Oncogenes: RAS, MYC, HER2, BCR-ABL and the table to know !
- Topic
Oncogenes are growth genes stuck in the ‘on’ position. One altered copy is enough to push a cell to divide.
Updated 2026-11-01
What it is
Proto-oncogenes are normal genes that promote growth: growth factors, receptors, signal transducers, transcription factors and cell-cycle regulators. A gain-of-function change (point mutation, amplification or translocation) turns them into oncogenes whose products signal without the normal stimulus. Because one altered allele suffices, oncogenes act dominantly at the cell level, and many are now direct drug targets.
Step by step
- A growth factor binds its receptor tyrosine kinase, which dimerises and phosphorylates itself.
- Adaptor proteins activate RAS by exchanging GDP for GTP.
- RAS-GTP switches on the RAF (BRAF), MEK, ERK kinase cascade and the PI3K-AKT pathway.
- ERK enters the nucleus and induces transcription factors such as MYC.
- MYC and cyclin D push the cell from G1 into S phase.
- Normally RAS hydrolyses its GTP (helped by GAP proteins such as neurofibromin) and switches off; mutant RAS cannot, so the signal never stops.
Oncogenes to know
| Oncogene | Type of protein | How it is activated | Main tumour |
|---|---|---|---|
| BCR-ABL | Non-receptor tyrosine kinase | Translocation t(9;22) | Chronic myeloid leukaemia |
| HER2 (ERBB2) | Growth factor receptor | Amplification | Breast cancer (also gastric) |
| N-MYC (MYCN) | Transcription factor | Amplification | Neuroblastoma |
| KIT | Receptor tyrosine kinase | Point mutation | Gastrointestinal stromal tumour |
| KRAS | GTP-binding protein | Point mutation | Pancreatic, colorectal, lung adenocarcinoma |
| BRAF (V600E) | Serine-threonine kinase | Point mutation | Melanoma, papillary thyroid carcinoma, hairy cell leukaemia |
| RET | Receptor tyrosine kinase | Point mutation (germline) or rearrangement | MEN2, medullary thyroid carcinoma |
| EGFR, ALK | Receptor tyrosine kinases | Mutation (EGFR), rearrangement (ALK) | Lung adenocarcinoma, often in non-smokers |
| JAK2 (V617F) | Non-receptor tyrosine kinase | Point mutation | Polycythaemia vera and other myeloproliferative neoplasms |
| MYC | Transcription factor | Translocation t(8;14) | Burkitt lymphoma |
| Cyclin D1 (CCND1) | Cell-cycle regulator | Translocation t(11;14) | Mantle cell lymphoma |
Clinical notes
- Targeted drugs block specific oncoproteins: imatinib for BCR-ABL and KIT, anti-HER2 antibodies, EGFR and ALK inhibitors, BRAF inhibitors.
- Tumours must be tested (immunohistochemistry, FISH, sequencing) before choosing these drugs.
Test yourself
Think of the answer, then tap the question to see it.
Why do oncogenes act dominantly?
Their mutations are gain of function: one altered allele produces an overactive protein that drives growth regardless of the normal allele.
Which translocation creates BCR-ABL and in which disease?
t(9;22), the Philadelphia chromosome, typical of chronic myeloid leukaemia (also present in some acute lymphoblastic leukaemias).
Why does a RAS point mutation keep the protein active?
The mutant RAS loses its ability to hydrolyse GTP, so it stays in the active GTP-bound form.
Which oncogene is amplified in high-risk neuroblastoma?
N-MYC (MYCN); amplification predicts aggressive behaviour.
Which oncogene mutation drives most gastrointestinal stromal tumours?
An activating mutation of the KIT receptor tyrosine kinase (some have PDGFRA mutations).
Related
- Tumour suppressor genes: RB, TP53, APC, BRCA and the two-hit hypothesis
- The hallmarks of cancer
- Translocations, amplifications and epigenetic changes in cancer
- The cell cycle in cancer: cyclins, CDKs and checkpoints
- Multistep carcinogenesis: the adenoma–carcinoma sequence
- Molecular pathology: PCR, FISH, sequencing and liquid biopsy
Related conditions
- Chronic myeloid leukaemia
- Breast cancer
- Neuroblastoma
- Gastrointestinal stromal tumour (GIST)
- Pancreatic cancer
- Colorectal cancer
- Lung cancer
- Melanoma
- Medullary thyroid carcinoma
- Multiple endocrine neoplasia (MEN 1, 2A, 2B)
- Thyroid cancer (papillary)
- Polycythaemia vera
- Non-Hodgkin lymphoma
Elsewhere in DurgiPedia
- Oncogenes and tumour suppressor genes
- Receptor tyrosine kinases
- JAK–STAT pathway
- Monoclonal antibodies and biologics: naming and targets
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: KRAS gene: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); ABL1 gene: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); What Is Cancer? (National Cancer Institute (NCI), 2026); Targeted Therapy to Treat Cancer (National Cancer Institute (NCI), 2026).
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Representative model, for educational purposes only.