targets

A growth receptor that is mutated in some lung cancers and overproduced in others; the first great success of targeted pills.

A growth-signal receptor. Some cancers make far too much of it, and drugs that block it or use it as a docking site have transformed those cancers.

PD-1 is a brake on T cells. Blocking it releases the immune system against the tumour and has cured some previously incurable cancers.

The signal tumours use to grow their own blood supply. Blocking it starves tumours and, surprisingly, helps immunotherapy work.

CD19 is a marker on B cells and B-cell cancers, and was the target of the first CAR-T therapies ever approved.

PD-L1 is the tumour's side of the PD-1 brake, and also the biomarker that decides who gets immunotherapy.

CD3 is the switch on every T cell. Bispecific drugs grab it with one arm and the tumour with the other, forcing the T cell to attack.

KRAS is the most commonly mutated cancer gene, called 'undruggable' for 40 years until 2021.

A receptor that is either mutated in some lung cancers or amplified as an escape route when other lung cancer drugs fail.

The hormone switch that drives prostate cancer, attacked by castration and by pills that block the receptor.

The hormone switch that drives most breast cancers. Blocking or destroying it is the oldest and most effective targeted therapy.

A tight-junction protein normally hidden in the stomach lining that becomes exposed in gastric and pancreatic cancers.

FGFR2 is a growth receptor fused in bile-duct cancer and overproduced in gastric cancer.

A protein on prostate cancer cells that lets doctors both see the cancer on a PET scan and hit it with a radioactive drug.

BCMA is a survival receptor on plasma cells, and the target that made CAR-T and bispecifics work in multiple myeloma.

KIT mutation is the driver behind most gastrointestinal stromal tumours, and the reason imatinib turned a sarcoma with a median survival of about a year into a chronic disease.

BRAF is a signalling kinase mutated in half of melanomas; blocking it with two drugs at once became a template for targeted therapy.

CD20 is a B-cell marker; rituximab against it was the first antibody approved for cancer, in 1997.

PIK3CA is the most commonly mutated gene in hormone-driven breast cancer. Drugs against it work, but hitting it cleanly without raising blood sugar took years.

ALK is a gene fusion driver in about 4 to 5% of non-small-cell lung cancers that responds to a succession of ALK inhibitor pills. Lorlatinib kept about 60% of patients progression-free at five years, alectinib is approved after surgery, and neladalkib targets compound resistance mutations.

The first immune brake ever targeted for cancer; releasing it won a Nobel Prize and cures a fraction of melanomas.

RET is a kinase altered in thyroid cancer and a small slice of lung cancer, treatable with one selective pill regardless of where the tumour is.

CDK4/6 is the engine that pushes a cell to copy its DNA. Blocking it alongside hormone therapy roughly doubled the time hormone-driven breast cancer stays controlled.

PARP is a DNA repair enzyme. Cancers that have already lost one repair system (BRCA) die when this second one is blocked; healthy cells survive.

Somatostatin receptor 2 is a hormone receptor densely present on neuroendocrine tumours, and was the first theranostic target to reach routine care.

The fusion that defines chronic myeloid leukaemia and a quarter of adult acute lymphoblastic leukaemia; the first cancer driver ever switched off by a pill.

The signalling enzyme that B-cell cancers use to survive. Blocking it turned chronic lymphocytic leukaemia into a disease controlled by a daily pill.

HER3 is a cousin of HER2 that cancers use as an escape route when HER2 or EGFR are blocked.

A metabolic enzyme whose mutant form produces a molecule that scrambles how genes are read; blocking it slows brain tumours and leukaemias.

Folate receptor alpha is a vitamin receptor that ovarian cancer cells carry in large numbers, used as the docking site for the ADC mirvetuximab.

TROP2 is a surface glycoprotein present at high levels on most epithelial cancers (breast, lung, urothelial, gastric, pancreatic) and at low levels on normal tissue. It does not drive the cancer; it is a delivery address, used by the approved ADCs sacituzumab govitecan and datopotamab deruxtecan and by sacituzumab tirumotecan, with a TROP2 PET tracer in development to pick patients.

A protein that appears on the surface of small-cell lung cancer cells, now hit by a drug that pulls T cells onto them.

FLT3 is a kinase mutated in about a third of acute myeloid leukaemias, where adding an inhibitor to chemotherapy improves survival.

The signalling enzyme that tells marrow cells to make red cells and platelets; a single mutation (V617F) leaves it switched on in most myeloproliferative neoplasms.

MEK is the relay in the growth-signal chain that sits just below RAS and RAF. Blocking it starves BRAF- and RAS-driven tumours of their go signal.

