{"slug":"kinase","tag":"kinase","variants":["kinase"],"description":"No description yet","count":16,"kinds":{"target":16},"related":[{"slug":"driver","tag":"driver","shared":11},{"slug":"adc-target","tag":"adc-target","shared":1},{"slug":"fusion","tag":"fusion","shared":1}],"records":[{"id":"ros1","kind":"target","name":"ROS1","route":"/targets/ros1/","tldr":"A gene fusion in about 1-2% of lung cancers that responds for years to targeted pills, now in their third generation."},{"id":"btk","kind":"target","name":"BTK (Bruton tyrosine kinase)","route":"/targets/btk/","tldr":"The signalling enzyme that B-cell cancers use to survive. Blocking it turned chronic lymphocytic leukaemia into a disease controlled by a daily pill."},{"id":"bcr-abl","kind":"target","name":"BCR::ABL1 (Philadelphia chromosome)","route":"/targets/bcr-abl/","tldr":"The fusion that defines chronic myeloid leukaemia and a quarter of adult acute lymphoblastic leukaemia; the first cancer driver ever switched off by a pill."},{"id":"egfr","kind":"target","name":"EGFR","route":"/targets/egfr/","tldr":"A growth receptor that is mutated in some lung cancers and overproduced in others; the first great success of targeted pills."},{"id":"braf","kind":"target","name":"BRAF","route":"/targets/braf/","tldr":"BRAF is a signalling kinase mutated in half of melanomas; blocking it with two drugs at once became a template for targeted therapy."},{"id":"alk","kind":"target","name":"ALK","route":"/targets/alk/","tldr":"ALK is a gene fusion driver in about 4 to 5% of non-small-cell lung cancers that responds to a succession of ALK inhibitor pills. Lorlatinib kept about 60% of patients progression-free at five years, alectinib is approved after surgery, and neladalkib targets compound resistance mutations."},{"id":"met","kind":"target","name":"MET","route":"/targets/met/","tldr":"A receptor that is either mutated in some lung cancers or amplified as an escape route when other lung cancer drugs fail."},{"id":"ret","kind":"target","name":"RET","route":"/targets/ret/","tldr":"RET is a kinase altered in thyroid cancer and a small slice of lung cancer, treatable with one selective pill regardless of where the tumour is."},{"id":"fgfr2","kind":"target","name":"FGFR2","route":"/targets/fgfr2/","tldr":"FGFR2 is a growth receptor fused in bile-duct cancer and overproduced in gastric cancer."},{"id":"kit","kind":"target","name":"KIT","route":"/targets/kit/","tldr":"KIT mutation is the driver behind most gastrointestinal stromal tumours, and the reason imatinib turned a sarcoma with a median survival of about a year into a chronic disease."},{"id":"flt3","kind":"target","name":"FLT3","route":"/targets/flt3/","tldr":"FLT3 is a kinase mutated in about a third of acute myeloid leukaemias, where adding an inhibitor to chemotherapy improves survival."},{"id":"pik3ca","kind":"target","name":"PIK3CA / PI3K-alpha","route":"/targets/pik3ca/","tldr":"PIK3CA is the most commonly mutated gene in hormone-driven breast cancer. Drugs against it work, but hitting it cleanly without raising blood sugar took years."},{"id":"akt","kind":"target","name":"AKT","route":"/targets/akt/","tldr":"AKT is a central survival kinase downstream of PI3K, blocked by capivasertib in breast and now prostate cancer."},{"id":"cdk4-6","kind":"target","name":"CDK4/6","route":"/targets/cdk4-6/","tldr":"CDK4/6 is the engine that pushes a cell to copy its DNA. Blocking it alongside hormone therapy roughly doubled the time hormone-driven breast cancer stays controlled."},{"id":"mek","kind":"target","name":"MEK1/2","route":"/targets/mek/","tldr":"MEK is the relay in the growth-signal chain that sits just below RAS and RAF. Blocking it starves BRAF- and RAS-driven tumours of their go signal."},{"id":"mtor","kind":"target","name":"mTOR","route":"/targets/mtor/","tldr":"mTOR is the cell's master growth controller, deciding whether to build proteins and divide. Rapamycin-like drugs clamp it down in kidney, breast and neuroendocrine cancers and in rare tumours driven by TSC gene loss."}]}