{"entity":{"id":"alk","kind":"target","name":"ALK","aka":[],"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.","summary":"ALK rearrangements occur in ~4-5% of NSCLC, typically in younger never-smokers. Lorlatinib achieved 5-year PFS of ~60% in CROWN, the longest of any targeted therapy in metastatic NSCLC. Alectinib is approved in the adjuvant setting (ALINA). Fourth-generation inhibitors (neladalkib) address compound resistance mutations.","asOf":"2026-09-04","wikipedia":"https://en.wikipedia.org/wiki/Anaplastic_lymphoma_kinase","links":[{"label":"Wikipedia","url":"https://en.wikipedia.org/wiki/Anaplastic_lymphoma_kinase"}],"tags":["driver","kinase"],"related":["alk-fusion","alk-resistance-mutation"],"cancers":["nsclc","neuroblastoma","pancreatic","colorectal"],"sections":[],"technologies":[],"targets":[],"drugs":["ceritinib","brigatinib","ensartinib","guardant360-cdx","tri-611"],"companies":["imagene-ai","inivata","lucence","triana-biomedicines"],"institutions":[],"pathways":["ras-mapk","pi3k-akt-mtor","nsclc-signalling"],"terms":["gene-fusion","resistance"],"trials":[],"people":[],"bottlenecks":[],"keyPapers":["paper-singhi-alk-rearrangements-pancreatic-jnccn-2017","paper-philip-kras-wild-type-pancreatic-ccr-2022","paper-soda-eml4-alk-fusion-nature-2007","paper-kris-lung-cancer-mutation-consortium-jama-2014"],"journals":[],"dependsOn":[],"notes":["Pancreatic ductal adenocarcinoma: ALK fusions in 5 of 3,170 tumours, 0.16%, all KRAS wild-type and all in patients under 50, among whom the rate is 1.3%; 3 of 4 treated with an ALK inhibitor benefited (Singhi 2017). It is the reason a young patient with a KRAS wild-type tumour should have fusion testing.","Colorectal cancer: ALK fusions in about 0.1% of tumours (cBioPortal). ALK point mutations read far higher on panels but are overwhelmingly passengers in hypermutated tumours; only a fusion is actionable.","Lung cancer: rearranged in 3 to 6% of adenocarcinomas, 5.6% in never smokers, with EML4 the partner in the large majority (cBioPortal; Soda 2007). Panel-based rates run below the fluorescence in situ hybridisation rate of 8% found by the Lung Cancer Mutation Consortium because a DNA panel sees a rearrangement only where it baits the breakpoint intron (Kris 2014). ALK point mutations found at diagnosis are almost all passengers; only a fusion is actionable. At progression the same gene is read again for a different purpose: each inhibitor generation selects its own resistance spectrum, G1202R dominates after a second-generation inhibitor, and the presence of an ALK mutation is what predicts benefit from lorlatinib (69% against 27% response) (Gainor 2016, Shaw 2019)."],"symbol":"ALK","role":[],"sources":[],"specificity":"tumour-specific","distribution":"few-types","specificityNote":"Tumour-specific alteration: 1 of 1 label readouts filed under it measure a sequence variant (ALK fusion (ALK-positive)) absent from normal cells. HPA ALK: RNA tissue enhanced (brain 2 nTPM, pituitary gland 2 nTPM, testis 2 nTPM); high antibody staining in 3 normal tissues; highest cancer staining skin cancer (4 of 10 high). Distribution: 2 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Lung cancer (all types), Childhood cancers (all types)); approvals of single-target medicines aimed at it also list Brain and spinal cord tumours (all types), not counted; Open Targets associates it with 5 specific cancer types at or above 0.5 (neuroblastoma, neuroblastoma, susceptibility to, 3, non-small cell lung carcinoma, lung cancer, anaplastic large cell lymphoma). (Rule 3 of scripts/fetch-target-specificity.ts.)","specificitySources":[{"label":"ALK fusion (ALK-positive) label threshold","url":"https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=42c49deb-713b-427a-9670-08af08adcffb","note":"ALK-positive (adjuvant, tumours >= 4 cm or node positive)"},{"label":"Human Protein Atlas ALK tissue","url":"https://www.proteinatlas.org/ENSG00000171094-ALK/tissue","note":"RNA tissue and blood lineage specificity, normal tissue antibody staining (version 25.1, CC BY-SA 3.0)"},{"label":"Open Targets ENSG00000171094 associations","url":"https://platform.opentargets.org/target/ENSG00000171094/associations","note":"cancer associations at or above 0.5 (CC0)"}],"hgnc":"HGNC:427","ensembl":"ENSG00000171094","uniprot":"Q9UM73","entrez":"238","firstDescribed":1994,"firstDescribedBasis":"sequence","firstDescribedNote":"Earliest sequence paper UniProt cites for the protein: Morris S.W. et al, Science, 1994, \"Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma\".","firstDescribedSource":"https://pubmed.ncbi.nlm.nih.gov/8122112/","biology":"ALK is a receptor tyrosine kinase; the EML4-ALK fusion is most common. It is also altered in anaplastic large-cell lymphoma and neuroblastoma.","whereFound":["NSCLC (~5%)","Anaplastic large-cell lymphoma","Neuroblastoma","Pancreatic ductal adenocarcinoma: gene fusion (eml4-alk, strn-alk) 0.2%","Colorectal cancer: gene fusion 0.1%","Non-small-cell lung cancer: rearrangement, usually eml4-alk 3-6%"],"targetClass":"kinase","prevalence":[{"cancerId":"nsclc","pct":"3-5","measure":"Rearrangement","source":"https://www.cbioportal.org/study/summary?id=luad_tcga_pan_can_atlas_2018","note":"Younger never-smokers"},{"cancerId":"neuroblastoma","pct":"8-14","measure":"Activating mutation/amplification","source":"https://en.wikipedia.org/wiki/Anaplastic_lymphoma_kinase","note":"Higher at relapse"},{"cancerId":"pancreatic","pct":"0.2","measure":"Gene fusion (EML4-ALK, STRN-ALK)","source":"https://doi.org/10.6004/jnccn.2017.0058","note":"5 of 3,170 profiled cancers, 0.16%, all KRAS wild-type and all under 50, where ALK fusions were 1.3% of tumours in patients under 50; 3 of 4 treated with an ALK inhibitor had stable disease, radiographic response or CA 19-9 normalisation (Singhi 2017); 1 of 2,336 (ASAP2-ALK) in pdac_msk_2024 (cBioPortal); 2.6% of 266 KRAS wild-type tumours (Philip 2022)."},{"cancerId":"colorectal","pct":"0.1","measure":"Gene fusion","source":"https://www.cbioportal.org/study/summary?id=crc_msk_2026","note":"cBioPortal structural variants: 9 of 7,237, 0.12%, in crc_msk_2026; 1 of 594 (PPP4R3B-ALK) in coadread_tcga_pan_can_atlas_2018. ALK point mutations read 388 of 7,237 in crc_msk_2026 but are overwhelmingly passengers in hypermutated tumours, not the fusions that matter."},{"cancerId":"nsclc","pct":"3-6","measure":"Rearrangement, usually EML4-ALK","source":"https://www.cbioportal.org/study/summary?id=luad_mskcc_2023_met_organotropism","note":"cBioPortal structural variants: 109 of 2,422, 4.5%, in luad_mskcc_2023_met_organotropism (EML4 the partner in 94 of the events); 31 of 915, 3.4%, in lung_msk_2017; 75 of 2,621, 2.9%, in nsclc_ctdx_msk_2022; 13 of 232, 5.6%, in lung_nci_2022; 6 of 181, 3.3%, in luad_oncosg_2020. The original description found the fusion in 5 of 75 patients, 6.7% (Soda 2007), and the Lung Cancer Mutation Consortium found ALK rearrangement in 57 of 733, 8%, by fluorescence in situ hybridisation (Kris 2014)."