NEET SS Medical Oncology (DM) Syllabus

Medical Oncology (DM) syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Medical Oncology (DM) in NEET SS, not a summary of it.

1. 1

   Principles of Cancer Biology and Therapeutics

   4 topics

   • Hallmarks of Cancer and Carcinogenesis
     • Oncogenes and tumor suppressor genes
     • Tumor microenvironment and angiogenesis
   • Principles of Chemotherapy
     • Drug classes and mechanisms
     • Toxicity management
   • Targeted Therapy and Immunotherapy
     • Tyrosine kinase inhibitors
     • Immune checkpoint inhibitors and irAEs
   • Cancer Screening, Staging and Prevention
     • TNM staging principles
2. 2

   Solid Tumors

   4 topics

   • Thoracic and Head-Neck Cancers
     • Lung cancer molecular subtypes
   • Gastrointestinal Malignancies
     • Colorectal, gastric and hepatobiliary cancers
   • Breast and Gynecological Cancers
     • Hormone receptor and HER2 status
   • Genitourinary and CNS Tumors
     • Prostate and renal cell carcinoma
3. 3

   Hematological Malignancies

   3 topics

   • Acute and Chronic Leukemias
     • AML, ALL classification and therapy
     • CML and tyrosine kinase inhibitors
   • Lymphomas
     • Hodgkin and non-Hodgkin lymphoma
   • Plasma Cell Disorders
     • Multiple myeloma
4. 4

   Supportive and Palliative Oncology

   3 topics

   • Oncologic Emergencies
     • Tumor lysis syndrome and febrile neutropenia
     • Spinal cord compression and SVC obstruction
   • Supportive Care
     • Antiemetics and growth factors
     • Cancer pain management
   • Paraneoplastic Syndromes
     • Endocrine and neurologic syndromes

Medical Oncology (DM) flashcards for NEET SS

25 of 51 cards from the Medical Oncology (DM) deck — real questions with worked answers.

1. What are the eight core Hallmarks of Cancer described by Hanahan and Weinberg (2011), beyond the original six?

   Original six: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion/metastasis. Two emerging: deregulating cellular energetics (Warburg effect) and avoiding immune destruction. Two enabling characteristics: genome instability/mutation and tumor-promoting inflammation.

2. What is the Warburg effect in cancer metabolism?

   The preference of tumor cells for aerobic glycolysis (glucose to lactate) even in the presence of oxygen, rather than oxidative phosphorylation; it supports rapid biosynthesis and is the basis of FDG-PET imaging.

3. Define the three stages of chemical carcinogenesis.

   Initiation (irreversible DNA mutation by a carcinogen), promotion (reversible clonal expansion of initiated cells by promoters), and progression (acquisition of malignant phenotype with genetic instability and invasion).

4. Differentiate oncogenes from tumor suppressor genes, including inheritance pattern of mutations.

   Oncogenes are gain-of-function, dominant (one mutated allele sufficient), e.g. RAS, MYC, HER2. Tumor suppressors are loss-of-function, recessive at cellular level requiring biallelic inactivation (Knudson two-hit hypothesis), e.g. TP53, RB1, APC.

5. What classes of viruses are linked to human cancers, with one example each?

   HPV (cervical, oropharyngeal), HBV/HCV (hepatocellular carcinoma), EBV (Burkitt lymphoma, nasopharyngeal carcinoma, Hodgkin), HHV-8 (Kaposi sarcoma), HTLV-1 (adult T-cell leukemia/lymphoma), Merkel cell polyomavirus (Merkel cell carcinoma).

6. Describe the cell-cycle phase specificity of antimetabolites versus alkylating agents.

   Antimetabolites (e.g. methotrexate, 5-FU, cytarabine) are S-phase specific (cell-cycle phase-specific). Alkylating agents (e.g. cyclophosphamide, cisplatin) are cell-cycle phase-nonspecific, acting in all phases including G0.

7. What is the log-kill hypothesis (Skipper) in chemotherapy?

   A given dose of chemotherapy kills a constant fraction (not a constant number) of tumor cells, regardless of tumor burden; this first-order kinetics rationale underlies multiple cyclical dosing to reduce tumor burden by successive logs.

8. State the dose-limiting and characteristic toxicities of anthracyclines (e.g. doxorubicin).

   Cumulative dose-dependent cardiotoxicity (dilated cardiomyopathy/CHF, lifetime limit ~450-550 mg/m2); also myelosuppression, mucositis, alopecia, vesicant extravasation, and red urine. Dexrazoxane is cardioprotective.

9. Match these chemotherapy drugs to their signature non-hematologic toxicities: cisplatin, bleomycin, vincristine, cyclophosphamide.

   Cisplatin: nephrotoxicity, ototoxicity, peripheral neuropathy. Bleomycin: pulmonary fibrosis. Vincristine: peripheral neuropathy (no myelosuppression). Cyclophosphamide: hemorrhagic cystitis (prevented by mesna).

