50 Year 2: Molecular Biology exam questions on TUMOR SUPPRESSOR GENES & CELL CYCLE CONTROL MCQs for medical students. Includes MCQs, answers, explanations and w
This MCQ set contains 50 questions on TUMOR SUPPRESSOR GENES & CELL CYCLE CONTROL MCQs in the Year 2: Molecular Biology unit. Each question includes the correct answer and a detailed explanation for active recall and exam preparation.
Correct answer: B – 13q14
The RB gene, the first tumor suppressor gene to be discovered, is located at chromosomal locus 13q14.
Correct answer: B – Two hits (mutations) are required
Knudson's two-hit hypothesis states that two hits are required to develop retinoblastoma - both copies of the RB tumor suppressor gene must be dysfunctional.
Correct answer: B – One mutation is inherited (germline), second is somatic
In familial cases, one hit (mutation) is inherited in the germline and the second hit develops when the normal Rb gene is lost by somatic mutation in retinoblasts.
Correct answer: C – G1/S transition
The Rb gene exerts antiproliferative effects by controlling the G1/S transition of the cell cycle, preventing cells from entering S phase inappropriately.
Correct answer: B – Hypophosphorylated
In its active form, Rb is hypophosphorylated and binds to E2F transcription factor, preventing transcription of genes required for DNA replication like cyclin E.
Correct answer: B – E2F
Hypophosphorylated Rb binds to E2F transcription factor, preventing E2F from activating transcription of genes required for cell cycle progression and DNA replication.
Correct answer: C – 70%
Approximately 70% of tumors demonstrate biallelic loss of TP53, highlighting its critical role as a tumor suppressor and "guardian of the genome."
Correct answer: B – Li-Fraumeni syndrome
Li-Fraumeni syndrome involves inheritance of one defective TP53 allele in the germline, with the second defect occurring in somatic cells, predisposing to multiple cancers.
Correct answer: B – Guardian of the genome
p53 is called the "guardian of the genome" because it serves as the central monitor of cellular stress and can initiate responses to maintain genomic integrity.
Correct answer: A – Anoxia, oncogene signaling, and DNA damage
p53 is the central monitor of stress in the cell and can be activated by anoxia, inappropriate oncogene signaling, or DNA damage.
Correct answer: B – Phosphorylation
DNA damage leads to activation of p53 by phosphorylation, which stabilizes the protein and activates its transcriptional functions.
Correct answer: C – CDKN1A (p21)
Activated p53 drives transcription of CDKN1A (which encodes p21), a CDK inhibitor that prevents Rb phosphorylation, thereby causing a G1-S block in the cell cycle.
Correct answer: B – To allow cells to repair DNA damage
The pause in cell cycle progression allows cells time to repair DNA damage. If damage cannot be repaired, p53 then induces cellular senescence or apoptosis.
Correct answer: B – Cellular senescence or apoptosis
If DNA damage cannot be repaired despite the cell cycle pause, p53 induces either cellular senescence (permanent growth arrest) or apoptosis (programmed cell death).
Correct answer: B – By encoding proteins that bind to RB and p53
Oncogenic DNA viruses like HPV encode proteins that bind to RB and p53, rendering them non-functional and allowing uncontrolled cell proliferation.
Correct answer: D – 100%
In 100% of pancreatic cancers and 83% of colon cancers, at least one component of the TGF-β pathway is mutated, highlighting its critical role as a growth inhibitor.
Correct answer: B – Potent inhibitor of proliferation
In most normal epithelial, endothelial, and hematopoietic cells, TGF-β is a potent inhibitor of proliferation, transmitting antiproliferative signals.
Correct answer: C – Epithelial-to-mesenchymal transition (EMT)
In late-stage tumors, TGF-β signaling can paradoxically activate epithelial-to-mesenchymal transition (EMT), promoting migration, invasion, and metastasis.
Correct answer: B – CDK inhibitors (CDKIs)
TGF-β signaling leads to transcriptional activation of CDK inhibitors (CDKIs) with growth-suppressing activity, while also repressing growth-promoting genes like MYC and cyclins.
Correct answer: C – MYC, CDK2, CDK4, and cyclins A and E
TGF-β signaling represses growth-promoting genes such as MYC, CDK2, CDK4, and those encoding cyclins A and E, contributing to its antiproliferative effects.
Correct answer: B – Contact inhibition
Contact inhibition is abolished in cancer cells, allowing them to pile on top of one another and continue proliferating despite cell-cell contact.
Correct answer: B – E-cadherin
E-cadherin maintains contact inhibition, which is lost in malignant cells, allowing them to overcome this normal growth-limiting mechanism.
Correct answer: C – Neurofibromin-2 (merlin)
The NF2 tumor suppressor gene produces neurofibromin-2 (merlin), which facilitates E-cadherin-mediated contact inhibition.
Correct answer: B – By regulating destruction of cytoplasmic β-catenin
The APC gene exerts antiproliferative actions by regulating the destruction of cytoplasmic β-catenin, preventing its nuclear translocation and transcriptional activity.
Correct answer: B – β-catenin accumulates, translocates to nucleus, acts as growth-promoting transcription factor
With APC mutation and loss, β-catenin is not destroyed, accumulates in the cytoplasm, translocates to the nucleus, and acts as a growth-promoting transcription factor.