Anticancer Drugs Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Anticancer Drugs. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Anticancer Drugs Indian Medical PG Question 1: Which of the following drugs act by inhibiting DNA replication?
- A. Mitomycin C
- B. 6-Mercaptopurine (Correct Answer)
- C. Actinomycin D
- D. Asparaginase
Anticancer Drugs Explanation: ***6-Mercaptopurine***
- This drug is a **purine analog** that acts as an **antimetabolite**, directly interfering with the **synthesis of purine nucleotides** required for DNA replication.
- By inhibiting enzymes like **PRPP amidotransferase** and getting incorporated into DNA as a fraudulent nucleotide, it blocks the **de novo synthesis** pathway, preventing normal DNA replication.
- This represents **direct inhibition of DNA synthesis** at the nucleotide building block level.
*Mitomycin C*
- This agent is an **alkylating agent** that **cross-links DNA** strands, causing DNA damage that prevents strand separation.
- While it does prevent DNA replication, its mechanism is through **DNA damage and structural disruption** rather than inhibition of the DNA synthesis machinery itself.
- It acts by damaging already-formed DNA rather than preventing new DNA synthesis.
*Actinomycin D*
- Actinomycin D is an **intercalating agent** that inserts itself between DNA base pairs, primarily **inhibiting RNA synthesis** by blocking RNA polymerase movement.
- While it binds to DNA, its primary therapeutic action is on **transcription (RNA synthesis)**, not direct inhibition of DNA replication.
*Asparaginase*
- Asparaginase is an enzyme that **depletes asparagine** from the blood, which is an essential amino acid for certain cancer cells (e.g., leukemic cells).
- Its mechanism is to starve cancer cells of asparagine, leading to **inhibition of protein synthesis**, not DNA replication.
Anticancer Drugs Indian Medical PG Question 2: All of the following are major subtypes of breast cancer based on Gene array analysis EXCEPT:
- A. Luminal A and Luminal B
- B. Triple negative
- C. Her-2 receptor positive
- D. Estrogen receptor positive (Correct Answer)
Anticancer Drugs Explanation: ***Oestrogen receptor positive***
- While **estrogen receptor (ER) positivity** is a critical prognostic and predictive marker in breast cancer, it is a single marker, not a distinct intrinsic subtype encompassing broader genomic categorization [1].
- The intrinsic subtypes are based on gene expression profiles that cluster tumors into biologically distinct groups, such as Luminal A, Luminal B, HER2-enriched, and Basal-like (including Triple Negative) [3].
*Luminal A and Luminal B*
- These are major intrinsic subtypes characterized by the expression of **hormone receptors** (ER and/or PR) and differing in their proliferation rates [2].
- **Luminal A** generally has high ER, low proliferation, and a good prognosis, while **Luminal B** often has higher proliferation (e.g., higher Ki-67) and a slightly worse prognosis [2].
*Triple negative*
- This is a major intrinsic subtype (**Basal-like**) defined by the absence of **estrogen receptors (ER)**, **progesterone receptors (PR)**, and **HER2 overexpression** [1], [4].
- It often correlates with a more aggressive clinical course and specific treatment approaches [4].
*Her-2 receptor positive*
- This is a major intrinsic subtype characterized by the **overexpression or amplification of the HER2 gene** [3].
- These cancers are often aggressive but respond well to targeted therapies like trastuzumab [3], [4].
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1064-1066.
[2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 10th ed. The Breast, pp. 1059-1060.
[3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, p. 1060.
[4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 258-259.
Anticancer Drugs Indian Medical PG Question 3: Which of the following is NOT a criterion for defining extensively drug-resistant tuberculosis (XDR-TB)?
- A. Isoniazid + Rifampicin + Fluoroquinolone
- B. Isoniazid + Rifampicin + Ethambutol + Fluoroquinolone
- C. Fluoroquinolone (Correct Answer)
- D. Isoniazid + Rifampicin + Kanamycin
Anticancer Drugs Explanation: ***Fluoroquinolone***
- Resistance to **fluoroquinolone alone** is NOT a criterion for XDR-TB because XDR-TB requires a **baseline of MDR-TB** (resistance to both rifampicin and isoniazid) plus additional resistances.
- XDR-TB definition (WHO 2021): **MDR-TB** + resistance to **any fluoroquinolone** + resistance to **at least one Group A drug** (bedaquiline or linezolid).
- Fluoroquinolone resistance in isolation does not meet any of these combined criteria.
