{"entity":{"id":"tumour-suppressor-gene","kind":"term","name":"Tumour suppressor gene","aka":["tumour suppressor","tumour suppressors","tumor suppressor","tumor suppressors","tumor suppressor gene","tumour suppressor genes","tumor suppressor genes","tumour-suppressor","tumor-suppressor"],"tldr":"A gene whose normal job is to stop cells dividing or to make damaged cells die. Losing it removes a brake, so the cell can grow unchecked even without a stuck accelerator.","summary":"Because a cell has two copies of each gene, a tumour suppressor is usually only disabled when both copies are lost, by mutation, deletion, or silencing; people who inherit one faulty copy (BRCA1, TP53 in Li-Fraumeni, APC) are one step closer and develop cancer young. TP53, mutated in about half of all cancers, halts division and triggers apoptosis after DNA damage; RB1 gates the cell cycle; PTEN restrains the PI3K pathway. Lost genes cannot be directly targeted by a drug, so treatment exploits the consequences: PARP inhibitors kill BRCA-deficient cells, and MDM2 inhibitors reactivate p53 in tumours where it is present but suppressed.","asOf":"2026-09-09","wikipedia":"https://en.wikipedia.org/wiki/Tumor_suppressor_gene","links":[{"label":"Wikipedia","url":"https://en.wikipedia.org/wiki/Tumor_suppressor_gene"}],"tags":[],"related":["oncogene","deletion","synthetic-lethality","evading-growth-suppressors","hereditary-cancer-syndromes","cell-cycle"],"cancers":[],"sections":[],"technologies":[],"targets":["tp53","brca","parp"],"drugs":[],"companies":[],"institutions":[],"pathways":["p53-cell-cycle","pi3k-akt-mtor"],"terms":[],"trials":[],"people":[],"bottlenecks":[],"keyPapers":[],"journals":[],"dependsOn":[],"notes":[],"category":"Biology basics"},"route":"/terms/tumour-suppressor-gene/","neighbours":{"term":[{"id":"apoptosis","kind":"term","name":"Apoptosis","route":"/terms/apoptosis/"},{"id":"cell-cycle","kind":"term","name":"Cell cycle","route":"/terms/cell-cycle/"},{"id":"deletion","kind":"term","name":"Deletion","route":"/terms/deletion/"},{"id":"driver-mutation","kind":"term","name":"Driver mutation","route":"/terms/driver-mutation/"},{"id":"gene","kind":"term","name":"Gene","route":"/terms/gene/"},{"id":"evading-growth-suppressors","kind":"term","name":"Hallmark: evading growth suppressors","route":"/terms/evading-growth-suppressors/"},{"id":"hereditary-cancer-syndromes","kind":"term","name":"Hereditary cancer syndromes","route":"/terms/hereditary-cancer-syndromes/"},{"id":"oncogene","kind":"term","name":"Oncogene","route":"/terms/oncogene/"},{"id":"somatic-mutation-theory","kind":"term","name":"Somatic mutation theory of cancer","route":"/terms/somatic-mutation-theory/"},{"id":"synthetic-lethality","kind":"term","name":"Synthetic lethality","route":"/terms/synthetic-lethality/"}],"target":[{"id":"brca","kind":"target","name":"BRCA1 / BRCA2 (HRD)","route":"/targets/brca/"},{"id":"parp","kind":"target","name":"PARP","route":"/targets/parp/"},{"id":"tp53","kind":"target","name":"TP53","route":"/targets/tp53/"}],"pathway":[{"id":"p53-cell-cycle","kind":"pathway","name":"p53 / RB / cell-cycle checkpoint","route":"/pathways/p53-cell-cycle/"},{"id":"pi3k-akt-mtor","kind":"pathway","name":"PI3K / AKT / mTOR","route":"/pathways/pi3k-akt-mtor/"}],"person":[{"id":"reuben-shaw","kind":"person","name":"Reuben Shaw","route":"/people/reuben-shaw/"}],"paper":[{"id":"paper-el-deiry-waf1-p21-cell-1993","kind":"paper","name":"El-Deiry 1993: WAF1, the gene through which p53 stops cell division","route":"/key-papers/paper-el-deiry-waf1-p21-cell-1993/"},{"id":"paper-hollstein-p53-mutations-science-1991","kind":"paper","name":"Hollstein 1991: p53 mutations in human cancers","route":"/key-papers/paper-hollstein-p53-mutations-science-1991/"},{"id":"paper-levine-p53-gatekeeper-cell-1997","kind":"paper","name":"Levine 1997: p53, the cellular gatekeeper for growth and division","route":"/key-papers/paper-levine-p53-gatekeeper-cell-1997/"},{"id":"paper-sherr-roberts-cdk-inhibitors-genesdev-1999","kind":"paper","name":"Sherr and Roberts 1999: CDK inhibitors as regulators of the G1 phase","route":"/key-papers/paper-sherr-roberts-cdk-inhibitors-genesdev-1999/"},{"id":"paper-vogelstein-surfing-p53-network-nature-2000","kind":"paper","name":"Vogelstein, Lane and Levine 2000: surfing the p53 network","route":"/key-papers/paper-vogelstein-surfing-p53-network-nature-2000/"}],"journal":[{"id":"pnas","kind":"journal","name":"Proceedings of the National Academy of Sciences","route":"/journals/pnas/"}]}}