MCQ Oncology Exam Preparation PDF

MCQ Oncology Exam Prepara4on 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...

MCQ Oncology Exam Prepara4on 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 aOack 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 ager 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 : 81. A 82. B 83. C 84. B 85. C 86. D 87. C 88. A 89. B 90. C 91. B 92. B 93. B 94. D 95. A 96. A 97. B 98. B 99. C 100. C 101. A 102. B 103. B 104. A 105. B 106. D 107. B 108. A 109. B 110. A 111. A 112. C 113. B 114. A 115. B 116. A 117. D 118. B 119. D 120. B 121. A 122. D 123. A