Missing content? – Request curation!
Request curation for specific Genes, Variants, or PubMed publications.
Have questions, comments, or suggestions? - Let us know!
Email us at : firstname.lastname@example.org
|Profile Name||ALK amp|
|Gene Variant Detail|
|Relevant Treatment Approaches|
|Molecular Profile||Indication/Tumor Type||Response Type||Relevant Treatment Approaches||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|ALK amp||neuroblastoma||no benefit||Crizotinib||Preclinical - Cell culture||Actionable||In a preclinical study, Xalkori (crizotinib) was less efficient than Lorlatinib (PF-06463922) to induced growth inhibition in ALK-amplified neuroblastoma cells in culture (PMID: 26554404).||26554404|
|ALK amp||neuroblastoma||sensitive||Lorlatinib||Preclinical - Cell culture||Actionable||In a preclinical study, Lorlatinib (PF-06463922) inhibited growth of ALK amplified neuroblastoma cells in culture (PMID: 26554404).||26554404|
|ALK amp||neuroblastoma||sensitive||CEP-28122||Preclinical - Cell culture||Actionable||In a preclinical study, CEP-28122 inhibited growth of ALK-amplified neuroblastoma cells in culture (PMID: 22203728).||22203728|
|ALK amp||lung non-small cell carcinoma||no benefit||Belizatinib||Phase I||Actionable||In a Phase I trial, treatment with Belizatinib (TSR-011) in ALK inhibitor-naive non-small cell lung cancer patients (n=14) harboring either an ALK mutation, ALK amplification, or an ALK rearrangement resulted in a partial response in 6 patients and stable disease in 8 patients, however, it was determined that the drug resulted in limited efficacy and development of the drug was discontinued (PMID: 31217479; NCT02048488).||31217479|
|ALK amp||neuroblastoma||no benefit||Crizotinib||Case Reports/Case Series||Actionable||In a Phase I/II trial (ADVL0912), Xalkori (crizotinib) treatment resulted in an objective response of 15% (3/20) in pediatric patients with relapsed/refractory neuroblastoma harboring ALK activating mutations or amplifications, although both patients harboring ALK amplification had disease progression after only 1 cycle of treatment (PMID: 33568345; NCT00939770).||33568345|
|ALK amp||neuroblastoma||predicted - sensitive||Repotrectinib||Case Reports/Case Series||Actionable||In a preclinical study, Augtyro (repotrectinib) treatment resulted in inhibition of cell proliferation in a neuroblastoma cell line harboring ALK amplification in culture (PMID: 34482287).||34482287|
|ALK amp||neuroblastoma||predicted - sensitive||Ensartinib||Preclinical - Cell culture||Actionable||In a preclinical study, Ensartinib (X-396) treatment resulted in inhibition of cell proliferation in a neuroblastoma cell line harboring ALK amplification in culture (PMID: 34482287).||34482287|
|ALK amp||neuroblastoma||sensitive||Lorlatinib||Preclinical - Pdx & cell culture||Actionable||In a preclinical study, Lorbrena (lorlatinib) inhibited viability of a panel of ALK-amplified neuroblastoma cell lines in culture, and inhibited tumor growth in a patient-derived xenograft (PDX) model (PMID: 36602782).||36602782|
|ALK amp||neuroblastoma||no benefit||Cyclophosphamide + Doxorubicin + Lorlatinib + Vincristine Sulfate||Preclinical - Pdx||Actionable||In a preclinical study, addition of Cytoxan (cyclophosphamide), Adriamycin (doxorubicin), and Oncovin (vincristine) to Lorbrena (lorlatinib) did not improve tumor growth inhibition in a patient-derived xenograft (PDX) model of neuroblastoma with ALK amplification and overexpression (PMID: 36602782).||36602782|
|ALK amp||neuroblastoma||predicted - sensitive||NUV-655||Preclinical - Cell culture||Actionable||In a preclinical study, NUV-655 inhibited proliferation of neuroblastoma cell lines with ALK amplification in culture (Cancer Res (2022) 82 (12_Supplement): 3337).||detail...|