}]},"route":"/targets/alk/","neighbours":{"biomarker":[{"id":"alk-fusion","kind":"biomarker","name":"ALK fusion (ALK-positive)","route":"/biomarkers/alk-fusion/"},{"id":"alk-resistance-mutation","kind":"biomarker","name":"ALK kinase-domain resistance mutation (G1202R and the rest)","route":"/biomarkers/alk-resistance-mutation/"}],"cancer":[{"id":"alk-negative-anaplastic-large-cell-lymphoma","kind":"cancer","name":"ALK-negative anaplastic large cell lymphoma","route":"/cancers/alk-negative-anaplastic-large-cell-lymphoma/"},{"id":"alk-positive-anaplastic-large-cell-lymphoma","kind":"cancer","name":"ALK-positive anaplastic large cell lymphoma","route":"/cancers/alk-positive-anaplastic-large-cell-lymphoma/"},{"id":"alk-positive-nsclc","kind":"cancer","name":"ALK-positive non-small-cell lung cancer","route":"/cancers/alk-positive-nsclc/"},{"id":"colorectal","kind":"cancer","name":"Colorectal cancer","route":"/cancers/colorectal/"},{"id":"histiocytoses","kind":"cancer","name":"Erdheim-Chester disease, Rosai-Dorfman disease and other histiocytic neoplasms","route":"/cancers/histiocytoses/"},{"id":"neuroblastoma-high-risk","kind":"cancer","name":"High-risk neuroblastoma","route":"/cancers/neuroblastoma-high-risk/"},{"id":"inflammatory-myofibroblastic-tumour","kind":"cancer","name":"Inflammatory myofibroblastic tumour (IMT)","route":"/cancers/inflammatory-myofibroblastic-tumour/"},{"id":"kras-wild-type-pdac","kind":"cancer","name":"KRAS wild-type pancreatic ductal adenocarcinoma","route":"/cancers/kras-wild-type-pdac/"},{"id":"lung-cancer","kind":"cancer","name":"Lung cancer (all types)","route":"/cancers/lung-cancer/"},{"id":"neuroblastoma","kind":"cancer","name":"Neuroblastoma (paediatric)","route":"/cancers/neuroblastoma/"},{"id":"nsclc","kind":"cancer","name":"Non-small-cell lung cancer","route":"/cancers/nsclc/"},{"id":"paediatric-high-grade-glioma","kind":"cancer","name":"Paediatric high-grade glioma (excluding diffuse midline glioma)","route":"/cancers/paediatric-high-grade-glioma/"},{"id":"pancreatic","kind":"cancer","name":"Pancreatic ductal adenocarcinoma","route":"/cancers/pancreatic/"},{"id":"peripheral-t-cell-lymphoma","kind":"cancer","name":"Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma)","route":"/cancers/peripheral-t-cell-lymphoma/"},{"id":"resectable-nsclc","kind":"cancer","name":"Resectable stage I to III non-small-cell lung cancer","route":"/cancers/resectable-nsclc/"},{"id":"uterine-sarcoma","kind":"cancer","name":"Uterine sarcoma","route":"/cancers/uterine-sarcoma/"}],"drug":[{"id":"alectinib","kind":"drug","name":"Alectinib","route":"/drugs/alectinib/"},{"id":"brigatinib","kind":"drug","name":"Brigatinib","route":"/drugs/brigatinib/"},{"id":"ceritinib","kind":"drug","name":"Ceritinib","route":"/drugs/ceritinib/"},{"id":"crizotinib","kind":"drug","name":"Crizotinib","route":"/drugs/crizotinib/"},{"id":"ensartinib","kind":"drug","name":"Ensartinib","route":"/drugs/ensartinib/"},{"id":"entrectinib","kind":"drug","name":"Entrectinib","route":"/drugs/entrectinib/"},{"id":"guardant360-cdx","kind":"drug","name":"Guardant360 