Tumor Immunology — MCQs
Nivolumab is used as checkpoint inhibitor in
A researcher is studying the interactions between foreign antigens and human immune cells. She has isolated a line of lymphocytes that is known to bind antigen-presenting cells. From this cell line, she has isolated a cell surface protein that binds to class I major histocompatibility complex molecules. The continued activation, proliferation and survival of this specific cell line requires which of the following signaling molecules?
Radiation exposure can lead to which type of thyroid carcinoma?
Which of the following is true? 1. BRCA1 is an oncogene 2. HER2neu is amplified only in a fraction of breast cancer 3. EGFR (+) is seen in non-small cell lung cancer 4. N-MYC is a tumor suppressor gene
What is the mechanism of action of Bevacizumab?
KEYNOTE-189 trial for pembrolizumab is done for?
Statement 1 - A 59-year-old patient presents with flaccid bullae. Histopathology shows a suprabasal acantholytic split. Statement 2 - The row of tombstones appearance is diagnostic of Pemphigus vulgaris.
With the lack of CD40 in B cells, which immunological abnormality is seen?
Which is the most immunogenic antigen of Salmonella Typhi?
Which of the following is true regarding lattice formation?
Tumor Immunology Indian Medical PG Practice Questions and MCQs
Question 1: Nivolumab is used as checkpoint inhibitor in
- A. Hodgkin's lymphoma (Correct Answer)
- B. Medulloblastoma
- C. Retinoblastoma
- D. Pleuropulmonary blastoma
Explanation: ***Hodgkin's lymphoma*** - **Nivolumab** is an **immune checkpoint inhibitor** targeting **PD-1**. It has shown significant efficacy in treating relapsed or refractory Hodgkin's lymphoma, particularly in patients who have failed prior therapies. - Hodgkin's lymphoma cells, specifically **Reed-Sternberg cells**, often overexpress PD-L1, which allows them to evade the immune system, making PD-1 blockade a rational therapeutic strategy. *Medulloblastoma* - **Medulloblastoma** is a common malignant brain tumor in children, and while immunotherapy research is ongoing, Nivolumab is **not a standard treatment** for this condition. - Treatment typically involves **surgery, radiation, and chemotherapy**, with targeted therapies under investigation. *Retinoblastoma* - **Retinoblastoma** is a malignant tumor of the retina, most commonly affecting young children. Treatment usually involves **chemotherapy, laser therapy, cryotherapy, or enucleation**. - There is **no established role for Nivolumab** or PD-1 inhibitors in the routine management of retinoblastoma. *Pleuropulmonary blastoma* - **Pleuropulmonary blastoma** is a rare, malignant lung tumor of childhood. Treatment primarily consists of **surgery and chemotherapy**. - While experimental, there is **no current evidence** supporting the use of Nivolumab as a standard treatment for pleuropulmonary blastoma.
Question 2: A researcher is studying the interactions between foreign antigens and human immune cells. She has isolated a line of lymphocytes that is known to bind antigen-presenting cells. From this cell line, she has isolated a cell surface protein that binds to class I major histocompatibility complex molecules. The continued activation, proliferation and survival of this specific cell line requires which of the following signaling molecules?
- A. Interleukin 1
- B. Interleukin 4
- C. Interleukin 2 (Correct Answer)
- D. Interleukin 8
- E. Interleukin 6
Explanation: ***Interleukin 2*** - The description of the lymphocyte binding the **constant portion of MHC class I** and requiring a signaling molecule for activation, proliferation, and survival points to a **T cell**. - **Interleukin-2 (IL-2)** is a crucial cytokine for the proliferation, differentiation, and survival of T lymphocytes, acting in an autocrine or paracrine fashion after T cell activation. *Interleukin 1* - **Interleukin-1 (IL-1)** is primarily involved in inflammation and fever, produced by macrophages and other innate immune cells. - While it can act as a costimulator for T cells, it is not the primary cytokine required for their sustained proliferation and survival after initial activation. *Interleukin 4* - **Interleukin-4 (IL-4)** is a key cytokine in humoral immunity, promoting B cell proliferation and differentiation, and inducing IgE class switching. - It also plays a role in the differentiation of naive T cells into **Th2 cells**, but it is not the main cytokine for general T cell proliferation and survival. *Interleukin 8* - **Interleukin-8 (IL-8)**, also known as CXCL8, is a chemokine primarily responsible for attracting and activating neutrophils to sites of infection or inflammation. - It does not have a direct role in the sustained proliferation and survival of activated lymphocytes. *Interleukin 6* - **Interleukin-6 (IL-6)** is a pleiotropic cytokine involved in acute phase reactions, hematopoiesis, and the immune response, particularly B cell differentiation and antibody production. - Although it can influence T cell responses, it is not the primary growth factor for activated T lymphocytes as IL-2 is.