*Isoniazid + Rifampicin + Fluoroquinolone*
- This represents **MDR-TB** (rifampicin + isoniazid resistance) plus **fluoroquinolone resistance**.
- This is a partial criterion approaching XDR-TB but still requires additional resistance to at least one Group A drug (bedaquiline or linezolid) for complete XDR-TB classification.
- However, this combination includes the essential MDR-TB base and fluoroquinolone component.
*Isoniazid + Rifampicin + Ethambutol + Fluoroquinolone*
- This includes **MDR-TB** (rifampicin + isoniazid), **fluoroquinolone resistance**, and ethambutol (first-line drug).
- While ethambutol resistance alone doesn't define XDR-TB, this combination includes the critical MDR-TB and fluoroquinolone components required for XDR-TB classification.
- Similar to above, would need Group A drug resistance for complete XDR-TB.
*Isoniazid + Rifampicin + Kanamycin*
- This represents **MDR-TB** plus resistance to **kanamycin** (a second-line injectable).
- Under previous WHO definitions (pre-2021), injectable resistance was part of XDR-TB criteria.
- This combination includes the MDR-TB base essential for any XDR-TB classification, though it lacks fluoroquinolone resistance.
Anticancer Drugs Indian Medical PG Question 4: A 55-year-old woman with non-small cell lung cancer is found to have an ALK gene rearrangement. How should this finding influence her treatment?
- A. Refer for surgical resection, if appropriate
- B. Switch to crizotinib, a targeted ALK inhibitor (Correct Answer)
- C. Consider radiation therapy, if indicated
- D. Continue standard chemotherapy, if appropriate for the patient's condition
Anticancer Drugs Explanation: ***Switch to crizotinib, a targeted ALK inhibitor***
- The presence of an **ALK gene rearrangement** in **non-small cell lung cancer (NSCLC)** is a strong indicator for **targeted therapy** with an **ALK inhibitor** like crizotinib.
- These drugs specifically block the aberrant activity of the ALK fusion protein, leading to **superior response rates** and **progression-free survival** compared to standard chemotherapy in ALK-positive patients.
*Refer for surgical resection, if appropriate*
- **Surgical resection** is primarily considered for **early-stage NSCLC** without evidence of metastatic disease [1].
- While surgery can be curative, the presence of specific gene rearrangements like ALK typically prompts consideration of **neoadjuvant or adjuvant targeted therapy** or systemic therapy for advanced disease.
*Consider radiation therapy, if indicated*
- **Radiation therapy** for NSCLC is usually employed for **local control**, either in curative intent for early stages or for **palliative management** of symptoms in advanced disease [2].
- It does not directly address the underlying **genetic driver** (ALK rearrangement) and would not be the primary systemic treatment.
*Continue standard chemotherapy, if appropriate for the patient's condition*
- While **standard chemotherapy** is a treatment option for NSCLC, the identification of a **driver mutation** like an ALK rearrangement makes **targeted therapy** a significantly more effective and preferred first-line approach.
- Continuing chemotherapy without considering targeted therapy would be **suboptimal** for a patient with an ALK rearrangement due to the availability of more effective treatments.
Anticancer Drugs Indian Medical PG Question 5: Which of the following is a monoclonal antibody used in cancer treatment?
- A. Cisplatin
- B. Rituximab (Correct Answer)
- C. 5-fluorouracil
- D. Methotrexate
Anticancer Drugs Explanation: ***Rituximab***
- **Rituximab** is a **chimeric monoclonal antibody** that targets the **CD20 protein** found on the surface of normal and malignant **B lymphocytes**.
- It is widely used in the treatment of various **lymphomas** and **leukemias**, as well as autoimmune diseases, by inducing the death of CD20-positive B cells.
*Cisplatin*
- **Cisplatin** is a **platinum-based chemotherapy drug** that works by forming **DNA adducts**, leading to DNA damage and apoptosis of cancer cells.
- It is used in various solid tumors but is not a monoclonal antibody; it's a **cytotoxic agent**.
*5-fluorouracil*
- **5-fluorouracil (5-FU)** is an **antimetabolite chemotherapy drug** that interferes with DNA and RNA synthesis, thereby inhibiting cell division.
- It is a **pyrimidine analog** and not a monoclonal antibody.
*Methotrexate*
- **Methotrexate** is a **folate analog antimetabolite** that inhibits **dihydrofolate reductase**, interfering with DNA synthesis and cell proliferation.
- It's a conventional chemotherapy agent and immunosuppressant, not a monoclonal antibody.
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