Tumor Immunity — MCQs
Which among the following drugs is the new FDA approved immune checkpoint inhibitor for endometrial carcinoma?
Which of the following is not a component of innate immunity?
Which of the following is considered a fundamental defense mechanism in psychology?
Which gene mutation is commonly associated with malignant melanoma?
Which marker is used to differentiate a thymoma from acute lymphoblastic leukemia (ALL)?
Which of the following is the platinum-based chemotherapeutic agent used as first-line treatment for ovarian carcinoma?
Therapeutic exposure is a core technique primarily used in which type of therapy?
Cell surface molecules involved in peripheral tolerance induction are
Which of the following is a function of MHC class I and II?
E-cadherin gene deficiency is associated with which type of cancer?
Tumor Immunity Indian Medical PG Practice Questions and MCQs
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
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.
Question 2: Which of the following is not a component of innate immunity?
- A. Epithelial barriers
- B. NK cells
- C. Dendritic cells
- D. Helper T lymphocytes (Correct Answer)
Explanation: ***Helper T lymphocyte*** - Helper T lymphocytes are a crucial part of **adaptive immunity** [4], facilitating responses against pathogens. - They specifically activate B cells and cytotoxic T cells [2], unlike components of innate immunity, which respond nonspecifically. *NK cells* - Natural Killer (NK) cells are integral to **innate immunity** [1], targeting infected or tumor cells without prior sensitization. - They play a role in the initial response to viral infections and can produce **cytokines** [2]. *Epithelial barriers* - Epithelial barriers act as the first line of defense in **innate immunity** [1], preventing pathogen entry. - They include physical and chemical barriers like skin and mucous membranes [3]. *Dendritic cells* - Dendritic cells are key antigen-presenting cells involved in **innate immunity** [1] and link to adaptive immunity. - They capture and present antigens [2], activating T cells to mount an immune response. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 194-196. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 207-208. [3] 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. 152-153. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 196-198.
Question 3: Which of the following is considered a fundamental defense mechanism in psychology?
- A. Alienation
- B. Confabulation
- C. Repression (Correct Answer)
- D. Suppression
Explanation: ***Repression*** - **Repression** is the **fundamental unconscious defense mechanism** where unacceptable thoughts, feelings, or memories are pushed out of conscious awareness to protect the ego. - It is considered the foundational defense mechanism because it operates automatically and without conscious effort, forming the basis for many other defense mechanisms. *Alienation* - **Alienation** refers to a feeling of estrangement or disconnection from others, society, or oneself, often due to social or psychological factors, but it is not a defense mechanism. - It describes a state of being rather than an active psychological process used to cope with anxiety. *Confabulation* - **Confabulation** is the creation of false autobiographical memories without the intent to deceive, often seen in neurological conditions like **Korsakoff's syndrome**. - It is a symptom of memory impairment, not an active psychological defense mechanism. *Suppression* - **Suppression** is a defense mechanism but is considered a mature/conscious defense; it involves deliberately and consciously putting unwanted thoughts or feelings out of mind. - Unlike **repression**, **suppression** is an intentional and relatively aware act of avoiding disturbing thoughts.
Question 4: Which gene mutation is commonly associated with malignant melanoma?
- A. MYCN
- B. CDKN2A (Correct Answer)
- C. RET
- D. BRAF
Explanation: ***CDK2A*** - CDK2A mutations are implicated in malignant melanoma as they disrupt the **cell cycle regulation**, contributing to uncontrolled cell growth [1]. - Loss of CDK2A function leads to reduced **p16INK4A**, a crucial inhibitor of cyclin-dependent kinases involved in **G1/S phase transition** [1,3]. - Germline mutations of p16 (CDKN2A) are present in 25% of melanoma-prone kindreds [2], and germline mutations in CDKN2A are associated with familial forms of melanoma [3]. *RET* - RET mutations are primarily associated with **medullary thyroid carcinoma** and **multiple endocrine neoplasia type 2**, not melanoma. - It is involved in the signaling pathways but does not have a direct link to melanoma pathogenesis. *None* - Suggesting "none" misrepresents the reality that specific mutations do occur in malignant melanoma, including **CDK2A** and **BRAF**. - This option fails to recognize the importance of genetic alterations in cancer development and progression. *N-myc* - N-myc mutations are primarily associated with **neuroblastoma** and not typically linked to malignant melanoma. - In melanoma, mutations of this gene do not play a significant role in its pathophysiology compared to another tumor suppressor gene like **CDK2A**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1150-1151. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-298. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 305-306.
