COMPETITIVE EXAM MCQs SERIES of LIFE SCIENCES for CSIR-UGC NET/JRF, SLET, GATE, and other entrance tests: CELL COMMUNICATION AND CELL SIGNALLING – Molecular and Cellular Biology of Cancer.
Syllabus Outline
- Genetic rearrangements in progenitor cells.
- Oncogenes and tumour suppressor genes.
- Cancer and the cell cycle.
- Virus-induced cancer.
- Metastasis and interaction of cancer cells with normal cells.
- Apoptosis and therapeutic interventions of uncontrolled cell growth.
This quiz contains concept-based, most frequently asked 25 MCQs of “CELL COMMUNICATION AND CELL SIGNALLING – Molecular and Cellular Biology of Cancer”. Each question has a single correct/most appropriate answer.
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1. Which of the following viral mechanisms is most directly associated with oncogenic transformation?
A) Inhibition of ribosomal RNA synthesis
B) Suppression of the host immune response
C) Cytoplasmic viral replication using host machinery
D) Integration of viral DNA disrupting tumour suppressor genes
2. A mutation in a proto-oncogene leads to constitutive activation of a signalling pathway promoting proliferation. Which of the following mutations is most consistent with this outcome?
A) Nonsense mutation in both alleles
B) Gain-of-function mutation in a single allele
C) Deletion of both alleles
D) Promoter methylation of the gene
3. Which of the following sequences most accurately reflects the chronological stages of tumorigenesis?
A) Gatekeeper mutation in somatic cells → Epigenetic silencing of tumour suppressors → Clonal genetic instability.
B) Epigenetic alteration of stem/progenitor cells → Gatekeeper mutation → Genetic and epigenetic instability.
C) Polyclonal genetic instability → Epigenetic fixation of tumour-progenitor genes → Rearrangement of oncogenes.
D) Rearrangement of oncogenes → Monoclonal expansion → Epigenetic alteration of the stem cell niche.
4. Which technique is most appropriate to detect the precise nucleotide-level breakpoint of a completely novel, uncharacterized chromosomal translocation in a patient sample?
A) Fluorescence in situ hybridisation using whole-chromosome paints.
B) Multi-colour flow cytometry analysis targeting extracellular cluster of differentiation markers.
C) Whole-genome sequencing coupled with bioinformatics alignment.
D) Western blotting utilising structurally specific monoclonal antibodies.
5. Which of the following scenarios most accurately illustrates a classical Loss of Heterozygosity event?
A) The spontaneous hypermutation of a proto-oncogene into an oncogene via gene amplification events during the S phase.
B) A single dominant-negative mutation in a transcription factor where the mutant protein actively suppresses the function of the remaining wild-type allele.
C) A somatic chromosomal deletion or mitotic recombination removes the remaining functional wild-type allele in a cell that already carries a germline mutation.
D) The widespread epigenetic hypermethylation of an entire chromosome, uniformly silencing all genes on that specific chromatid.
6. A naturally occurring mutant form of the p53 protein can form stable tetramers with wild-type p53 proteins in a heterozygous cell. However, these mixed tetramers completely lose their ability to bind DNA in a sequence-specific manner. In classical genetic terms, how is this type of mutation best classified?
A) Recessive suppression
B) Haploinsufficiency
C) Dominant-negative effect
D) Gain-of-function allostery
7. Highly aggressive malignant tumours commonly show reactivation and strong overexpression of the enzyme telomerase. Why is this reactivation essential for the long-term survival of most cancer cells?
A) Telomerase functions as a ligase that repairs DNA double-strand breaks caused by chemotherapy.
B) Telomerase produces large amounts of ribonucleotides to support the high metabolic demands of cancer cells.
C) Telomerase prevents the shortening of chromosome ends during repeated cell divisions, allowing cancer cells to escape replicative senescence.
D) Telomerase acts as a transcription factor that activates genes involved in metastasis, such as matrix metalloproteinases.
8. Which of the following best describes the primary mechanism by which the tumour suppressor p53 causes cell cycle arrest at the G1/S checkpoint in response to severe DNA damage?
A) p53 moves to the cytoplasm and directly binds to inhibit CDK2 activity.
B) p53 functions as a transcription factor and increases the expression of the CDK inhibitor p21
C) p53 acts as a ubiquitin ligase that targets Cyclin D for rapid degradation.
