Molecular Basis of Cancer — MCQs
The following gene mutation protects tumor cells from apoptosis:
Which of the following helps in cell-to-cell adhesion?
Li–Fraumeni syndrome is associated with mutations in which of the following genes?
DNA Methylation is not related to?
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
Tyrosine kinase receptor is associated with proto-oncogene -
The image below shows the life cycle of a virus. Which of the proteins of the virus act as oncogenes?
Chimney sweeper's cancer is also known as
Which enzyme is responsible for the immortality of cancer cells?
What does the term 'Stage M' indicate in colon cancer according to the TNM staging system?
Molecular Basis of Cancer Indian Medical PG Practice Questions and MCQs
Question 1: The following gene mutation protects tumor cells from apoptosis:
- A. BRCA
- B. RB
- C. TGFβ
- D. Bcl-2 (Correct Answer)
Explanation: ***bcl-2*** - The **bcl-2 gene** produces a protein that inhibits apoptosis, thereby allowing tumor cells to evade programmed cell death [1][2]. - Overexpression of **bcl-2** is associated with various cancers, making it pivotal in cancer biology [1]. *RB* - The **RB gene** is primarily a tumor suppressor, regulating the cell cycle, and does not directly prevent apoptosis. - Loss of RB function leads to unregulated cell division rather than inhibition of cell death. *TGFβ* - **TGFβ** acts as a tumor suppressor and can induce apoptosis in certain contexts, particularly in oncogenic processes. - Its primary role involves regulating cell growth and differentiation, not directly protecting against apoptosis. *BRCA* - **BRCA genes** (BRCA1 and BRCA2) are involved in DNA repair mechanisms; mutations increase cancer susceptibility but do not prevent apoptosis directly. - Dysfunction in BRCA proteins primarily impacts the repair of DNA damage, leading to genomic instability rather than apoptosis resistance. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310.
Question 2: Which of the following helps in cell-to-cell adhesion?
- A. Interleukins
- B. Interferons
- C. E-Cadherin (Correct Answer)
- D. Matrix metalloproteinases
Explanation: ***E-Cadherin*** - E-Cadherin is a **cell adhesion molecule** that plays a crucial role in maintaining the structure of tissues by promoting **cell-to-cell adhesion** [1]. - It is mainly involved in the **adherens junctions**, helping cells stick together, especially in epithelial tissues. *Matrix metallo proteinase* - Matrix metallo proteinases (MMPs) are enzymes that degrade **extracellular matrix** components, rather than promoting adhesion between cells. - They are involved in **tissue remodeling** and **wound healing**, not in direct cell-to-cell interactions. *Interleukins* - Interleukins are a group of **cytokines** that mediate **immune responses**, but they do not facilitate direct cell adhesion. - Their primary function involves **cell signaling** and communication, rather than adhesion processes. *Interferons* - Interferons are signaling proteins involved in the **immune defense against viral infections** and do not have a role in cell-to-cell adhesion. - They primarily act to induce an **antiviral state** in neighboring cells and modulate the immune response. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 314-315.
Question 3: Li–Fraumeni syndrome is associated with mutations in which of the following genes?
- A. Gene RB1
- B. Gene BRCA1
- C. Gene P21
- D. Gene TP53 (Correct Answer)
Explanation: ***Gene TP53*** - Li-Fraumeni syndrome is a rare, inherited cancer susceptibility syndrome associated with germline mutations in the **TP53 tumor suppressor gene**. - The **TP53 gene** encodes the p53 protein, which plays a critical role in cell cycle arrest, DNA repair, and initiation of apoptosis in response to cellular stress, thus preventing tumor formation. *Gene P21* - The **p21 gene** (CDKN1A) is a cyclin-dependent kinase inhibitor that acts downstream of p53, mediating p53-induced cell cycle arrest. - While p21 is involved in the p53 pathway, mutations in p21 itself are not the primary cause of Li-Fraumeni syndrome. *Gene RB1* - The **RB1 gene** encodes the retinoblastoma protein, a tumor suppressor involved in cell cycle regulation, particularly in controlling passage from G1 to S phase. - Mutations in **RB1** are primarily associated with hereditary retinoblastoma and osteosarcoma, not Li-Fraumeni syndrome. *Gene BRCA1* - The **BRCA1 gene** is a tumor suppressor gene involved in DNA repair, especially homologous recombination. - Germline mutations in **BRCA1** are strongly associated with hereditary breast and ovarian cancer syndrome, not Li-Fraumeni syndrome.