Question 5: Which marker is used to differentiate a thymoma from acute lymphoblastic leukemia (ALL)?
- A. Cytokeratin (Correct Answer)
- B. CD1a
- C. CD3
- D. TdT
Explanation: ***Cytokeratin*** - **Thymomas** are epithelial tumors and express **cytokeratin**, which is a marker for epithelial cells, while **ALL** (Acute Lymphoblastic Leukemia) does not express this marker. - The presence of **cytokeratin** indicates a **thymic origin**, differentiating it from lymphoid neoplasms like **ALL**. *CD1a* - This marker is primarily associated with **Hodgkin's lymphoma** and some **T-cell neoplasms**, not thymomas [2]. - The lack of expression in **ALL** makes it an unsuitable differentiator for thymomas. *Tdt* - **Tdt** (Terminal deoxynucleotidyl transferase) is a marker typically found in lymphoid progenitor cells, especially in **ALL**. - Its presence would not indicate a **thymoma**, which does not express **Tdt**. *CD3* - While **CD3** is a marker of **T-cells** [2], it is not specific for thymomas, which can be **CD3-positive**, but it is also seen in various **lymphoid proliferations** including **ALL** [1]. - Therefore, it cannot be definitively used to distinguish between a thymoma and **ALL**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 599-600. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 598.
Question 6: Which of the following is the platinum-based chemotherapeutic agent used as first-line treatment for ovarian carcinoma?
- A. Cyclophosphamide
- B. Methotrexate
- C. Cisplatin (Correct Answer)
- D. Dacarbazine
Explanation: ***Cisplatin*** - **Cisplatin** is a platinum-based chemotherapy drug that forms **DNA cross-links**, inhibiting DNA synthesis and leading to the death of rapidly dividing cells, making it highly effective against **ovarian carcinoma**. - It is a cornerstone of chemotherapy regimens for ovarian cancer, often used in combination with other agents such as paclitaxel. *Methotrexate* - **Methotrexate** is an **antimetabolite** that inhibits dihydrofolate reductase, thereby interfering with DNA synthesis. - While it is used in various cancers like leukemia, lymphoma, and some solid tumors (e.g., breast cancer, gestational trophoblastic disease), it is **not a primary recommended drug for ovarian carcinoma**. *Cyclophosphamide* - **Cyclophosphamide** is an **alkylating agent** that causes DNA damage, leading to cell death. - It is used in many cancers, including lymphoma, breast cancer, and some leukemias, but it is **not a first-line or primary agent for ovarian carcinoma** in contemporary treatment guidelines. *Dacarbazine* - **Dacarbazine** is an **alkylating agent** primarily used in the treatment of **malignant melanoma** and Hodgkin lymphoma. - It is **not indicated for the treatment of ovarian carcinoma**.
Question 7: Therapeutic exposure is a core technique primarily used in which type of therapy?
- A. Behavior therapy with exposure techniques (Correct Answer)
- B. Cognitive therapy modifying thought patterns
- C. Supportive therapy providing emotional support
- D. Psychoanalysis focusing on unconscious conflicts
Explanation: ***Behavior therapy with exposure techniques*** - **Exposure therapy** is a core component of **behavior therapy**, specifically designed to address **anxiety disorders** and phobias by gradually exposing individuals to feared stimuli. - The goal is to reduce fear and avoidance behaviors by helping the individual learn that the feared object or situation is harmless and that their anxiety will naturally decrease over time (habituation). *Cognitive therapy modifying thought patterns* - **Cognitive therapy** focuses on identifying and changing **maladaptive thought patterns** and beliefs that contribute to psychological distress. - While it may be combined with behavioral techniques, **exposure** itself is not its primary methodology but rather a behavioral intervention. *Supportive therapy providing emotional support* - **Supportive therapy** aims to reduce distress by offering **emotional support**, encouragement, and practical advice, helping patients cope with current stressors. - It does not typically involve structured techniques like exposure to modify specific behaviors or thought patterns, but rather a more empathetic and less directive approach. *Psychoanalysis focusing on unconscious conflicts* - **Psychoanalysis** is a long-term, intensive therapy that explores **unconscious conflicts**, repressed memories, and past experiences to bring them to conscious awareness. - Its techniques include **free association**, dream analysis, and transference interpretation, rather than direct exposure to feared stimuli.
