QCM EVs Quiz - Questions and Answers PDF
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This document contains a set of multiple choice questions and answers (QCM) regarding extracellular vesicles (EVs). The quiz focuses on various aspects of these vesicles, including their functions, isolation techniques, and roles in cancer progression.
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**1. What are extracellular vesicles (EVs)?**\ a. Enzymes that degrade extracellular matrix proteins.\ b. Phospholipid-delimited particles released by cells into the extracellular environment.\ c. Specialized immune cells that regulate cancer growth.\ d. Mutated proteins secreted by cancer cells.\ *...
**1. What are extracellular vesicles (EVs)?**\ a. Enzymes that degrade extracellular matrix proteins.\ b. Phospholipid-delimited particles released by cells into the extracellular environment.\ c. Specialized immune cells that regulate cancer growth.\ d. Mutated proteins secreted by cancer cells.\ **Answer:** b **2. Which of the following is NOT a main function of EVs?**\ a. Transferring content between cells.\ b. Triggering apoptosis in recipient cells.\ c. Disposing of harmful cellular components.\ d. Modifying the extracellular matrix.\ **Answer:** b **3. What types of molecules can be found in EVs?**\ a. Proteins, nucleic acids, lipids, and sugars.\ b. Only proteins and DNA.\ c. Cytokines and growth factors exclusively.\ d. Only phospholipids.\ **Answer:** a **4. What is a challenge in isolating extracellular vesicles?**\ a. Low yield in isolation techniques.\ b. Overlapping biophysical properties between EV subtypes.\ c. Lack of specific surface markers.\ d. All of the above.\ **Answer:** d **5. Which isolation technique is commonly used for EVs?**\ a. Density gradients (DG).\ b. Precipitation (P).\ c. Differential ultracentrifugation (dUC).\ d. All of the above.\ **Answer:** d **6. EVs are heterogeneous in terms of their:**\ a. Size, origin, content, and functions.\ b. Only size and lipid content.\ c. Receptors and nucleic acid content.\ d. Density and immunogenicity.\ **Answer:** a **7. What is the size range of EVs?**\ a. 50--150 nm.\ b. 30 nm to ≥5 µm.\ c. 50 nm to 400 nm.\ d. 100 µm to 1 mm.\ **Answer:** b **8. Which EV subtype is enriched with CD63?**\ a. Ectosomes.\ b. Exosomes.\ c. Apoptotic bodies.\ d. Microvesicles.\ **Answer:** b **9. What determines the content of EVs?**\ a. The cellular origin of the vesicle.\ b. External environmental conditions.\ c. The size of the EV.\ d. Interaction with recipient cells.\ **Answer:** a **10. How can EVs interact with their target cells?**\ a. Cargo transfer.\ b. Receptor-mediated signaling.\ c. Modifying the extracellular matrix.\ d. All of the above.\ **Answer:** d **11. What is one major role of tumor-derived EVs in cancer progression?**\ a. Suppressing tumor angiogenesis.\ b. Transferring RNA, cytokines, and growth factors to recipient cells.\ c. Inducing apoptosis in cancer cells.\ d. Enhancing immune surveillance.\ **Answer:** b **12. How do EVs contribute to metastatic disease?**\ a. By reducing cancer cell migration.\ b. By carrying components that promote invasion and metastasis.\ c. By suppressing the tumor microenvironment.\ d. By preventing angiogenesis.\ **Answer:** b **13. Which feature of EVs makes them useful as biomarkers for cancer?**\ a. Their size and density.\ b. Their nucleic acid and protein content derived from cancer cells.\ c. Their ability to degrade extracellular matrix proteins.\ d. Their secretion by immune cells.\ **Answer:** b **14. What is the effect of tumor-derived EVs on the tumor microenvironment (TME)?**\ a. Remodeling the TME to promote cancer growth and survival.\ b. Inhibiting cancer progression by disrupting the TME.\ c. Blocking immune cell recruitment to the TME.\ d. Increasing oxygen levels in the TME.\ **Answer:** a **15. How do EVs promote cancer cell survival?**\ a. By eliminating neo-antigens.\ b. By delivering survival signals to recipient cells.\ c. By blocking angiogenesis.\ d. By inducing apoptosis in neighboring cells.\ **Answer:** b **16. What was the finding of Thery's lab on EVs from triple-negative breast cancer cells?**\ a. They suppress immune responses.\ b. They promote pro-inflammatory macrophages associated with better clinical outcomes.\ c. They reduce the secretion of cytokines in macrophages.\ d. They directly target tumor suppressor genes.\ **Answer:** b **17. How were CD63+ and CD9+ EVs tagged in Thery's study on EV secretion?**\ a. With fluorescent dyes.\ b. With nanoluciferase enzymes.\ c. With radioactive markers.\ d. With lipid-based dyes.\ **Answer:** b **18. What was discovered about drugs affecting EV release in Thery's lab?**\ a. 104 compounds were identified that modify EV release.\ b. Drugs exclusively reduced EV secretion.\ c. No drugs impacted EV release.\ d. Only lipid-modifying drugs were effective.\ **Answer:** a **19. What is a limitation in studying EV subtypes?**\ a. Difficulty in distinguishing between subtypes due to lack of specific markers.\ b. Limited availability of EV-producing cell lines.\ c. EVs are too large for current imaging techniques.\ d. EVs do not survive isolation procedures.\ **Answer:** a **20. How do MDA-MB-231-derived EVs affect monocyte-derived macrophages?**\ a. Induce M1 macrophage polarization.\ b. Convert macrophages into T cells.\ c. Suppress macrophage activity.\ d. Increase IL-10 secretion.\ **Answer:** a **21. What is a potential clinical application of EVs?**\ a. Direct tumor removal.\ b. Biomarker discovery for cancer diagnosis.\ c. Promoting metastasis in cancer patients.\ d. Blocking immune checkpoint therapy.\ **Answer:** b **22. Which molecules are transferred by EVs to modulate the immune response?**\ a. Cytokines, PD-L1, and RNA.\ b. Chemokines and angiogenic factors.\ c. Only DNA and lipids.\ d. Caspases and IL-12.\ **Answer:** a **23. Why are EVs significant in cancer therapy research?**\ a. They degrade tumor antigens.\ b. They allow targeted delivery of therapeutic agents.\ c. They suppress immune evasion.\ d. They prevent angiogenesis.\ **Answer:** b **24. How do EVs affect tumor-associated macrophages (TAMs)?**\ a. Polarize them into M2 macrophages, promoting tumor growth.\ b. Prevent macrophage recruitment to the TME.\ c. Reduce immune suppression.\ d. Inhibit cytokine release by macrophages.\ **Answer:** a **25. What role does PD-L1 in EVs play in cancer?**\ a. Promotes immune cell activation.\ b. Contributes to immunosuppression by exhausting T cells.\ c. Increases tumor antigen recognition.\ d. Enhances angiogenesis.\ **Answer:** b