دورية أكاديمية
أعرض في EDS

Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors.

التفاصيل البيبلوغرافية
العنوان: Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors.
المؤلفون: Pecci F; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Nakazawa S; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Ricciuti B; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Harada G; Department of Medical Oncology, Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College, New York, New York., Lee JK; Foundation Medicine, Cambridge, Massachusetts., Alessi JV; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Barrichello A; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Vaz VR; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Lamberti G; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Di Federico A; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Gandhi MM; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Gazgalis D; Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts., Feng WW; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Jiang J; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Baldacci S; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Locquet MA; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Gottlieb FH; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Chen MF; Department of Medical Oncology, Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College, New York, New York., Lee E; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Haradon D; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Smokovich A; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Voligny E; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Nguyen T; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Goel VK; Turning Point Therapeutics, Bristol Myers Squibb Company, San Diego, California., Zimmerman Z; Turning Point Therapeutics, Bristol Myers Squibb Company, San Diego, California., Atwal S; Turning Point Therapeutics, Bristol Myers Squibb Company, San Diego, California., Wang X; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Harvard University, Boston, Massachusetts., Bahcall M; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Heist RS; Massachusetts General Hospital, Boston, Massachusetts., Iqbal S; The Center for the Development of Therapeutics, Broad Institute of MIT and Harvard, Cambridge, Massachusetts.; Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, Massachusetts., Gandhi N; Caris Life Sciences, Phoenix, Arizona., Elliott A; Caris Life Sciences, Phoenix, Arizona., Vanderwalde AM; Caris Life Sciences, Phoenix, Arizona., Ma PC; Penn State Cancer Institute, Penn State College of Medicine, Penn State University, Hershey, Pennsylvania., Halmos B; Montefiore Einstein Cancer Center, Bronx, New York., Liu SV; Georgetown University, Washington, DC., Che J; Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts., Schrock AB; Foundation Medicine, Cambridge, Massachusetts., Drilon A; Department of Medical Oncology, Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College, New York, New York., Jänne PA; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts., Awad MM; Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
المصدر: Cancer discovery [Cancer Discov] 2024 Aug 02; Vol. 14 (8), pp. 1440-1456.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: American Association for Cancer Research Country of Publication: United States NLM ID: 101561693 Publication Model: Print Cited Medium: Internet ISSN: 2159-8290 (Electronic) Linking ISSN: 21598274 NLM ISO Abbreviation: Cancer Discov Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Philadelphia, PA : American Association for Cancer Research
مواضيع طبية MeSH: Proto-Oncogene Proteins c-met*/genetics , Proto-Oncogene Proteins c-met*/antagonists & inhibitors , Lung Neoplasms*/genetics , Lung Neoplasms*/drug therapy , Lung Neoplasms*/pathology , Protein Kinase Inhibitors*/therapeutic use , Protein Kinase Inhibitors*/pharmacology , Point Mutation*, Humans ; Animals ; Mice ; Cell Line, Tumor
مستخلص: Activating point mutations in the MET tyrosine kinase domain (TKD) are oncogenic in a subset of papillary renal cell carcinomas. Here, using comprehensive genomic profiling among >600,000 patients, we identify activating MET TKD point mutations as putative oncogenic driver across diverse cancers, with a frequency of ∼0.5%. The most common mutations in the MET TKD defined as oncogenic or likely oncogenic according to OncoKB resulted in amino acid substitutions at positions H1094, L1195, F1200, D1228, Y1230, M1250, and others. Preclinical modeling of these alterations confirmed their oncogenic potential and also demonstrated differential patterns of sensitivity to type I and type II MET inhibitors. Two patients with metastatic lung adenocarcinoma harboring MET TKD mutations (H1094Y, F1200I) and no other known oncogenic drivers achieved confirmed partial responses to a type I MET inhibitor. Activating MET TKD mutations occur in multiple malignancies and may confer clinical sensitivity to currently available MET inhibitors. Significance: The identification of targetable genomic subsets of cancer has revolutionized precision oncology and offers patients treatments with more selective and effective agents. Here, we demonstrate that activating, oncogenic MET tyrosine kinase domain mutations are found across a diversity of cancer types and are responsive to MET tyrosine kinase inhibitors.
(©2024 The Authors; Published by the American Association for Cancer Research.)
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معلومات مُعتمدة: R01 CA222823 United States CA NCI NIH HHS; T32 CA009207 United States CA NCI NIH HHS; T32-CA009207 American Society of Clinical Oncology (ASCO); AAPMRC2.2020.LCC/SB Ligue Contre le Cancer (French League Against Cancer)
المشرفين على المادة: EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
0 (Protein Kinase Inhibitors)
EC 2.7.10.1 (MET protein, human)
تواريخ الأحداث: Date Created: 20240402 Date Completed: 20240802 Latest Revision: 20240804
رمز التحديث: 20240804
مُعرف محوري في PubMed: PMC11294820
DOI: 10.1158/2159-8290.CD-23-1217
PMID: 38564707
قاعدة البيانات: MEDLINE
الوصف
تدمد:2159-8290
DOI:10.1158/2159-8290.CD-23-1217