 55. A 100. C 11. A 56. B 101. A 12. A 57. D 102. B 13. B 58. C 103. B 14. C 59. A 104. A 15. A 60. A 105. B 16. A 61. B 106. D 17. B 62. A 107. B 18. D 63. C 108. A 19. B 64. B 109. B 20. B 65. C 110. A 21. B 66. D 111. A 22. A 67. A 112. C 23. C 68. B 113. B 24. D 69. B 114. A 25. A 70. B 115. B 26. D 71. A 116. A 27. A 72. D 117. D 28. D 73. B 118. B 29. C 74. A 119. D 30. C 75. B 120. B 31. C 76. C 121. A 32. A 77. B 122. D 33. C 78. B 123. A 34. B 79. D 35. B 80. A 36. B 81. A 37. C 82. B 38. A 83. C 39. B 84. B 40. C 85. C 41. A 86. D 42. B 87. C 43. C 88. A 44. B 89. B 45. A 90. C