Explore Genes

Tumor Protein P53

>50% of cancers carry TP53 mutations. Missense hotspots gain dominant-negative and oncogenic gain-of-function activities beyond simple p53 loss.

KRAS Proto-Oncogene, GTPase

Mutated in ~90% of pancreatic, ~40% colorectal, ~25% lung adenocarcinomas. G12C covalent inhibitors (sotorasib, adagrasib) are the first direct KRAS therapy.

Epidermal Growth Factor Receptor

Exon 19 deletions and L858R drive NSCLC. Osimertinib overcomes T790M gatekeeper resistance via Cys797 covalent bond — 18.9 months PFS in FLAURA.

BRCA1 DNA Repair Associated

~70% lifetime breast cancer risk. BRCA1 deficiency creates synthetic lethality with PARP inhibitors (olaparib, niraparib) via homologous recombination loss.

B-Raf Proto-Oncogene

V600E in ~50% of melanomas. BRAF + MEK inhibitors exceed 60% ORR. Colorectal cancer requires triple therapy (+ EGFR antibody) due to EGFR feedback.

MYC Proto-Oncogene, bHLH Transcription Factor

Dysregulated in ~70% of cancers via amplification or translocation. BET bromodomain inhibitors suppress super-enhancer-driven MYC transcription.

PI3K Catalytic Subunit Alpha

H1047R/E545K mutations in ~30% of HR+ breast cancers. Alpelisib + fulvestrant improved PFS by 5.3 months in SOLAR-1 (HR 0.65).

Human Epidermal Growth Factor Receptor 2

Amplified in ~20% of breast cancers. T-DXd extends HER2-targeted benefit to HER2-low (IHC 1+/2+), expanding the actionable population to ~40% of breast cancers.

Phosphatase and Tensin Homolog

Second most mutated tumour suppressor after TP53. PTEN loss drives constitutive AKT/mTOR — capivasertib is FDA-approved for PTEN-altered HR+ breast cancer.

AKT Serine/Threonine Kinase 1

Central PI3K/AKT hub. E17K PH domain mutation (~5% HR+ breast cancer) causes PIP3-independent membrane tethering. Capivasertib approved 2023.

Mechanistic Target of Rapamycin Kinase

mTORC1 inhibitors approved in RCC, breast, and NETs. Paradoxical AKT activation via S6K→IRS-1 feedback limits monotherapy efficacy; dual PI3K/mTOR inhibitors address this.

Vascular Endothelial Growth Factor A

Primary mediator of tumour angiogenesis. Bevacizumab and VEGFR TKIs (sunitinib, axitinib) are approved across colorectal, lung, and kidney cancers.

ATM Serine/Threonine Kinase

Master DSB response kinase. Germline mutations cause ataxia-telangiectasia; somatic loss in ~15% of CLL creates PARP inhibitor and platinum sensitivity.

Cyclin Dependent Kinase 4

CDK4/6 inhibitors (palbociclib, ribociclib, abemaciclib) extend PFS >12 months in HR+/HER2− breast cancer by preventing pRb phosphorylation.

MDM2 Proto-Oncogene

Primary p53 E3 ubiquitin ligase. Amplified in ~90% of liposarcomas; MDM2 inhibitors (navtemadlin, milademetan) are active in TP53-wild-type MDM2-amplified tumours.

RB Transcriptional Corepressor 1

Archetypal tumour suppressor controlling the G1/S restriction point. RB1 loss is near-universal in SCLC (~90%) and is the primary CDK4/6 inhibitor resistance biomarker.

Cyclin Dependent Kinase Inhibitor 2A

Encodes p16INK4a and p14ARF from overlapping reading frames — a single deletion simultaneously disables both the RB and p53 tumour suppressor pathways.

BCL2 Apoptosis Regulator

t(14;18) translocation drives follicular lymphoma. Venetoclax (BH3-mimetic) produces responses within hours in BCL2-dependent CLL and AML.

Signal Transducer and Activator of Transcription 3

Constitutively activated by IL-6/JAK2 in ~70% of haematological malignancies, driving BCL-XL, cyclin D1, and immunosuppressive cytokine expression.

Hypoxia Inducible Factor 1 Subunit Alpha

Master transcription factor of hypoxic response. VHL loss in clear cell RCC causes normoxic HIF-1/2α accumulation; belzutifan directly inhibits HIF-2α.