Loading…
Especially relevant to University of Oxford and University of Cambridge.
Say your answer out loud first, then jot down the key points you made. Writing it helps you spot gaps — and it's what the AI feedback reads.
0 words
Reasoning about probability, mutation and evolution from first principles, generating and testing hypotheses — a classic tutorial-style problem (Peto's paradox).
A structure to build your own answer on — not a script.
Why it's surprising
Cancer arises from mutations during cell division; more cells and longer life → more divisions → more chances of cancer-causing mutations.
Generate hypotheses
Better DNA repair; more tumour-suppressor genes; more readily triggered cell death (apoptosis); slower metabolism; tumours that are themselves attacked.
Evolutionary reasoning
Large, long-lived animals would be under strong selection for cancer suppression, otherwise they'd die before reproducing.
Evidence (if known)
Elephants have many extra copies of the tumour suppressor gene TP53, which may make damaged cells more likely to die.
Test
Compare cancer rates across species; study cell responses to DNA damage in the lab.
A strong but not perfect answer. Read the notes to see why it works — then make your own version with your experiences.
It's surprising because cancer is thought to arise when cells accumulate mutations, and mutations happen mainly when DNA is copied during cell division. An elephant has many more cells than a human and lives a long time, so you'd expect vastly more cell divisions, and therefore many more chances for a cell to become cancerous. If every cell had the same risk1, elephants should get cancer far more often than we do.
Since they don't, something must be different. A few possibilities2: their cells might repair DNA damage more effectively; they might be quicker to kill off damaged cells through apoptosis; they might have extra tumour-suppressor genes; or their cells might divide more slowly.
From an evolutionary point of view3, it makes sense that they'd have some protection. A large animal that takes years to reach reproductive age would be under strong pressure not to die of cancer first — so any mutation that reduced cancer risk would be strongly selected for.
I've read that elephants actually have many copies of the gene TP53, which codes for p53, a protein that stops damaged cells dividing or triggers their death. So one idea is that their cells are more likely to die when their DNA is damaged, instead of carrying on and potentially becoming cancerous.
To test that4, you could compare how elephant and human cells respond to DNA-damaging radiation in the lab — if elephant cells undergo apoptosis more readily, that would support it. And if we understood the mechanism, it might suggest ways of boosting similar pathways in humans, though I imagine that's very hard to do safely.
Real interviews are won and lost here. Answer each one aloud.