How cancer drugs work
Each of these explainers takes one targeted cancer drug or drug class and works through the same questions: what does it bind, why does the target matter, where does it sit in treatment, and how do tumours become resistant. Every claim links to a trial registry, regulator document or primary publication.
These pages describe how drugs work at a mechanistic level. They are educational and are not treatment advice; approvals, eligibility and evidence change, and drug decisions belong with a treating clinician.
EGFR inhibitors
EGFR gene profile →Tyrosine kinase inhibitors for EGFR-mutant lung cancer, and how the three generations differ.
KRAS G12C inhibitors
KRAS gene profile →The first drugs to hit KRAS, why they only work for one mutation, and how the two agents compare.
BRAF / MEK inhibitors
BRAF gene profile →Blocking the MAPK pathway in BRAF V600 disease — and why the two drugs are given together.
Fusion-kinase inhibitors
ALK, RET and NTRK inhibitors for tumours driven by gene fusions, including tumour-agnostic approvals.
DNA-repair and cell-cycle drugs
PARP inhibitors that exploit homologous-recombination deficiency, and CDK4/6 inhibitors that hold the RB brake.
HER2 agents and antibody-drug conjugates
HER2 gene profile →The original HER2 antibody, and the ADC design that delivers chemotherapy more selectively.
PI3K / AKT / mTOR pathway drugs
Isoform-selective PI3K-alpha inhibition, and why rapalogs only block part of mTOR.
Apoptosis-targeting drugs
BCL2 gene profile →How a BH3-mimetic re-enables the cell-death programme that leukaemia cells suppress.
Keep up with what is being trialled
These explainers cover how established drugs work. For the newer agents and combinations moving through trials, the GeneAnalyses digest summarises the changes each day.
Clinical Trials News
A daily, plain-language digest of new oncology and life-sciences clinical trials, with a weekly deep-dive roundup — every update linked to its trial registry or primary source.