loss of cell-cycle control

Meaning: The cell cycle is driven by cyclins and cyclin-dependent kinases (CDKs) and policed by checkpoints at G1/S, G2/M and the spindle checkpoint in M phase. Loss of control means mutations break these brakes or jam the accelerator, so cells divide despite DNA damage or missing growth signals. Two gene classes matter. Proto-oncogenes (for example Ras) promote division; when mutated into oncogenes they show gain of function, and one mutant allele often suffices. Tumor suppressors (p53, Rb) halt the cycle, allow repair, or trigger apoptosis; their loss of function typically requires both alleles to be inactivated. Cancer usually requires several accumulated mutations, not one.

On the MCAT: A passage describes a mutation, a knockout or a drug and asks which checkpoint fails, or whether a cell would arrest or keep dividing. Expect p53 questions: with DNA damage, functional p53 stops cells at G1/S or sends them to apoptosis, while cells lacking p53 enter S phase with damaged DNA and pass on mutations. Also expect dominant versus recessive reasoning for oncogenes versus tumor suppressors, and cancer traits such as rapid division, loss of contact inhibition, evasion of apoptosis and telomerase activity.

Common confusion: Students treat oncogenes and tumor suppressors as the same kind of mutation. An activated oncogene acts like a stuck accelerator and is usually dominant in effect. A single damaged tumor suppressor allele usually leaves a working copy, so control often persists until the second allele is lost.