The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors
Published version of a preprint
Abstract
Focal amplification and activating point mutation of the MET gene are well-characterized oncogenic drivers that confer susceptibility to targeted MET inhibitors. Recurrent somatic splice site alterations at MET exon 14 (METex14) that result in exon skipping and MET activation have been characterized, but their full diversity and prevalence across tumor types are unknown. Here, we report analysis of tumor genomic profiles from 38,028 patients to identify 221 cases with METex14 mutations (0.6%), including 126 distinct sequence variants. METex14 mutations are detected most frequently in lung adenocarcinoma (3%), but also frequently in other lung neoplasms (2.3%), brain glioma (0.4%), and tumors of unknown primary origin (0.4%). Further in vitro studies demonstrate sensitivity to MET inhibitors in cells harboring METex14 alterations. We also report three new patient cases with METex14 alterations in lung or histiocytic sarcoma tumors that showed durable response to two different MET-targeted therapies. The diversity of METex14 mutations indicates that diagnostic testing via comprehensive genomic profiling is necessary for detection in a clinical setting. Significance: Here we report the identification of diverse exon 14 splice site alterations in MET that result in constitutive activity of this receptor and oncogenic transformation in vitro. Patients whose tumors harbored these alterations derived meaningful clinical benefit from MET inhibitors. Collectively, these data support the role of METex14 alterations as drivers of tumorigenesis, and identify a unique subset of patients likely to derive benefit from MET inhibitors. Cancer Discov; 5(8); 850–9. ©2015 AACR. See related commentary by Ma, p. 802. See related article by Paik et al., p. 842. This article is highlighted in the In This Issue feature, p. 783
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In the citing paper
“Importantly, large-scale profiling studies utilizing either whole exome sequencing or broad targeted sequencing panels in NSCLC tumors have revealed multiple non-random patterns of co-occurring or mutually exclusive mutations, which typically vary depending on the particular oncogenic driver mutation15, 34, 58–62.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“Landmark large scale sequencing studies have established a census of major KRAS co-mutations in both early-stage and advanced LUAD15, 34, 59, 62.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“Although EGFR –mutant tumors represent the prototypical oncogene-addicted LUAD subgroup that spearheaded adoption of the single-driver model, the overwhelming majority of EGFR-mutant lung tumors harbor one or more co-mutations, even when the analysis is limited to pre-defined sets of cancer-relevant genes within established panels (FoundationOne, Guardant360, MSK-IMPACT)15, 59, 72, 73.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“NKX2–1 amplification is significantly enriched in EGFR-mutant LUAD”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“earlier studies that identified a central role for WNT signaling in LUAD metastasis”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“like CTNNB1 mutations, are encountered preferentially in advanced-stage tumors15, 34, 72, 73”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“but are less likely to harbor TP53 alterations (23.8%−26.5%) compared with other driver subgroups15, 128.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“experimental data demonstrating increased invasive potential of EGFR and CTNNB1 co-mutated NSCLC cells in vitro15, 34, 72, 73, 120, 121”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“PIK3CA mutations, including classical kinase (H1074R and H1074L) and helical (E545K and E542K) domain mutations are observed in 9%−12.4% of advanced stage EGFR-mutant LUAD”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“Activating mutations in CTNNB1 represent one of the most consistently co-selected alterations in EGFR-mutant LUAD across different studies.