{"entity":{"id":"sustaining-proliferative-signaling","kind":"term","name":"Hallmark: sustaining proliferative signalling","aka":[],"tldr":"Cancer cells keep telling themselves to divide, by making their own growth signals or jamming the receptors on.","summary":"Sustaining proliferative signalling is the hallmark by which cancer cells keep instructing themselves to divide, either by producing their own growth signals or by locking growth receptors in the on position. It is achieved through receptor mutation or amplification (EGFR, HER2, ALK), downstream activation (KRAS, BRAF, PIK3CA) or autocrine ligand production, and it runs through the RAS / RAF / MEK / ERK (MAPK), PI3K / AKT / mTOR and MYC pathways. This is the hallmark behind Small-molecule kinase inhibitors, Monoclonal antibodies such as HER2 antibodies, and KRAS & RAS inhibitors, and it underpins the concept of Oncogene addiction. Readers reach it from the Hallmarks of Cancer overview and the original 2000 hallmarks paper, and from the Oncogene, Growth signal and Proliferation entries.","asOf":"2026-09-08","wikipedia":"https://en.wikipedia.org/wiki/The_Hallmarks_of_Cancer","links":[{"label":"Hanahan, Hallmarks of Cancer: New Dimensions (Cancer Discovery 2022)","url":"https://doi.org/10.1158/2159-8290.CD-21-1059"}],"tags":["hallmark"],"related":[],"cancers":[],"sections":[],"technologies":["kinase-inhibitors","monoclonal-antibody","kras-inhibitors"],"targets":["egfr","her2","kras","braf","pik3ca","alk"],"drugs":[],"companies":[],"institutions":[],"pathways":["ras-mapk","pi3k-akt-mtor","myc"],"terms":["oncogene-addiction"],"trials":[],"people":[],"bottlenecks":[],"keyPapers":[],"journals":[],"dependsOn":[],"notes":[],"category":"Cancer biology"},"route":"/terms/sustaining-proliferative-signaling/","neighbours":{"technology":[{"id":"kras-inhibitors","kind":"technology","name":"KRAS & RAS inhibitors","route":"/technologies/kras-inhibitors/"},{"id":"monoclonal-antibody","kind":"technology","name":"Monoclonal antibodies","route":"/technologies/monoclonal-antibody/"},{"id":"kinase-inhibitors","kind":"technology","name":"Small-molecule kinase inhibitors","route":"/technologies/kinase-inhibitors/"}],"target":[{"id":"alk","kind":"target","name":"ALK","route":"/targets/alk/"},{"id":"braf","kind":"target","name":"BRAF","route":"/targets/braf/"},{"id":"egfr","kind":"target","name":"EGFR","route":"/targets/egfr/"},{"id":"her2","kind":"target","name":"HER2","route":"/targets/her2/"},{"id":"kras","kind":"target","name":"KRAS","route":"/targets/kras/"},{"id":"pik3ca","kind":"target","name":"PIK3CA / PI3K-alpha","route":"/targets/pik3ca/"}],"pathway":[{"id":"myc","kind":"pathway","name":"MYC","route":"/pathways/myc/"},{"id":"pi3k-akt-mtor","kind":"pathway","name":"PI3K / AKT / mTOR","route":"/pathways/pi3k-akt-mtor/"},{"id":"ras-mapk","kind":"pathway","name":"RAS / RAF / MEK / ERK (MAPK)","route":"/pathways/ras-mapk/"}],"term":[{"id":"growth-signal","kind":"term","name":"Growth signal","route":"/terms/growth-signal/"},{"id":"hallmarks-of-cancer","kind":"term","name":"Hallmarks of Cancer","route":"/terms/hallmarks-of-cancer/"},{"id":"hallmarks-synthesis","kind":"term","name":"Hallmarks of cancer as a synthesis of the theories","route":"/terms/hallmarks-synthesis/"},{"id":"oncogene","kind":"term","name":"Oncogene","route":"/terms/oncogene/"},{"id":"oncogene-addiction","kind":"term","name":"Oncogene addiction","route":"/terms/oncogene-addiction/"},{"id":"proliferation","kind":"term","name":"Proliferation","route":"/terms/proliferation/"}],"paper":[{"id":"paper-hallmarks-of-cancer-cell-2000","kind":"paper","name":"The Hallmarks of Cancer: six capabilities every tumour must acquire","route":"/key-papers/paper-hallmarks-of-cancer-cell-2000/"}]}}