Question 4: DNA Methylation is not related to?
- A. DNA Replication
- B. Gene silencing
- C. Capping (Correct Answer)
- D. Mismatch repair
Explanation: ***Capping*** - **Capping** is a modification of messenger RNA (mRNA) that occurs during **mRNA processing** in eukaryotes, involving the addition of a 7-methylguanosine cap to the 5' end of the mRNA molecule. - This process is crucial for mRNA stability, translation initiation, and nuclear export, and is entirely **independent of DNA modifications** like DNA methylation. *DNA Replication* - DNA methylation plays a role in **DNA replication** to distinguish newly synthesized strands from parental strands during **DNA repair**. - In bacteria, methylation at specific sites (**Dam methylase**) helps in **mismatch repair** by identifying the parental strand. *Gene silencing* - **DNA methylation** of CpG islands in promoter regions is a well-established mechanism for **gene silencing** by altering chromatin structure and preventing transcription factor binding. - This epigenetic modification leads to stable transcriptional repression and is critical for processes like X-chromosome inactivation and genomic imprinting. *Mismatch repair* - In prokaryotes, **DNA methylation** marks the parental strand, which is used by the **mismatch repair system** to correct errors on the newly synthesized, unmethylated strand. - In eukaryotes, while not directly marking strands, DNA methylation can influence the efficiency of mismatch repair pathways by altering chromatin accessibility.
Question 5: 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 6: Tyrosine kinase receptor is associated with proto-oncogene -
- A. RAS (RAt Sarcoma)
- B. RET (REarranged during Transfection) (Correct Answer)
- C. RB (Retinoblastoma gene)
- D. MYC (Myelocytomatosis oncogene)
Explanation: ***RET*** - RET is a **tyrosine kinase receptor** that plays a crucial role in cell signaling and development [1][2]. - It is associated with several **neoplasms**, including medullary thyroid carcinoma and multiple endocrine neoplasia type 2 [1]. *RB* - RB (Retinoblastoma protein) is a **tumor suppressor gene**, not a proto-oncogene or receptor. - Its role is largely in regulating the **cell cycle**, particularly in preventing excessive cell growth. *RAS* - RAS is a family of **GTPase proteins** involved in transmitting signals within cells, but it is not a receptor itself [1]. - It is classified as an **oncogene**, but does not function as a tyrosine kinase receptor [2]. *MYC* - MYC is a **transcription factor** involved in cell cycle progression and growth, not a tyrosine kinase receptor [2]. - It is considered an **oncogene** that promotes cellular proliferation, but it doesn't have tyrosine kinase activity [3][4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1097-1098. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 291-292. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 28-29. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 293-294.
Question 7: The image below shows the life cycle of a virus. Which of the proteins of the virus act as oncogenes?
- A. L1, L2
- B. E1, E2, E5
- C. E1, E2
- D. E6, E7 (Correct Answer)
Explanation: ***E6, E7*** - The **E6** and **E7** proteins of high-risk human papillomaviruses (HPVs) are considered **oncogenes** because they interfere with critical tumor suppressor pathways [1][2]. - **E6** promotes the degradation of **p53**, a tumor suppressor protein, while **E7** inactivates **retinoblastoma protein (pRb)**, leading to uncontrolled cell proliferation and increased risk of malignant transformation [2]. *L1, L2* - **L1** and **L2** are **late proteins** (structural proteins) that form the **viral capsid** (outer shell) of the HPV virion. - They are essential for assembling new viral particles but do not directly contribute to the oncogenic process by disrupting host cell cycle regulation. *E1, E2, E5* - **E1** is involved in **viral DNA replication**, acting as a helicase and ATPase. - **E2** regulates **viral gene expression** and DNA replication, while **E5** is a small transmembrane protein that can contribute to cell growth but is generally considered less potent in oncogenesis than E6 and E7, and its exact role varies by HPV type. *E1, E2* - **E1** is critical for **viral DNA replication**, and **E2** regulates viral gene transcription and DNA replication. - While important for the viral life cycle, neither E1 nor E2 are the primary drivers of oncogenesis in the way E6 and E7 are, as they do not directly target key tumor suppressor proteins like p53 and pRb. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1007-1008. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 334-335.
