# Tumour suppressor gene

Source: https://onco.cc/terms/tumour-suppressor-gene/  
OnCo record `tumour-suppressor-gene` (Term). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

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.

## Fields

- Kind: Term
- Last checked: 2026-09-09
- Also known as: tumour suppressor; tumour suppressors; tumor suppressor; tumor suppressors; tumor suppressor gene; tumour suppressor genes; tumor suppressor genes; tumour-suppressor; tumor-suppressor

## Sources

- Wikipedia: https://en.wikipedia.org/wiki/Tumor_suppressor_gene
- Wikipedia: https://en.wikipedia.org/wiki/Tumor_suppressor_gene

## Connected records

- terms: [Apoptosis](https://onco.cc/terms/apoptosis/), [Cell cycle](https://onco.cc/terms/cell-cycle/), [Deletion](https://onco.cc/terms/deletion/), [Driver mutation](https://onco.cc/terms/driver-mutation/), [Gene](https://onco.cc/terms/gene/), [Hallmark: evading growth suppressors](https://onco.cc/terms/evading-growth-suppressors/), [Hereditary cancer syndromes](https://onco.cc/terms/hereditary-cancer-syndromes/), [Oncogene](https://onco.cc/terms/oncogene/), [Somatic mutation theory of cancer](https://onco.cc/terms/somatic-mutation-theory/), [Synthetic lethality](https://onco.cc/terms/synthetic-lethality/)
- targets: [BRCA1 / BRCA2 (HRD)](https://onco.cc/targets/brca/), [PARP](https://onco.cc/targets/parp/), [TP53](https://onco.cc/targets/tp53/)
- pathways: [p53 / RB / cell-cycle checkpoint](https://onco.cc/pathways/p53-cell-cycle/), [PI3K / AKT / mTOR](https://onco.cc/pathways/pi3k-akt-mtor/)
- people: [Reuben Shaw](https://onco.cc/people/reuben-shaw/)
- key papers: [El-Deiry 1993: WAF1, the gene through which p53 stops cell division](https://onco.cc/key-papers/paper-el-deiry-waf1-p21-cell-1993/), [Hollstein 1991: p53 mutations in human cancers](https://onco.cc/key-papers/paper-hollstein-p53-mutations-science-1991/), [Levine 1997: p53, the cellular gatekeeper for growth and division](https://onco.cc/key-papers/paper-levine-p53-gatekeeper-cell-1997/), [Sherr and Roberts 1999: CDK inhibitors as regulators of the G1 phase](https://onco.cc/key-papers/paper-sherr-roberts-cdk-inhibitors-genesdev-1999/), [Vogelstein, Lane and Levine 2000: surfing the p53 network](https://onco.cc/key-papers/paper-vogelstein-surfing-p53-network-nature-2000/)
- journals: [Proceedings of the National Academy of Sciences](https://onco.cc/journals/pnas/)

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