CDx","route":"/drugs/guardant360-cdx/"},{"id":"iruplinalkib","kind":"drug","name":"Iruplinalkib","route":"/drugs/iruplinalkib/"},{"id":"lorlatinib","kind":"drug","name":"Lorlatinib","route":"/drugs/lorlatinib/"},{"id":"neladalkib","kind":"drug","name":"Neladalkib","route":"/drugs/neladalkib/"},{"id":"tri-611","kind":"drug","name":"TRI-611","route":"/drugs/tri-611/"}],"company":[{"id":"imagene-ai","kind":"company","name":"Imagene AI","route":"/companies/imagene-ai/"},{"id":"inivata","kind":"company","name":"Inivata","route":"/companies/inivata/"},{"id":"lucence","kind":"company","name":"Lucence","route":"/companies/lucence/"},{"id":"triana-biomedicines","kind":"company","name":"Triana Biomedicines","route":"/companies/triana-biomedicines/"}],"pathway":[{"id":"oncogene-activation-two-hit","kind":"pathway","name":"Drivers, passengers & the two-hit model","route":"/pathways/oncogene-activation-two-hit/"},{"id":"drug-efflux-pumps","kind":"pathway","name":"Drug efflux pumps (ABC transporters)","route":"/pathways/drug-efflux-pumps/"},{"id":"nsclc-signalling","kind":"pathway","name":"Non-small cell lung cancer (KEGG map)","route":"/pathways/nsclc-signalling/"},{"id":"organ-tropism-seed-soil","kind":"pathway","name":"Organ tropism: seed and soil","route":"/pathways/organ-tropism-seed-soil/"},{"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/"},{"id":"rtk-activation","kind":"pathway","name":"Receptor tyrosine kinase activation","route":"/pathways/rtk-activation/"},{"id":"resistance-routes-map","kind":"pathway","name":"Resistance routes: how a blocked pathway comes back","route":"/pathways/resistance-routes-map/"},{"id":"blood-brain-barrier-metastasis","kind":"pathway","name":"The blood-brain barrier & brain metastasis","route":"/pathways/blood-brain-barrier-metastasis/"}],"term":[{"id":"driver-mutation","kind":"term","name":"Driver mutation","route":"/terms/driver-mutation/"},{"id":"resistance","kind":"term","name":"Drug resistance (primary and acquired)","route":"/terms/resistance/"},{"id":"gene-fusion","kind":"term","name":"Gene fusion","route":"/terms/gene-fusion/"},{"id":"sustaining-proliferative-signaling","kind":"term","name":"Hallmark: sustaining proliferative signalling","route":"/terms/sustaining-proliferative-signaling/"},{"id":"histologic-transformation","kind":"term","name":"Histologic transformation","route":"/terms/histologic-transformation/"},{"id":"kinase","kind":"term","name":"Kinase","route":"/terms/kinase/"},{"id":"gatekeeper-mutation","kind":"term","name":"On-target resistance mutations (gatekeeper, solvent-front, compound)","route":"/terms/gatekeeper-mutation/"},{"id":"oncogene","kind":"term","name":"Oncogene","route":"/terms/oncogene/"},{"id":"segmental-chromosomal-aberrations","kind":"term","name":"Segmental chromosomal aberrations and ploidy (neuroblastoma)","route":"/terms/segmental-chromosomal-aberrations/"}],"paper":[{"id":"paper-wu-alina-adjuvant-alectinib-nejm-2024","kind":"paper","name":"Alectinib in resected ALK-positive non-small-cell lung cancer","route":"/key-papers/paper-wu-alina-adjuvant-alectinib-nejm-2024/"},{"id":"paper-peters-alex-alectinib-crizotinib-nejm-2017","kind":"paper","name":"Alectinib versus crizotinib in untreated ALK-positive non-small-cell lung cancer","route":"/key-papers/paper-peters-alex-alectinib-crizotinib-nejm-2017/"},{"id":"paper-shaw-alk-resistance-mutations-lorlatinib-jco-2019","kind":"paper","name":"ALK resistance mutations and efficacy of lorlatinib in advanced anaplastic lymphoma kinase-positive non-small-cell lung 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