The G1 checkpoint chiefly assesses whether
Answer: C
Size, nutrients, growth signals and DNA integrity are all weighed before the cell commits. The other options describe what is tested at the G2 and spindle checkpoints instead. Each checkpoint asks a different question at a different moment.
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The spindle assembly checkpoint delays the cell until
Answer: D
A single unattached kinetochore is enough to hold the cell at metaphase. The delay prevents chromosomes being distributed unequally, which would leave both daughters abnormal. Aneuploidy of this kind is a hallmark of many tumours.
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The protein p53 is often described as the guardian of the genome because it
Answer: A
It arrests the cell so that repair can happen, and directs the cell to die if the damage proves too great. It does not carry out the repair itself, which is done by other proteins it summons. Calling it a guardian describes its supervisory role rather than any repair activity.
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State whether the following is true or false.
The p53 protein repairs damaged DNA directly.
Answer: B
It is a transcription factor that halts the cycle and switches on repair genes, or triggers apoptosis when repair is hopeless. Confusing the manager with the workforce is the usual error here. Its job is to decide what happens next, not to mend the damage itself.
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The gene most frequently mutated in human cancers is
Answer: C
Roughly half of all human tumours carry a mutation in it, which reflects how central the checkpoint it controls is to preventing cancer. Losing it lets damaged cells continue dividing. Restoring p53 function is a long-standing goal of cancer therapy.
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Assertion (A): Loss of p53 function makes a cell more likely to become cancerous.
Reason (R): Without p53 a cell with damaged DNA can continue through the cycle and divide.
Answer: D
Both are true and the reason gives the consequence: damage accumulates instead of being repaired or removed, so mutations pile up across successive divisions and the cell drifts towards malignancy. It is the commonest single genetic change found in human tumours.
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A tumour suppressor gene differs from an oncogene in that a tumour suppressor
Answer: A
Cancer results from losing both copies of a tumour suppressor or from gaining an overactive version of a proto-oncogene. The two therefore behave quite differently in inheritance. An inherited oncogene mutation is dominant, a suppressor loss recessive at the cell level.
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State whether the following is true or false.
A single mutated copy of a tumour suppressor gene is usually enough to cause cancer.
Answer: B
Both copies must normally be lost, which is the two-hit hypothesis. An inherited faulty copy explains why some families develop tumours far earlier, since only one further hit is then needed. Knudson worked the idea out from the ages at which retinoblastoma appears.
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Consider the following statements about cancer genes.
1. An oncogene is an overactive version of a normal gene.
2. A tumour suppressor normally acts as a brake on division.
3. Both types require the loss of two copies to have an effect.
Answer: C
The first two are correct. The third applies only to tumour suppressors: a single activated copy of an oncogene is enough, because the fault is a gain of function rather than a loss. One mutated copy of an oncogene therefore suffices, unlike a suppressor.
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The retinoblastoma protein, Rb, restrains the cycle by
Answer: D
Phosphorylation by a cyclin-CDK complex releases E2F, which then switches on the genes needed for S phase. Loss of Rb removes that restraint and the cell enters S phase regardless. Rb was the first tumour suppressor to be identified.
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