Question 8: Chimney sweeper's cancer is also known as
- A. Carcinoma colon
- B. Carcinoma penis
- C. Carcinoma scrotum (Correct Answer)
- D. Carcinoma lung
Explanation: ***Carcinoma scrotum*** - **Chimney Sweeper's cancer** is a historical term for **squamous cell carcinoma** of the scrotum, first described by Percivall Pott in 1775. - It was highly prevalent among chimney sweepers due to prolonged occupational exposure to **soot** (coal tar), which contains **polycyclic aromatic hydrocarbons (PAHs)**. *Carcinoma colon* - This cancer affects the **large intestine** and is linked to polyps, genetic factors, and lifestyle, not specifically soot exposure to external skin. - While PAHs can be ingested and metabolized, the direct association with "Chimney Sweeper's cancer" is specific to external skin carcinogenicity [1]. *Carcinoma penis* - This is a rare cancer associated with **HPV infection**, poor hygiene, and phimosis, primarily affecting the penile shaft or glans [2]. - It is not historically linked to occupational soot exposure in the way scrotal cancer is. *Carcinoma lung* - **Lung cancer** is strongly associated with **smoking** and exposure to airborne carcinogens like asbestos and radon, or general air pollution [1]. - While chimney sweepers might inhale soot, the term "Chimney Sweeper's cancer" specifically refers to the external **scrotal carcinoma** due to direct skin contact. **References:** [1] 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. 217-218. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 975-976.
Question 9: Which enzyme is responsible for the immortality of cancer cells?
- A. Telomerase (Correct Answer)
- B. RNA polymerase
- C. DNA reverse transcriptase
- D. DNA polymerase
Explanation: ***Telomerase*** - **Telomerase** is an enzyme that adds repetitive DNA sequences (telomeres) to the ends of chromosomes, counteracting telomere shortening that normally occurs with cell division [1]. - In cancer cells, activated telomerase prevents **telomere attrition**, allowing cells to bypass replicative senescence and achieve **immortality** [1], [2]. *DNA reverse transcriptase* - **Reverse transcriptase** synthesizes DNA from an RNA template, a process mainly found in retroviruses for replication. - While some cancer cells may activate viral pathways, DNA reverse transcriptase itself isn't the primary enzyme responsible for their intrinsic immortality. *RNA polymerase* - **RNA polymerase** is responsible for transcribing DNA into RNA, a fundamental process for gene expression and protein synthesis in all cells. - It plays a general role in cell survival and function, but not specifically in the indefinite replication characteristic of cancer cells. *DNA polymerase* - **DNA polymerase** is crucial for DNA replication and repair, ensuring the accurate duplication of genetic material during cell division. - While essential for cancer cell proliferation, it does not directly prevent telomere shortening or confer cellular immortality. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 311-312. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 312.
Question 10: What does the term 'Stage M' indicate in colon cancer according to the TNM staging system?
- A. Local extension to serosa and lymph nodes.
- B. Local extension to serosa only.
- C. Local extension to mucosa.
- D. Distant metastasis to the liver. (Correct Answer)
Explanation: ***Local extension to serosa and lymph nodes.*** - Stage M in colon cancer indicates **involvement beyond the primary tumor**, typically affecting the **serosa** and nearby **lymph nodes**. - This stage represents **regional spread** rather than distant metastases, making it a critical point in cancer staging [1]. *Local extension to mucosa.* - This refers to early disease confined to the **innermost layer** of the colon and does not denote advanced disease like Stage M. - It reflects the **initial stages** of colon cancer, not involving lymphatic or serosal spread. *Local extension to serosa.* - While it indicates some **local progression**, it does not encompass the involvement of **lymph nodes**, which is essential for Stage M. - It misses a critical component of the classification, as it is not just about serosal involvement alone. *Metastasis to the liver.* - This describes **distant metastatic spread**, which is categorized beyond local extension and is indicative of a more advanced stage than M. - Stage M specifically refers to local disease rather than **distant metastasis**, such as to the liver. **References:** [1] 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. 236-237.
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