Oncology Exam Preparation - MCQs

Oncology Exam Preparation - MCQ Questions

• Primary characteristic of cancer: Uncontrolled cell division in specific tissues or organs.
• Biological carcinogens: Tobacco, UV rays, viruses, bacteria, parasites, benzene, and ionizing radiation. Sedentary lifestyle and obesity are also contributing factors.
• G1/S checkpoint processes: Checks for sufficient nutrients and DNA damage, activates DNA polymerase and centrosome duplication.
• Error-prone DNA repair mechanism: Non-homologous end joining (NHEJ).
• Tumor suppressor genes: They are hypoactivated in cancer and contribute to activating cell growth and differentiation. They are not responsible for autosomal recessive inheritance.
• DNA replication phase: S phase of the cell cycle.
• Role of Rb protein: Prevents progression from G1 to S phase until appropriate conditions are met.
• DNA repair mechanism using a complementary strand: Homologous recombination.
• M phase of cell cycle: DNA is replicated, chromosomes are segregated to daughter cells, nutrient levels are checked, DNA damage is repaired.
• Cancer most likely to have BRCA1 or BRCA2 mutation: Breast and ovarian cancer.
• Feature defining a malignant tumor: Metastatic potential.
• Therapy using small molecules or antibodies: Targeted therapy.
• Cell cycle checkpoint preventing mitosis with DNA damage: G2/M checkpoint.
• Characteristic allowing tumors to evade apoptosis: Overexpression of Bcl-2.
• Pathway commonly activated in cancer to promote growth: MAPK pathway.
• Immune cell type directly killing tumor cells: CD8+ T-cells.
• Metabolic adaptation seen in cancer cells: Reliance on oxidative phosphorylation.
• Role of tumor microenvironment in cancer progression: Supports immune activation and provides nutrients and growth signals to tumor cells.
• Checkpoint protein involved in preventing cell cycle progression with DNA damage: ATM.
• Feature allowing cancer cells to grow uncontrollably: Loss of contact inhibition.
• Mechanism of radiation therapy in treating cancer: Inducing DNA damage in cancer cells.
• Tumor suppressor gene example: p53.
• Hallmark of cancer involving avoiding immune destruction: Evading immune system responses
• Purpose of PET scan in oncology: Measure glucose uptake in tissues.
• Process of angiogenesis: Formation of new blood vessels.
• Cells part of adaptive immune system: B cells.
• Stage of immunoediting allowing tumor avoidance of immune destruction: Escape.
• Protein involved in homologous recombination repair: BRCA1.
• Effect of IL-10 in tumor microenvironment: Suppresses immune responses.
• Role of tumor-associated macrophages (TAMs): Promote tumor growth and suppress immune activity.
• Hallmark addressed by anti-VEGF therapy: Inducing angiogenesis
• Role of dendritic cells in cancer immunity: Presenting antigens to T-cells
• Cancer treatment using precise radiation targeting: Proton therapy
• Enzyme unwinding DNA for replication: Helicase
• Process disrupted in cancers with mismatch repair deficiency: Replication fidelity.
• Mechanism of action of anti-PD-1 antibodies: Block tumor-induced immune suppression.
• Difference between CAR-T cells and natural T cells: CAR-T cells are genetically engineered to target specific antigens.
• Effect of hypoxia in tumor microenvironment on immune cells: Suppresses immune cell activity.
• Cytokine involved in increasing T-cell sensitivity to apoptosis: IFN-γ
• Macrophage transformation under tumor conditions: M1 macrophages become M2 macrophages.
• Role of regulatory T cells (Tregs): Promote tumor immune suppression.
• Mechanism by which tumors interfere with immune cell navigation: Producing nonfunctional ligands blocking CXCR3/secreting functional chemokine ligands.
• Effect of fibroblasts conversion into CAFs: Builds a protective barrier around the tumor.
• Warburg effect characteristic in tumors: Tumors switch to glycolysis even in the presence of oxygen.
• Reason for immune cell anergy in tumor microenvironment: Excess glucose availability
• Effect of lactate production by tumors: Lowers pH of tumor microenvironment.
• Immune cells affected by glucose depletion: T-cells.
• Dual role of immune system in cancer: Acts as suppressor and inducer of tumorigenesis.