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“advanced-stage ALK-rearrangement -positive LUAD are enriched in somatic alterations in CDKN2A (32.5%)”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“and CDKN2B (26.5%)”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“their prevalence increases in late-stage tumors (5.3% - 9.6%)”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“these tumors are characterized by highly significant enrichment of MDM2 and CDK4 amplification (41.6%) compared with other driver oncogenes”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“both RET and ROS1 fusion-positive LUAD are characterized by high rates of concurrent CDKN2A loss (29.8% and 30.4% for RET and ROS1-rearranged tumors respectively)”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“CDKN2B loss (25% and 17.7% respectively)”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“The spectrum of co-occurring alterations in BRAF-mutant NSCLC mirrors the background frequency of alterations in TP53 (53.3%), LKB1 (16.2%), ATM (5.8%), NF1 (6.9%), PIK3CA (6.6%), KEAP1 (6.6%), MYC (10.8%), NKX2–1 (7.3%)”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“as well as frequent mutations in RB1 (8.9%)”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“whereas loss of CDKN2A (24.1%) and CDKN2B (17.5%) occur with similar frequencies to that in the overall population of patients with NSCLC15.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“both RET and ROS1 fusion-positive LUAD are characterized by high rates of concurrent CDKN2A loss (29.8% and 30.4% for RET and ROS1-rearranged tumors respectively)”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“although the frequency of TP53 mutations appears to be somewhat higher compared to ALK-rearranged tumors (34.6%−45.5% for RET-and 45.6% for ROS1- rearranged tumors)15, 131.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“patients with ERBB2-mutant NSCLC exhibit preferential amplification of NKX2–1 (19.4%) and ERBB2 itself (14.4%)”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“as well as amplification of MET itself15.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“CDKN2B loss (25% and 17.7% respectively)”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“relative paucity of TP53 mutations”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“but the frequencies of co-mutations in TP53 (51.7%), CDKN2A (27.2%), CDKN2B (17.2%), PIK3CA (5%), CTNNB1 (4.4%) and MDM2 amplification (7.2%) are similar to that observed in the overall population of patients with NSCLC15.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“In contrast, mutations in TP53 (33.57%) are under-represented”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
In the citing paper
“although alterations in RB1, MDM2, CDKN2A (16.6%) and CDKN2B (11.2%) are less frequent within this molecular subgroup15.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [15]
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“Regardless, it has been hypothesized that combination of METi with an added targeted therapy such as a CDK 4/6 or MDM2 inhibitor could prove useful in patients with MDM2 or CDK4 co-amplification [22], presenting an interesting avenue of research in the coming years.”
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“%) and infrequently in other tumor types such as urothelial carcinoma, head and neck squamous cell carcinoma, clear cell kidney cancer, and colorectal adenocarcinoma [22, 23].”
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“20 27 These inhibitors primarily benefit tumors dependent on c-Met pathway activation, whereas c-Met overexpression does not necessarily correlate with pathway activity, 28 limiting their clinical benefit in broader populations with c-Met-overexpressing tumors.”
Genomic Applications in Pulmonary Malignancies
Büttner, R., Odenthal, M., & Merkelbach‐Bruse, S. (2014) · Springer eBooks · doi:10.1007/978-1-4939-0727-4_24 · Cited by 1
Stratification in advanced non-small cell lung cancer: precision medicine in practice
Brustugun, O. T. (2016) · Expert Review of Precision Medicine and Drug Development · doi:10.1080/23808993.2016.1176861 · Cited by 1
“Preliminary data, although scarce, also indicate clinical effectiveness in squamous cell carcinoma with skipped exon 14-mutations [75].”
BackgroundAltérations moléculaires anciennes et émergentes : quand les rechercher ?