A gene fusion in about 1-2% of lung cancers that responds for years to targeted pills, now in their third generation.

The enzyme that cuts both DNA strands to untangle chromosomes before cell division. Etoposide and the anthracyclines hold it in the cut state, filling dividing cells with double-strand breaks.

B7-H3 is an immune checkpoint-like surface protein found on 60 to 70% of small-cell lung cancers and 80 to 90% of castration-resistant prostate cancers, with little on normal tissue. It is used as an ADC address, chiefly by ifinatamab deruxtecan, now in phase 3 in small-cell lung cancer; whether blocking its immune-dampening role adds anything beyond payload delivery is unresolved.

DNA repair genes. Inheriting a broken copy raises breast and ovarian cancer risk, but tumours that lose them become uniquely vulnerable to PARP inhibitors and platinum.

CD38 is a myeloma surface enzyme and the target of daratumumab, which is now given as a quick under-the-skin injection.

Rare gene fusions found across dozens of cancer types; the first target where a drug was approved for any tumour carrying it.

An enzyme that cancers lacking the MTAP gene (about 10-15% of all tumours) depend on more than normal cells do; new inhibitors designed to exploit that difference are in late trials.

AKT is a central survival kinase downstream of PI3K, blocked by capivasertib in breast and now prostate cancer.

CD22 is a B-cell surface protein and the docking site for the leukaemia ADC inotuzumab ozogamicin.

The classic 'CEA' tumour marker measured in blood, also present on the cell surface where ADCs can reach it.

The receptor that macrophages depend on; blocking it shrinks tenosynovial giant cell tumour (a CSF1-driven tumour) and depletes tumour-supporting macrophages, though the latter has not yet helped patients with common cancers.

HLA-A is the molecule that holds up short pieces of a cell's proteins for T cells to inspect. Engineered T-cell receptor therapies such as tebentafusp and afami-cel only work in people with the HLA-A*02 variant, because the receptor recognises the tumour peptide sitting in that particular groove.

Ikaros is a transcription factor that myeloma cells depend on. Lenalidomide, pomalidomide and the newer CELMoDs work by gluing Ikaros to the cell's disposal machinery so it is destroyed, which kills the plasma cell and wakes up T cells.

LAG-3 is the third immune brake to reach approval, combined with PD-1 blockade in melanoma.

Nectin-4 is an adhesion protein plentiful on bladder cancer cells, used as the docking site for the ADC enfortumab vedotin.

The switch in the hedgehog developmental pathway that is stuck on in basal cell carcinoma and some medulloblastomas; three approved pills block it.

The enzyme that makes the thymine building block of DNA. Fluorouracil, capecitabine and pemetrexed jam it, starving dividing cells of thymidine.

TP53 is the 'guardian of the genome', broken in half of all cancers. Fixing it directly has so far defeated every attempt, so drugs exploit what its loss makes cancers depend on.

The protein that builds the microtubule scaffolding a cell needs to pull its chromosomes apart. Taxanes freeze the scaffold and vinca alkaloids and eribulin stop it forming; either way the dividing cell stalls and dies.

ABL1 is the kinase half of the BCR::ABL1 fusion that causes chronic myeloid leukaemia. The CML drugs bind the ABL1 kinase domain, most in its ATP pocket and asciminib in a separate pocket that locks it shut.

The enzyme that turns androgens into oestrogen in fat, muscle and breast tissue after the menopause. Aromatase inhibitors remove the oestrogen that drives most breast cancers in post-menopausal women.

BRD4 is a reader protein that docks on acetylated DNA packaging and pulls in the machinery that switches growth genes such as MYC on. BET inhibitors such as pelabresib and ZEN-3694 block that docking; in NUT carcinoma the cancer's own driver is a BRD4 fusion.

CD47 is the 'don't eat me' signal: it binds SIRP-alpha on macrophages to stop them engulfing the cell, and over 90% of AML blasts and large B-cell lymphoma cells display it. Blocking it should let macrophages eat tumour cells, but red cells carry CD47 too, so anaemia is built in, and the lead antibody magrolimab was dropped after failed trials.

EZH2 is an enzyme that silences genes. The first drug against it treated a rare sarcoma and some lymphomas until it was withdrawn in 2026 for causing second blood cancers.

FAK is the kinase that tells a cell it is anchored to its surroundings, letting it survive, move and resist drugs. Defactinib, given with the RAF/MEK inhibitor avutometinib, removes that escape route in low-grade serous ovarian cancer; other FAK inhibitors are in trials in meningioma and solid tumours.