Oncology Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Oncology. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Oncology Indian Medical PG Question 1: Which among the following drugs is the new FDA approved immune checkpoint inhibitor for endometrial carcinoma?
- A. Ipilimumab
- B. Pembrolizumab (Correct Answer)
- C. Trastuzumab
- D. Nivolumab
Oncology Explanation: **Pembrolizumab**
* **Pembrolizumab** (Keytruda), a **PD-1 inhibitor**, received accelerated FDA approval for patients with **advanced endometrial carcinoma** that is mismatch repair deficient (dMMR) or microsatellite instability-high (MSI-H), and has progressed following prior systemic therapy or is not a candidate for curative surgery or radiation.
* This approval was based on data from the KEYNOTE-158 study, demonstrating **durable responses** in these specific subsets of endometrial cancer, highlighting its role in precision oncology.
*Ipilimumab*
* **Ipilimumab** (Yervoy) is a **CTLA-4 inhibitor** primarily approved for the treatment of **melanoma** and renal cell carcinoma, often in combination with nivolumab.
* While it is an immune checkpoint inhibitor, its primary indications and specific FDA approvals do not include **endometrial carcinoma**.
*Trastuzumab*
* **Trastuzumab** (Herceptin) is a **monoclonal antibody** that targets the **HER2 protein**, commonly used in the treatment of **HER2-positive breast cancer** and certain types of gastric cancer.
* It is not an immune checkpoint inhibitor and its mechanism of action is distinct from blocking immune checkpoints like PD-1 or CTLA-4.
*Nivolumab*
* **Nivolumab** (Opdivo) is a **PD-1 inhibitor** with broad FDA approvals for various cancers, including melanoma, non-small cell lung cancer, renal cell carcinoma, classical Hodgkin lymphoma, and others.
* While a potent immune checkpoint inhibitor, **pembrolizumab** received the specific accelerated approval for advanced endometrial carcinoma in the context described, making it the most direct answer for the "new FDA approved" status in this specific indication.
Oncology Indian Medical PG Question 2: Which enzymatic activity is primarily responsible for the immortality of cancer cells?
- A. RNA polymerase
- B. Telomerase (Correct Answer)
- C. DNA polymerase
- D. DNA reverse transcriptase
Oncology Explanation: ***Telomerase***
- **Telomerase** is an enzyme that adds repetitive nucleotide sequences to the ends of chromosomes (**telomeres**), preventing their shortening during DNA replication [1].
- In normal somatic cells, **telomerase** activity is low or absent, leading to progressive telomere shortening and eventual cellular senescence or apoptosis; however, in cancer cells, **telomerase** is highly active, maintaining telomere length and enabling indefinite cell division, contributing to their **immortality** [1].
*DNA reverse transcriptase*
- **DNA reverse transcriptase** synthesizes DNA from an RNA template, a process characteristic of retroviruses (e.g., HIV) and not typically involved in the immortality of human cancer cells.
- While some endogenous retroelements exist in the human genome, this enzyme's primary role is not in maintaining the replicative potential of cancer cells.
*RNA polymerase*
- **RNA polymerase** is responsible for synthesizing RNA from a DNA template (**transcription**), a fundamental process in gene expression.
- While critical for cell growth and division, **RNA polymerase** does not directly prevent telomere shortening or contribute to cellular immortality.
*DNA polymerase*
- **DNA polymerase** is involved in DNA replication and repair, synthesizing new DNA strands and ensuring genetic fidelity.
- While essential for cell proliferation, it does not directly address the issue of **telomere shortening**, which is key to cellular aging and immortality.
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 311-312.
Oncology Indian Medical PG Question 3: Most frequently altered oncogene in pancreatic cancer is:
- A. K-RAS (Correct Answer)
- B. CDKN2A
- C. SMAD4
- D. TP53
Oncology Explanation: ***K-RAS***
- **K-RAS** mutations are present in approximately **90%** of pancreatic adenocarcinomas, making it the most frequently altered oncogene in this cancer type [1].
- It plays a major role in the **Ras signaling pathway**, which is crucial for cell proliferation and survival.