Question 3: Radiation exposure can lead to which type of thyroid carcinoma?
- A. Lymphoma
- B. Papillary carcinoma (Correct Answer)
- C. Medullary carcinoma
- D. Follicular carcinoma
Explanation: ***Papillary carcinoma*** - Papillary thyroid carcinoma is strongly associated with **radiation exposure**, particularly during childhood [1]. - It is the most prevalent type of thyroid cancer and typically has a **good prognosis** [1]. *Lymphoma* - Thyroid lymphoma is rare and generally not linked to **radiation exposure**; it often presents as a **rapidly enlarging goiter**. - It is more commonly associated with **autoimmune thyroiditis**, not primary radiation effects. *Follicular carcinoma* - Follicular carcinoma shows a correlation with **iodine deficiency** rather than radiation exposure [1]. - Its presentation is more subtle, compared to the classical association of **radiation with papillary carcinoma**. *Medullary carcinoma* - Medullary thyroid carcinoma is primarily linked to **familial syndromes** like MEN 2 and not radiation exposure. - It arises from **parafollicular C cells**, making it clinically distinct from radiation-related types. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1098-1099.
Question 4: Which of the following is true? 1. BRCA1 is an oncogene 2. HER2neu is amplified only in a fraction of breast cancer 3. EGFR (+) is seen in non-small cell lung cancer 4. N-MYC is a tumor suppressor gene
- A. 1,3
- B. 1,2
- C. 2,3 (Correct Answer)
- D. All of the options
Explanation: ***Correct Option: 2,3*** - **Statement 2 is TRUE**: HER2neu amplification occurs in only a fraction (~15-20%) of breast cancers, making it a specific subset requiring targeted therapy with trastuzumab (Herceptin) [1]. - **Statement 3 is TRUE**: EGFR (epidermal growth factor receptor) mutations or overexpression are commonly seen in non-small cell lung cancer (NSCLC) and serve as important therapeutic targets for tyrosine kinase inhibitors. *Incorrect Option: 1,3* - Statement 1 is **FALSE**: BRCA1 is a **tumor suppressor gene**, not an oncogene. It functions in DNA double-strand break repair, and loss-of-function mutations increase the risk of breast and ovarian cancers. - Statement 3 is TRUE, but the inclusion of the false statement about BRCA1 makes this option incorrect. *Incorrect Option: 1,2* - Statement 1 is **FALSE**: BRCA1 is a **tumor suppressor gene**, not an oncogene. - Statement 2 is TRUE [1], but the false classification of BRCA1 invalidates this option. *Incorrect Option: All of the options* - Statement 1 is **FALSE**: BRCA1 is a tumor suppressor gene, not an oncogene. - Statement 4 is **FALSE**: N-MYC is an **oncogene** that is amplified in neuroblastoma and other cancers, not a tumor suppressor gene. - Since two of the four statements are incorrect, "All of the options" cannot be true. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1059-1060.
Question 5: What is the mechanism of action of Bevacizumab?
- A. Anti VEGF antibody (Correct Answer)
- B. Histone deacetylase inhibitor
- C. HER2 neu inhibitor
- D. Proteasome inhibitor
Explanation: ***Anti VEGF antibody*** - **Bevacizumab** is a **monoclonal antibody** that specifically targets and binds to vascular endothelial growth factor (VEGF). - By inhibiting VEGF, bevacizumab prevents the formation of new blood vessels (**angiogenesis**) that tumors need to grow and metastasize. *Histone deacetylase inhibitor* - **Histone deacetylase (HDAC) inhibitors** influence gene expression by modifying chromatin structure, leading to cell cycle arrest and apoptosis in cancer cells. - They are used in certain hematologic malignancies and solid tumors but do not directly interfere with angiogenesis. *Proteasome inhibitor* - **Proteasome inhibitors** like bortezomib block the action of proteasomes, leading to an accumulation of ubiquitinated proteins and induction of apoptosis in cancer cells. - This mechanism is distinct from blocking new blood vessel formation. *HER2 neu inhibitor* - **HER2 neu inhibitors** (e.g., trastuzumab) specifically target the HER2/neu receptor, which is overexpressed in certain breast and gastric cancers. - Their action primarily involves blocking growth signals transmitted through this receptor, not inhibiting VEGF or angiogenesis.
Question 6: KEYNOTE-189 trial for pembrolizumab is done for?
