[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [Biochemistry](https://durgical.com/en/biochemistry/) › Oncogenes and tumour suppressor genes [Biochemistry](https://durgical.com/en/biochemistry/) · Topic # Oncogenes and tumour suppressor genes Cancer arises from mutations that speed up division (oncogenes) or remove its brakes (tumour suppressors); this is the basic outline. Updated 2026-11-01 ## Key facts - Proto-oncogene: a normal gene that drives growth (factors, receptors, RAS, MYC); mutated or amplified it becomes an oncogene and acts with one copy (dominant in the cell). - Tumour suppressor: brakes the cycle or repairs DNA (TP53, RB1, APC, BRCA1/2); both copies must be damaged: Knudson's two-hit hypothesis. - Mutant RAS (KRAS) stays bound to GTP and always on; it is common in pancreas, colon and lung. - p53, «guardian of the genome», halts the cycle in G1 (via p21), triggers repair or apoptosis; it is mutated in about half of cancers. - RB brakes the G1→S transition by holding E2F; cyclin–CDK complexes phosphorylate it to release it. ## In detail - Normal signal: a growth factor activates its receptor tyrosine kinase, then RAS–RAF–MEK–ERK, and genes such as MYC switch on. - Oncogene by point mutation (KRAS, BRAF V600E), amplification (HER2/ERBB2, N-MYC) or translocation (BCR-ABL in chronic myeloid leukaemia, MYC in Burkitt lymphoma). - Lost suppressor: the first mutation can be inherited (familial retinoblastoma, Li-Fraumeni, BRCA) and the second happens in the tissue. - Repair genes (MLH1, MSH2 in Lynch; BRCA1/2) are «caretaker» suppressors: their loss speeds up every other mutation. - Cancer gathers several changes: self-sufficient growth signals, escape from brakes and apoptosis, immortality (telomerase), angiogenesis, invasion and reprogrammed metabolism (Warburg effect). - Many targeted drugs hit specific oncogenes: imatinib (BCR-ABL), trastuzumab (HER2), BRAF and EGFR inhibitors. ## Clinical notes - Familial adenomatous polyposis (APC): hundreds of polyps and almost certain colon cancer without colectomy. - BRCA1/2: high risk of breast and ovarian cancer; PARP inhibitors exploit the faulty repair. - Li-Fraumeni (germline TP53): sarcomas, breast, brain and adrenal tumours at young ages. - This is an outline: the molecular genetics of cancer is expanded in the molecular biology section. ## Related conditions - [Colorectal cancer](https://durgical.com/en/conditions/colorectal-cancer/) - [Breast cancer](https://durgical.com/en/conditions/breast-cancer/) - [Ovarian cancer](https://durgical.com/en/conditions/ovarian-cancer/) - [Lung cancer](https://durgical.com/en/conditions/lung-cancer/) - [Pancreatic cancer](https://durgical.com/en/conditions/pancreatic-cancer/) - [Glioblastoma](https://durgical.com/en/conditions/glioblastoma/) - [Hereditary paraganglioma and pheochromocytoma (SDH)](https://durgical.com/en/conditions/hereditary-paraganglioma-and-pheochromocytoma/) ## Related - [Warburg effect (aerobic glycolysis in cancer)](https://durgical.com/en/biochemistry/topics/warburg-effect/) - [Drugs acting on nucleotide metabolism](https://durgical.com/en/biochemistry/topics/drugs-acting-on-nucleotide-metabolism/) - [Thymidylate synthase](https://durgical.com/en/biochemistry/enzymes/thymidylate-synthase/) - [Dihydrofolate reductase (DHFR)](https://durgical.com/en/biochemistry/enzymes/dihydrofolate-reductase/) ## Test yourself Think of the answer, then tap the question to see it. ## Why is one mutated oncogene copy enough but two suppressor copies are needed? The oncogene gains a function that dominates; the suppressor loses a brake, and the healthy copy keeps braking until it is lost too. ## What does p53 do when it detects DNA damage? It halts the cycle in G1 through p21, activates repair and, if the damage is large, apoptosis. ## How is RAS activated as an oncogene? A point mutation stops it hydrolysing GTP, so it stays switched on. ## Which tumour suppressor gene is mutated in familial adenomatous polyposis? APC, which normally tags β-catenin for degradation. [Add to my cards (4)](https://durgical.app/estudiar/?add=/en/biochemistry/topics/oncogenes-and-tumour-suppressor-genes/) Educational information, not medical advice. For any symptom, see a health professional. Sources: [TP53 gene: MedlinePlus Genetics](https://medlineplus.gov/genetics/gene/tp53/) (MedlinePlus, US National Library of Medicine, 2026); [KRAS gene: MedlinePlus Genetics](https://medlineplus.gov/genetics/gene/kras/) (MedlinePlus, US National Library of Medicine, 2026); [RB1 gene: MedlinePlus Genetics](https://medlineplus.gov/genetics/gene/rb1/) (MedlinePlus, US National Library of Medicine, 2026); [APC gene: MedlinePlus Genetics](https://medlineplus.gov/genetics/gene/apc/) (MedlinePlus, US National Library of Medicine, 2026); [BRCA1 gene: MedlinePlus Genetics](https://medlineplus.gov/genetics/gene/brca1/) (MedlinePlus, US National Library of Medicine, 2026); [Li-Fraumeni syndrome: MedlinePlus Genetics](https://medlineplus.gov/genetics/condition/li-fraumeni-syndrome/) (MedlinePlus, US National Library of Medicine, 2026); [Signaling by RAS mutants](https://reactome.org/PathwayBrowser/#/R-HSA-6802949) (Reactome, 2026); [Cancer](https://www.who.int/news-room/fact-sheets/detail/cancer) (World Health Organization, 2026). 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