D) p53 acts as a kinase that phosphorylates the Retinoblastoma protein, keeping it in its active, E2F-inhibiting state.
9. Which of the following protein complexes is actively inhibited by the Spindle Assembly Checkpoint until all sister chromatids are properly attached to the spindle?
A) The Anaphase-Promoting Complex/Cyclosome bound to its activator Cdc20
B) The Cyclin B/CDK1 complex
C) The Origin Recognition Complex at DNA replication origins
D) The Mitotic Checkpoint Complex containing BubR1
10. In a controlled experiment, rapidly dividing human cancer cells are treated with a small molecule that specifically inhibits the protease separase. At which stage of the cell cycle will these cells arrest?
A) At the G1/S boundary
B) In prometaphase
C) In metaphase
D) In telophase
11. Which of the following correctly describes how the viral proteins E6 and E7 from high-risk Human Papillomavirus strains 16 and 18 promote cervical cancer?
A) E6 binds to Retinoblastoma and promotes its degradation; E7 binds to p53, releasing active E2F transcription factors.
B) E6 binds to p53 and promotes its degradation; E7 binds to Retinoblastoma, releasing active E2F transcription factors
C) E6 functions as a tyrosine kinase; E7 acts as a transcription factor for Cyclin D
D) Both E6 and E7 inhibit the Anaphase Promoting Complex
12. Which molecular change caused by Epstein–Barr virus infection increases the risk of cancer in B lymphocytes?
A) Integration of viral DNA near the c-Myc gene causes a mutation
B) Destruction of the Golgi apparatus, disrupting protein transport
C) Production of a viral protein that blocks p53 in nearby cells
D) Disruption of normal B cell growth control
13. Which statement correctly describes Hepatitis Delta virus and its role in liver cancer?
A) It directly mutates host DNA using reverse transcriptase
B) It is a DNA virus that remains inactive in liver cells
C) It produces the same oncogenic proteins as Human Papillomavirus
D) It is a defective RNA virus that does not cause cancer directly
14. How can integrated Human Papillomavirus DNA be distinguished from episomal DNA using restriction digestion followed by Southern blotting?
A) Episomal DNA shows multiple bands, while integrated DNA shows a single band
B) Episomal DNA shows a single band, while integrated DNA shows multiple bands
C) Both show the same pattern
D) Integrated DNA does not bind the probe and shows no bands
15. Which molecular change is a hallmark of epithelial–mesenchymal transition?
A) Decreased E-cadherin and increased vimentin and N-cadherin
B) Increased E-cadherin and decreased vimentin
C) Increased tight junction proteins such as claudin and occludin
D) Decreased epithelial–mesenchymal transition transcription factors
16. What is the main function of matrix metalloproteinases in cancer metastasis?
A) Promote actin filament formation for cell movement
B) Act as transcription factors to increase Vascular Endothelial Growth Factor
C) Degrade extracellular matrix components to allow cell invasion
D) Form a protective capsule around the tumour
17. Exosomes secreted by cancer cells into the surrounding tumour microenvironment have recently been heavily implicated in modifying nearby healthy stromal cells. Which of the following specific mechanisms best explains how these exosomes can promote the “Reverse Warburg effect” in neighbouring normal cells?
A) By delivering massive, fully assembled mitochondria that physically replace the stromal cell’s own organelles.
B) By delivering highly specific microRNAs or proteins that translationally suppress oxidative phosphorylation genes and strongly upregulate glycolytic enzymes in the recipient cells.
C) By physically forming giant gap junctions between the cancer cell and the normal cell to siphon ATP out of the stroma directly.
D) By secreting concentrated hydrochloric acid that chemically denatures respiratory chain proteins in the extracellular space.
18. What is the mechanism of action of BH3 mimetics?
A) Mimic BH3 domains and inhibit Bcl-2 to trigger apoptosis
B) Activate caspase-3 by mimicking to induce apoptosis
C) Activate death receptors by mimicking on the cell surface
D) Inhibit tyrosine kinases by mimicking those involved in cell cycle control
19. Which mechanism explains how tumour-secreted soluble Fas ligand decoy receptors promote long-term immune evasion?
A) They bind and neutralise Fas ligand from cytotoxic T cells, preventing activation of the extrinsic apoptosis pathway in tumour cells.