- A. Nivolumab with chemo given for NSCLC
- B. Only Pembrolizumab for NSCLC
- C. Pembrolizumab with chemo given for NSCLC (Correct Answer)
- D. Only nivolumab for NSCLC
Explanation: ***Pembrolizumab with chemo given for NSCLC*** - The **KEYNOTE-189 trial** investigated the efficacy of **pembrolizumab** in combination with chemotherapy as first-line treatment for **metastatic nonsquamous non-small cell lung cancer (NSCLC)**. - This trial demonstrated significant improvements in overall survival and progression-free survival, leading to the approval of pembrolizumab in this setting. *Nivolumab with chemo given for NSCLC* - **Nivolumab** is another PD-1 inhibitor, but studies specifically combining nivolumab with chemotherapy for NSCLC (e.g., CheckMate 227) are distinct from KEYNOTE-189. - While both drugs are used in NSCLC, their pivotal trials and specific combination regimens differ. *Only Pembrolizumab for NSCLC* - Although pembrolizumab monotherapy is approved for certain NSCLC patients with high PD-L1 expression, the **KEYNOTE-189 trial specifically focused on a combination approach** with chemotherapy. - Other KEYNOTE trials, like KEYNOTE-024, evaluated pembrolizumab monotherapy in NSCLC. *Only nivolumab for NSCLC* - **Nivolumab monotherapy** has been studied and approved for NSCLC, particularly in the second-line setting or for patients with high PD-L1 expression, but this was not the focus of the KEYNOTE-189 trial. - Trials like CheckMate 017 and 057 investigated nivolumab as a single agent in NSCLC.
Question 7: Statement 1 - A 59-year-old patient presents with flaccid bullae. Histopathology shows a suprabasal acantholytic split. Statement 2 - The row of tombstones appearance is diagnostic of Pemphigus vulgaris.
- A. Statements 1 & 2 are correct, 2 is not explaining 1 (Correct Answer)
- B. Statements 1 and 2 are correct and 2 is the correct explanation for 1
- C. Statements 1 and 2 are incorrect
- D. Statement 1 is incorrect
Explanation: ***Correct: Statements 1 & 2 are correct, 2 is not explaining 1*** **Analysis of Statement 1:** - A 59-year-old patient with **flaccid bullae** and **suprabasal acantholytic split** on histopathology is the classic presentation of **Pemphigus vulgaris** - The flaccid (easily ruptured) nature of bullae distinguishes it from tense bullae seen in bullous pemphigoid - The suprabasal location of the split (just above the basal layer) with acantholysis (loss of cell-to-cell adhesion) is pathognomonic - **Statement 1 is CORRECT** ✓ **Analysis of Statement 2:** - The **"row of tombstones" or "tombstone appearance"** is indeed a diagnostic histopathological feature of Pemphigus vulgaris - This appearance results from basal keratinocytes remaining attached to the basement membrane while suprabasal cells separate due to acantholysis - The intact basal cells standing upright resemble a row of tombstones - **Statement 2 is CORRECT** ✓ **Does Statement 2 explain Statement 1?** - Statement 2 describes a **histopathological appearance** (tombstone pattern) that is a **consequence** of the suprabasal split - However, it does NOT explain the **underlying cause** of the flaccid bullae or the suprabasal split - The true explanation involves **IgG autoantibodies against desmoglein 3 (and desmoglein 1)**, which attack intercellular adhesion structures (desmosomes), causing **acantholysis** - Therefore, **Statement 2 does NOT explain Statement 1** ✗ *Incorrect: Statement 2 is the correct explanation for Statement 1* - While both statements describe features of Pemphigus vulgaris, the tombstone appearance is a descriptive finding, not an explanatory mechanism *Incorrect: Statements 1 and 2 are incorrect* - Both statements are medically accurate descriptions of Pemphigus vulgaris features *Incorrect: Statement 1 is incorrect* - Statement 1 correctly describes the cardinal clinical and histopathological features of Pemphigus vulgaris
Question 8: With the lack of CD40 in B cells, which immunological abnormality is seen?