• Method of tumor inducing apoptosis in immune cells: Producing exosomes carrying Fas-ligand.
• Goal of immunotherapy: Boost the immune system to attack cancer cells.
• Type of immunotherapy using genetically engineered T cells: Cellular immunotherapy.
• Mechanism CAR-T cells bypass MHC-I down-regulation: Recognize entire proteins on tumor cell surfaces.
• Limitation of 1st generation CAR T-cells: Lack of CD3Z chains or inability to induce cytokine production.
• Advancement made to 2nd generation CAR-T cells: Addition of CD28 co-stimulatory domain.
• Signaling pathway step critical for T-cell activation: CD3 phosphorylation and ZAP70 recruitment
• Function of LAT-SLP76 signalosome: Amplify T-cell signaling.
• Clinical issue associated with 2nd generation CAR-T cells: Poor persistence and sensitivity.
• Purpose of introducing IL-2 receptor domain: To enhance glycolysis or auto-produce cytokines and boost responses or eliminate MHC-I dependency.
• What does "proof of concept" refer to in CAR-T cell development?: Demonstrated potential to activate T-cells.
• Factor limiting CAR-T cell sensitivity recognizing low antigen levels: Absence of CD28 co-stimulation
• Major cause of relapse in CAR-T cell therapy: Tumor antigen variance or reduced surface expression.
• Signaling domain combination found in 2nd generation CAR-T cells: CD28+ LAT
• Difference between CAR receptor and TCR activation: CAR recognizes entire proteins, TCR requires MHC-I.
• Reason for 1st generation CAR-T cells failing in clinical trials: Lacked antigen recognition, caused rapid tumor progression, or induced excessive toxicity.
• Advancement made to 2nd generation CAR-T cells: Integration of co-stimulatory signals
• Role of ZAP70 in T-cell activation: Phosphorylates LAT and amplifies signaling.
• Reason for 1st generation CAR-T cell failure in clinical trials: Lack of antigen recognition ability, rapid tumor progression, failed to form memory cells.
• Reason for 2nd generation CAR-T cells being more effective: Improved targeting and integration of co-stimulatory signals.
• Mechanism indicating complete CAR-T cell signaling activation: LAT phosphorylation.
• Problem with CAR-T cells recognizing tumors with low antigen levels: High antigen thresholds required for activation
• Reason for tumor relapse after initial CAR-T therapy success: Tumors develop resistance via antigen downregulation.
• Major challenge in creating next generation CAR-T cells: Balancing sensitivity with safety.
• Definition of extracellular vesicles (EVs): Lipid bilayer enclosed particles secreted by cells.
• Prime function of tumor-derived EVs in cancer progression: Deliver oncogenic molecules to recipient cells.
• Type of molecules carried by EVs: Proteins, lipids, and nucleic acids.
• Process promoted by EVs in tumor microenvironment: Immune cell activation
• Role of EVs as biomarkers in cancer: Reflects genetic and proteomic content of the tumor.
• Technique to isolate extracellular vesicles: Density gradient centrifugation
• Role of tumor-derived EVs in immune modulation: Activate immune checkpoints; suppress immune responses by carrying inhibitory molecules.
• Size range of exosomes: 30-150 nm.
• Protein marker typically present in exosomes: CD63.
• Mechanism by which EVs contribute to "seed and soil" hypothesis in metastasis: Modifying the microenvironment of distant organs to support tumor growth.
• Distinguishing feature of microvesicles from exosomes: Microvesicles bud directly from the plasma membrane; exosomes originate from multivesicular bodies.
• Effect of PD-L1 transfer by EV in cancer: Promote immune evasion by suppressing T-cell function.
• Role of exosomal miRNAs in cancer progression: Regulate gene expression in recipient cells to promote tumor growth.
• Mechanism of how EVs facilitate therapy resistance: By carrying drug efflux pumps or delivering oncogenes.
• Method to track EV uptake: Fluorescent labeling or mass spectrometry.

Prepare for your oncology exam with this comprehensive set of multiple-choice questions. The quiz covers essential topics such as cancer characteristics, biological carcinogens, cell cycle checkpoints, and DNA repair mechanisms. Test your knowledge and ensure you're ready for your exam!