B) They attract massive numbers of macrophages to the tumour site to phagocytose the surrounding healthy tissue, creating space for expansion.
C) They act as highly efficient competitive inhibitors for the PD-1 receptor, causing systemic autoimmune reactions that distract the immune system.
D) They bind directly to cytochrome c upon release, completely preventing apoptosome formation within the cytoplasm of the tumour cell.
20. Chromosomal translocations in progenitor cells can contribute to oncogenesis. Which of the following statements are correct?
I – Translocations can place proto-oncogenes under the control of strong promoters.
II – Fusion proteins generated by translocations can have novel activities.
III – All chromosomal translocations result in loss of gene function.
IV – Translocations are restricted only to haematological malignancies.
A) I and II only
B) I, II and III
C) II and IV only
D) I, II and IV
21. Which of the following statements relating to the intricate mechanisms of cell cycle checkpoints is correct:
I – The anaphase-promoting complex is an E3 ubiquitin ligase that targets specific proteins for degradation, facilitating exit from mitosis.
II – The phosphorylation of Retinoblastoma is a permanent, irreversible modification that lasts until the cell undergoes apoptosis.
III – CDC25 is a phosphatase that removes inhibitory phosphates from CDKs, driving the cell cycle forward.
IV – ATM and ATR kinases are solely active during the G1 phase of the cell cycle.
A) I and III
B) II and IV
C) I, II, and III
D) III and IV
22. Which statement correctly explains how the Hepatitis B virus and the Hepatitis C virus cause liver cancer?
I – Hepatitis B virus integrates into the host genome and produces HBx protein.
II – Hepatitis C virus alters cell signalling and causes chronic inflammation.
III – Hepatitis B virus is an RNA virus, while Hepatitis C virus is a DNA virus.
IV – Hepatitis B virus destroys the Retinoblastoma protein, and Hepatitis C virus destroys the p53 protein.
A) I and II
B) II, III and IV
C) I, II, III and IV
D) III and IV
23. Which statements about virus-induced cancers are correct?
I – SV40 promoters are widely used in gene expression systems
II – Epstein–Barr virus is often found in some cancers, such as Hodgkin lymphoma
III – Rous Sarcoma Virus carries v-src, a viral version of a tumour suppressor gene
IV – Tumour-causing viruses often block apoptosis to keep infected cells alive
A) I and IV
B) I, III, and IV
C) II and III
D) I, II and IV
24. Which statements about the tumour microenvironment are correct?
I – Low oxygen increases Vascular Endothelial Growth Factor and Matrix Metalloproteinases, promoting metastasis
II – Tumour-associated macrophages always prevent metastasis
III – Cancer-associated fibroblasts support tumour growth and metastasis
IV – Acidic pH prevents cancer cell migration
A) I, III and IV
B) II and IV only
C) I and III only
D) I, II and III
25. Assertion (A): Most human cancer cells carry mutations that disrupt the G1/S checkpoint, but they rarely show complete inactivation of the G2/M or spindle assembly checkpoints.
Reason (R): Complete loss of the spindle assembly checkpoint causes severe chromosomal missegregation and rapid cell death, making such mutations unfavourable for tumour survival.
A) Both A and R are true, and R correctly explains A.
B) Both A and R are true, but R does not correctly explain A.
C) A is true, but R is false.
D) A is false, but R is true.
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References
- Nelson, David L. & Cox, Michael M. (2021). Lehninger Principles of Biochemistry, W. H. Freeman, 8th Edition.
- Willey, J. M., Sandman, K. M., & Wood, D. H. (2022). Prescott’s Microbiology, McGraw-Hill, 12th Edition
- Kuby, J., Kindt, T. J., Osborne, B. A., & Goldsby, R. A. (2019). Kuby Immunology, W. H. Freeman, 8th Edition.
- Alberts, B., Johnson, A., Lewis, J., Morgan, D., Raff, M., Roberts, K., & Walter, P. (2014). Molecular Biology of the Cell, Garland Science, 4th Edition.
- Geoffrey Cooper and Kenneth Adams (2022). The Cell: A Molecular Approach, Oxford University Press, 9th Edition
- Robert A Weinberg, Robert A. Weinberg (2006). The Biology of Cancer, Taylor & Francis, 1st Edition.
- Gupta, P.K. (2022). Cell and Molecular Biology, Rastogi Publications, 5th Edition.
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