*TP53*
- While **TP53** mutations are also common in various cancers, they are not the most prevalent in pancreatic cancer, where K-RAS is more frequently mutated [1].
- Typically associated with **tumor progression**, rather than initiating changes seen in pancreatic carcinogenesis [1].
*SMAD4*
- **SMAD4** mutations occur in about **55%** of pancreatic cancers but are generally involved in the later stages of tumor progression, rather than being an initiating oncogenic event [1].
- Primarily functions in the **TGF-beta signaling pathway**, which is different from the K-RAS pathway.
*CDKN2A*
- Although **CDKN2A** deletions are implicated in pancreatic cancer, they are not as frequently altered as K-RAS mutations [1].
- This gene is related to the regulation of the **cell cycle**, but its alterations are secondary in the context of pancreatic oncogenesis [1].
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 897-898.
Oncology Indian Medical PG Question 4: Field carcinogenesis theory is commonly seen in
- A. Head and neck cancer (Correct Answer)
- B. Cervical cancer
- C. Prostate cancer
- D. Breast cancer
Oncology Explanation: ***Head and neck cancer***
- **Field carcinogenesis** refers to the concept that a large area of tissue is exposed to carcinogens, leading to multiple primary tumors or recurrences [1].
- In **head and neck squamous cell carcinoma**, extensive exposure of the mucosal lining to tobacco and alcohol promotes widespread genetic alterations [1].
*Cervical cancer*
- Primarily linked to **human papillomavirus (HPV) infection**, which causes localized lesions that may progress [2].
- While different areas of the cervix can be affected, the underlying mechanism is more focal infection rather than diffuse field exposure.
*Prostate cancer*
- Development is often associated with **age**, **genetics**, and **hormonal factors** (androgens).
- It typically arises from a single or a few distinct foci within the prostate gland, not pervasive field change [3].
*Breast cancer*
- Characterized by distinct lesions originating from ductal or lobular epithelium and influenced by **hormones** and **genetics** [4].
- While multifocal breast cancer can occur, it is generally considered the result of multiple independent events or spread from an initial lesion, not a widespread "field" of precancerous tissue in the same way as head and neck.
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 738-739.
[2] 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. 222-223.
[3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 993-994.
[4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1059-1060.
Oncology Indian Medical PG Question 5: Knudson two-hit hypothesis is classically exemplified by
- A. Crohn disease
- B. Ulcerative colitis
- C. Retinoblastoma (Correct Answer)
- D. Melanoma
Oncology Explanation: ***Retinoblastoma***
- The **Knudson two-hit hypothesis** was **originally formulated** based on studies of **retinoblastoma** by Alfred Knudson in 1971 [1].
- It posits that **two separate mutational events** are required to inactivate **both alleles** of the **Rb tumor suppressor gene** in the same cell, leading to tumor formation [1], [2].
- This explains both **hereditary** (germline mutation + somatic mutation) and **sporadic** (two somatic mutations) forms of retinoblastoma [1], [2].
- Retinoblastoma remains the **paradigmatic example** of this hypothesis and tumor suppressor gene inactivation [2].
*Crohn disease*
- This is an **inflammatory bowel disease**, not a neoplasm, with complex etiology involving genetic susceptibility, environmental factors, and immune dysregulation.
- Its pathogenesis does **not follow the Knudson two-hit hypothesis**, which specifically relates to tumor suppressor gene inactivation in cancer.
*Ulcerative colitis*
- Similar to Crohn disease, **ulcerative colitis** is an **inflammatory bowel disease** with multifactorial etiology, not a neoplastic condition.
- While chronic UC can increase colorectal cancer risk through accumulated mutations, the disease itself does **not represent the two-hit hypothesis model**.
*Melanoma*
- **Melanoma** is a skin cancer often linked to **UV radiation** and mutations in oncogenes like **BRAF** and tumor suppressors like **PTEN** and **CDKN2A**. [3]
- While some familial melanomas involve tumor suppressor genes, melanoma is **not the classic example** used to illustrate the Knudson hypothesis—**retinoblastoma holds that distinction**.
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 300.
[2] 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. 227-228.
[3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-298.
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