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.

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.

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

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.

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

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

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

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

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

PARP inhibitors block DNA repair. Some cancers with defective repair are especially vulnerable, but the gene, disease setting and treatment combination determine which evidence applies.

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

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

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

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.

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.

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

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

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

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

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.

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.

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.

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.

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

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

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.

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

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.

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.

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

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

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.

PALB2 (Partner and localizer of BRCA2) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a drug target, a tumour suppressor, a biomarker and a DNA repair gene, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Breast cancer, Ovarian cancer, Colorectal cancer and 5 more.

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.

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

The pituitary receptor that starts the hormone chain leading to testosterone and oestrogen. Agonists overstimulate it into silence and antagonists block it outright, the basis of medical castration in prostate cancer and ovarian suppression in breast cancer.

MLH1 (DNA mismatch repair protein Mlh1) is a gene. The public catalogues list it as a drug target, a biomarker and a DNA repair gene, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Colorectal cancer, Ovarian cancer, Endometrial cancer and 4 more.

MSH2 (DNA mismatch repair protein Msh2) is a gene. The public catalogues list it as a drug target, a biomarker and a DNA repair gene, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Colorectal cancer, Endometrial cancer, Ovarian cancer and 5 more.

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

CD123 is the interleukin-3 receptor alpha chain, present on every blastic plasmacytoid dendritic cell neoplasm and on the blasts and leukaemia stem cells of 70 to 80% of acute myeloid leukaemias. Tagraxofusp and pivekimab sunirine target it in that rare neoplasm, and CAR-T cells against it in AML must spare the normal blood-forming progenitors that also carry it.

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.

CDK2 (Cyclin-dependent kinase 2) is a protein kinase, an enzyme that switches other proteins on by adding phosphate groups. The public catalogues list it as a drug target, a biomarker and a DNA repair gene, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Triple-negative breast cancer.

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.

mTOR is the cell's master growth controller, deciding whether to build proteins and divide. Rapamycin-like drugs clamp it down in kidney, breast and neuroendocrine cancers and in rare tumours driven by TSC gene loss.

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.

CD25 is the part of the interleukin-2 receptor found on activated T cells and on some lymphoma cells; denileukin diftitox uses it as a doorway to deliver a toxin.

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

CD73 is an enzyme on tumour and immune cells that converts AMP into adenosine, which switches off T and natural killer cells through A2A and A2B receptors. Oleclumab (anti-CD73) with durvalumab slowed progression in a phase 2 lung cancer trial and quemliclustat is in phase 3 in pancreatic cancer, but A2A blockers gave only modest signals and several were dropped.

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.

An adhesion protein on almost all carcinoma cells and the capture molecule for circulating tumour cell tests; the target of the first bispecific antibody ever approved (catumaxomab, 2009).

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.

FAP (fibroblast activation protein) sits on the cancer-associated fibroblasts that scaffold more than 90% of epithelial cancers and is almost absent from normal adult tissue. FAPI PET tracers therefore light up tumours with high contrast, including pancreatic, gastric and low-grade cancers where FDG PET is weak, and FAP-targeted radioligands are in development.

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.