- A. Total lack of NK cells
- B. Lack of CD8 mediated cytotoxicity
- C. Inability of neutrophil against infections
- D. Decreased IgG and increase in IgM (Correct Answer)
Explanation: ***Decreased IgG and increase in IgM*** - The interaction between **CD40 on B cells** and **CD40L (CD154) on T helper cells** is crucial for **B cell activation**, proliferation, and **class switch recombination** (CSR). - Without this interaction, B cells cannot undergo CSR, leading to a failure to produce **IgG, IgA, or IgE**, while **IgM levels remain high** because IgM production is the initial default. *Total lack of NK cells* - **Natural Killer (NK) cells** are part of the innate immune system and their development is largely independent of CD40-CD40L signaling. - The absence of CD40 on B cells primarily affects adaptive humoral immunity, not NK cell numbers or function. *Lack of CD8 mediated cytotoxicity* - **CD8+ T cells** mediate cytotoxicity against infected or cancerous cells and their activation is primarily dependent on antigen presentation by **MHC class I molecules** and costimulation, not directly on B cell CD40. - While B cells can act as APCs, their CD40 interaction is more critical for T helper cell help for humoral responses. *Inability of neutrophil against infections* - **Neutrophils** are phagocytic cells important in innate immunity, and their function is largely independent of CD40 on B cells. - Neutrophil activity relies on pathogen recognition, phagocytosis, and degranulation, which are not directly regulated by the B cell CD40-CD40L pathway.
Question 9: Which is the most immunogenic antigen of Salmonella Typhi?
- A. O antigen
- B. H antigen (Correct Answer)
- C. Vi antigen
- D. Somatic antigen
Explanation: **Explanation:** The immunogenicity of an antigen is determined by its chemical complexity and size. In *Salmonella Typhi*, the **H (Flagellar) antigen** is the most immunogenic because it is composed of proteins (flagellin). Proteins are more potent triggers of the immune system compared to polysaccharides, leading to a robust antibody response. This is why H-agglutinins appear earlier and reach higher titers than O-agglutinins during a *Salmonella* infection. **Analysis of Options:** * **A & D. O Antigen (Somatic Antigen):** These are the same entity. The O antigen is a lipopolysaccharide (LPS) located on the outer membrane. While it is important for serogrouping, polysaccharides are generally less immunogenic than proteins. O-antibodies appear later and disappear sooner than H-antibodies. * **C. Vi Antigen:** This is a surface polysaccharide capsular antigen (Virulence antigen). It is poorly immunogenic and primarily functions by masking the O antigen from antibodies. Its main clinical utility is in identifying chronic carriers and for use in certain vaccines (e.g., Typhim VI). **High-Yield Clinical Pearls for NEET-PG:** * **Widal Test:** Measures antibodies against O and H antigens. A titer of **>1:160 for O** and **>1:160 for H** is usually considered significant in endemic areas. * **Sequence of Appearance:** In Enteric fever, O antibodies appear first (around the end of the 1st week), but H antibodies reach higher peaks and persist longer. * **Carrier State:** Persistent high titers of **Vi antibodies** (1:10 or more) suggest a chronic carrier state, as the bacteria continue to harbor the capsule in the gallbladder or urinary tract.
Question 10: Which of the following is true regarding lattice formation?
- A. Associated with precipitation and not agglutination
- B. Associated with agglutination and not precipitation
- C. Associated with both precipitation and agglutination (Correct Answer)
- D. Associated with neither precipitation nor agglutination
Explanation: **Explanation:** The **Lattice Hypothesis**, proposed by Marrack (1934), is the fundamental principle governing all visible antigen-antibody (Ag-Ab) reactions. It states that for a visible reaction to occur, multivalent antigens must be cross-linked by bivalent antibodies to form a large, insoluble three-dimensional network or "lattice." **Why Option C is correct:** Lattice formation is the prerequisite for both **precipitation** and **agglutination**. * In **precipitation**, the antigen is **soluble**. When it reacts with its specific antibody at the "Zone of Equivalence," they form a lattice that becomes too large to remain in solution and settles as a visible precipitate. * In **agglutination**, the antigen is **particulate** (e.g., bacteria, RBCs). The antibodies act as bridges between these particles, forming a lattice that results in visible clumping. **Why other options are incorrect:** * **Options A & B:** These are incorrect because they suggest the lattice phenomenon is exclusive to one type of reaction. While the physical state of the antigen differs (soluble vs. particulate), the underlying mechanism of cross-linking to form a lattice remains identical. * **Option D:** This is incorrect as no visible Ag-Ab reaction can occur without the formation of a lattice. **NEET-PG High-Yield Pearls:** 1. **Zone of Equivalence:** This is the specific ratio of Ag to Ab where lattice formation is maximal. 2. **Prozone Phenomenon:** False negative result due to **antibody excess**. No lattice forms because every antigenic site is saturated by a single antibody, preventing cross-linking. 3. **Postzone Phenomenon:** False negative result due to **antigen excess**. 4. **Valency:** For a lattice to form, the antigen must be multivalent and the antibody must be at least bivalent (IgG) or multivalent (IgM).
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