Question 8: Cell surface molecules involved in peripheral tolerance induction are
- A. CD40 and CD40L
- B. CD34 and CD51
- C. B7 and CD28 (Correct Answer)
- D. B7 and CD3
Explanation: ***B7 and CD28*** - B7 is crucial for providing a **costimulatory signal** to T cells via interaction with CD28, promoting **T cell activation** and peripheral tolerance [1][2]. - This interaction is essential in preventing autoimmune responses by ensuring T cells require both antigen and costimulatory signals for full activation [1][3]. *B7 and CD3* - CD3 is a part of the T cell receptor (TCR) complex, primarily involved in **T cell activation**, not specifically in peripheral tolerance. - The interaction of B7 with **CD3** does not provide the costimulatory signal necessary for peripheral tolerance [3]. *CD34 and CD51* - CD34 is primarily involved in **hematopoietic stem cell trafficking** and does not play a role in T cell tolerance mechanisms. - CD51 is associated with **integrins** and plays a role in adhesion rather than in peripheral tolerance induction. *CD40 and CD40L* - While CD40-CD40L interactions are important for **B cell activation** and other immune responses, they are not directly involved in the inductive mechanisms of **peripheral tolerance** in T cells. - They primarily mediate costimulatory signals in **adaptive immunity**, not specifically for tolerance purposes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 204-206. [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. 157-158. [3] 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. 176-177.
Question 9: Which of the following is a function of MHC class I and II?
- A. Antibody class switching
- B. Signal transduction in T cell
- C. Antigen presentation to T cell (Correct Answer)
- D. Increase the secretion of cytokine
Explanation: ***Antigen presentation to T cell*** - **MHC class I** molecules present **endogenous antigens** to **CD8+ cytotoxic T cells**, leading to the destruction of infected or cancerous cells. - **MHC class II** molecules present **exogenous antigens** to **CD4+ helper T cells**, which then coordinate the immune response. *Antibody class switching* - This process is primarily influenced by **cytokines** secreted by helper T cells, rather than direct MHC function. - While T cells interact with B cells to facilitate class switching, the direct role is not performed by the MHC molecules themselves. *Signal transduction in T cell* - **T cell receptor (TCR)** and associated co-receptors (like **CD3 complex**) are responsible for signal transduction upon antigen recognition. - MHC molecules present the antigen, but they do not directly mediate the intracellular signaling cascades within the T cell. *Increase the secretion of cytokine* - Cytokine secretion is a downstream effect of T cell activation, which occurs after successful antigen presentation by MHC molecules. - MHC molecules' direct function is presentation, not the direct increase in cytokine secretion.
Question 10: E-cadherin gene deficiency is associated with which type of cancer?
- A. Intestinal cancer
- B. Pancreatic cancer
- C. Thyroid cancer
- D. Gastric cancer (Correct Answer)
Explanation: **Correct: Gastric cancer** - **E-cadherin** is a crucial cell adhesion molecule, and its deficiency is strongly linked to **diffuse-type gastric cancer**. - Mutations in the **CDH1 gene**, which encodes E-cadherin, predispose individuals to **hereditary diffuse gastric cancer (HDGC)** due to loss of cell-cell adhesion. - This is a classic tumor suppressor gene, and germline mutations lead to an autosomal dominant cancer syndrome. *Incorrect: Intestinal cancer* - While E-cadherin plays a role in various epithelial cancers, its deficiency is not the primary driver or defining feature of intestinal cancer (colorectal cancer). - **Colorectal cancer** is more commonly associated with mutations in genes like **APC**, **KRAS**, **TP53**, and mismatch repair genes. *Incorrect: Thyroid cancer* - E-cadherin expression can be altered in thyroid cancers, but its deficiency is not the hallmark genetic event. - **Thyroid cancer** (especially papillary and follicular types) is more frequently linked to gene rearrangements (e.g., **RET/PTC**, **PAX8/PPARγ**) or point mutations (e.g., **BRAF**, **RAS**). *Incorrect: Pancreatic cancer* - Although E-cadherin can be down-regulated in pancreatic cancer, it is not the principal genetic deficiency. - **Pancreatic ductal adenocarcinoma** typically involves mutations in **KRAS**, **TP53**, **SMAD4**, and **CDKN2A**.
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