10. What is the mechanism of action of taxanes and vinca alkaloids on microtubules?

    Taxanes (paclitaxel, docetaxel) stabilize microtubules preventing depolymerization; vinca alkaloids (vincristine, vinblastine) bind tubulin and inhibit microtubule assembly/polymerization. Both arrest cells in M phase (mitotic spindle poisons).

11. Name the targeted agent and its target for: CML, HER2-positive breast cancer, EGFR-mutant lung cancer, and BCR-ABL-independent BRAF V600E melanoma.

    CML: imatinib (BCR-ABL tyrosine kinase). HER2 breast: trastuzumab (HER2/ERBB2). EGFR lung: gefitinib/osimertinib (EGFR). BRAF melanoma: vemurafenib/dabrafenib (BRAF V600E).

12. How do immune checkpoint inhibitors work, and name the main targets?

    They block inhibitory immune checkpoints to restore T-cell antitumor activity. Targets: CTLA-4 (ipilimumab), PD-1 (nivolumab, pembrolizumab), and PD-L1 (atezolizumab, durvalumab).

13. What is CAR-T cell therapy and a key approved indication?

    Chimeric Antigen Receptor T-cell therapy: patient T-cells are genetically engineered to express a receptor against a tumor antigen (e.g. CD19) and reinfused. Approved for relapsed/refractory B-ALL and B-cell lymphomas (e.g. tisagenlecleucel, axicabtagene).

14. What is cytokine release syndrome (CRS), the major toxicity of CAR-T therapy, and its treatment?

    A systemic inflammatory response from massive cytokine release (high IL-6) causing fever, hypotension, hypoxia, and organ dysfunction; treated with tocilizumab (anti-IL-6 receptor) and corticosteroids.

15. List the recommended screening tests and target populations for breast, cervical, and colorectal cancer.

    Breast: mammography every 1-2 years from age 40-50. Cervical: Pap smear/HPV testing from age 21-25 every 3-5 years. Colorectal: colonoscopy every 10 years (or FIT/FOBT annually) from age 45-50.

16. Explain the TNM staging system components.

    T = size/extent of primary Tumor (T1-T4), N = regional lymph Node involvement (N0-N3), M = distant Metastasis (M0/M1). These combine into stage groups I-IV.

17. Define lead-time bias and length-time bias in cancer screening.

    Lead-time bias: apparent increase in survival because diagnosis is earlier, without changing time of death. Length-time bias: screening preferentially detects slow-growing, indolent tumors with better prognosis, overstating screening benefit.

18. What tumor markers are used for: ovarian, prostate, colorectal, hepatocellular, and testicular cancers?

    Ovarian: CA-125. Prostate: PSA. Colorectal: CEA. Hepatocellular: AFP. Testicular: AFP and beta-hCG (plus LDH).

19. What is the most common type of lung cancer, and which subtype is most associated with smoking and central location with paraneoplastic syndromes?

    Adenocarcinoma is the most common (and most common in non-smokers, peripheral). Small cell lung cancer (SCLC) is strongly smoking-associated, central, and causes paraneoplastic syndromes (SIADH, ectopic ACTH, Lambert-Eaton).

20. What is the most common cause of head and neck squamous cell carcinoma, and what biomarker confers better prognosis in oropharyngeal cancer?

    Tobacco and alcohol are classic causes; HPV (p16-positive) oropharyngeal cancer has a significantly better prognosis and treatment response.

21. Name the molecular subtypes/key biomarkers tested in colorectal cancer that guide therapy.

    RAS (KRAS/NRAS) and BRAF mutation status (anti-EGFR antibodies like cetuximab work only in RAS wild-type), and microsatellite instability (MSI-H/dMMR), which predicts immunotherapy response and Lynch syndrome.

22. What is the Barcelona Clinic Liver Cancer (BCLC) significance and first-line systemic therapy for advanced HCC?

    BCLC staging integrates tumor stage, liver function (Child-Pugh), and performance status to guide HCC treatment. First-line systemic therapy for advanced HCC is atezolizumab plus bevacizumab.

23. Which gene mutation is associated with gastrointestinal stromal tumors (GIST) and what targeted drug is used?

    Activating mutations in KIT (CD117) or PDGFRA; treated with imatinib (and sunitinib/regorafenib for resistance).

24. Define the molecular subtypes of breast cancer based on receptor status.

    Luminal A (ER+/PR+, HER2-, low Ki-67), Luminal B (ER+, higher Ki-67 or HER2+), HER2-enriched (ER-/HER2+), and Triple-negative/Basal-like (ER-/PR-/HER2-).

25. What hereditary syndrome predisposes to breast and ovarian cancer, and what therapy exploits this defect?

    BRCA1/BRCA2 germline mutations (hereditary breast-ovarian cancer syndrome); PARP inhibitors (olaparib, niraparib) exploit synthetic lethality in homologous recombination-deficient tumors.

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