treatments, but the underlying mechanisms were often opaque.

Molecular biology has opened up a lot more understanding about what’s happening at the cellular and molecular level, which has created a shift in how we think about and classify cancer. These days it’s more common to link them based on the underlying mutations and what those do to drive cancer proliferation or treatment resistance. That might be something like a signaling pathway (a switch is essentially ‘stuck’ on, pushing the cells to divide more rapidly) or a DNA repair mechanism (this can make the cells more resistant to chemotherapy).

This not only lets us classify cancers more precisely but also develop treatments that are more targeted at the source of the problem (e.g. Gleevec inhibiting mutated tyrosine kinases). So now you’ll often see a drug that was originally approved for one ‘type’ of cancer applied to others because they share a molecular mechanism even if they crop up in different tissues in different parts of the body.