Mignard, X., Ruppert, A.-M., Rabbe, N., Pontdeme, G., Antoine, M., Lacave, R., Lavolé, A., Cadranel, J. L., & Wislez, M. (2017) · Revue des Maladies Respiratoires Actualités · doi:10.1016/s1877-1203(17)30053-8 · Cited by 3
Lategahn, J., Keul, M., & Rauh, D. (2017) · Angewandte Chemie · doi:10.1002/ange.201710398 · Cited by 1
Absenger, G. (2019) · memo - Magazine of European Medical Oncology · doi:10.1007/s12254-019-0488-3 · Cited by 1
Oncogenèse pulmonaire: comprendre les addictions oncogéniques et les résistances
Baldacci, S., Mascaux, C., & Cortot, A. B. (2019) · Revue des Maladies Respiratoires Actualités · doi:10.1016/s1877-1203(19)30085-0 · Cited by 1
Brisudová, A., & Škarda, J. (2020) · Biomedical Papers · doi:10.5507/bp.2020.015 · Cited by 1
Malignant Epithelial Tumors of the Lung
Weissferdt, A. (2020) · Springer eBooks · doi:10.1007/978-3-030-36438-0_12 · Cited by 1
Secuenciación de nueva generación (NGS) y oncología de precisión
Recondo, G. (2021) · Medicina · doi:10.56050/01205498.1572 · Cited by 1
“Las mutaciones o deleciones que afectan los sitios dadores y aceptores de empalme o “splicing” del exón 14 pueden ser detectados por NGS con paneles genómicos que comprendan toda la extensión del exón y sus intrones flanqueantes, permitiendo detectar las más de 100 variantes que dan como resultado un empalme patológic…”
Genomic Applications in Pulmonary Malignancies
Büttner, R., Heydt, C., & Merkelbach‐Bruse, S. (2018) · Springer eBooks · doi:10.1007/978-3-319-96830-8_27 · Cited by 1
Grodkiewicz, M., Kozieł, P., Chmielewska, I., Grenda, A., Krawczyk, P. A., & Milanowski, J. (2023) · Oncology in Clinical Practice · doi:10.5603/ocp.2023.0041 · Cited by 1
Molecular Pathology of Lung Tumors
Lo, Y., & Lindeman, N. I. (2023) · Springer eBooks · doi:10.1007/978-3-031-35118-1_9 · Cited by 1
Смолин, С., Zhukova, L., Smolin, A., Bubenko, D. N., & Гречухина, К. С. (2023) · Malignant tumours · doi:10.18027/2224-5057-2023-13-3-37-48 · Cited by 1
Development of clinical trials for non-small cell lung cancer drugs in China from 2005 to 2023
Jia, W., Yu, H., Li, S., Wang, J., Niu, S., Zang, G., Liang, M., Liu, J., & Na, R. (2023) · Frontiers in Medicine · doi:10.3389/fmed.2023.1239351 · Cited by 1
Yang, Y., He, X., Xiao, W., Bai, J., & Liu, Y. (2023) · Anti-Cancer Drugs · doi:10.1097/cad.0000000000001559 · Cited by 1
Toumi, E., Hesson, L. B., Lin, V. Y., Wright, D. C., Hajdu, E., Lim, L. S., Giblin, M., Zhou, F., Hoffmeister, A., Zabih, F., et al. (2024) · Cancers · doi:10.3390/cancers16244152 · Cited by 1
Isaacs, J. M., & Clarke, J. M. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-800684-9.00006-x · Cited by 1
Precision Medicine in Lung Cancer
Kerr, K. M., & Laing, G. M. (2017) · Molecular pathology library · doi:10.1007/978-3-319-62941-4_1 · Cited by 1
Molecular Pathology of Lung Cancer
Bozkurtlar, E. B., & Kaya, H. (2018) · Nuclear Medicine Seminars · doi:10.4274/nts.2018.004 · Cited by 1
Clinical Next-Generation Sequencing Assays for Solid Tumors
Hsiao, S. J., Aisner, D. L., & Ewalt, M. D. (2018) · Advances in Molecular Pathology · doi:10.1016/j.yamp.2018.07.008 · Cited by 1
Classification histomoléculaire des cancers pulmonaires
Antoine, M., Moroch, J., Kebir, F., Georges, M., Ruppert, A.-M., Wislez, M., & Cadranel, J. L. (2018) · Revue des Maladies Respiratoires Actualités · doi:10.1016/s1877-1203(18)30016-8 · Cited by 1
Dickinson, E., Zhao, D., & Reckamp, K. L. (2018) · Elsevier eBooks · doi:10.1016/b978-0-323-55433-6.00009-2 · Cited by 1
Hosseini, S. M., Khanafshar, E., Seeley, E. J., & Ruiz‐Cordero, R. (2021) · Diagnostic Cytopathology · doi:10.1002/dc.24694 · Cited by 1
“A review of 38 028 tumor specimens sequenced at FoundationOne detected MET exon 14 skipping mutations mostly in lung primary tumors, but also in brain gliomas.(2) Similarly, The Cancer Genome Atlas data (query of 10 967 samples on cBioPortal) shows MET exon 14 skipping mutations only in cases of lung adenocarcinoma an…”
BackgroundSong, P., Liu, L., Liu, Y., Zhang, T., Guo, L., Li, W., Ying, J., Yang, L., & Gao, S. (2019) · Translational Cancer Research · doi:10.21037/tcr.2019.03.14 · Cited by 1
“Crizotinib, a potent tyrosine kinase inhibitor (TKI) of anaplastic lymphoma kinase (ALK) and ROS1, has demonstrated its remarkable therapeutic effect in patients with MET amplified or MET exon 14 skipping mutated advanced-stage non-small-cell lung cancer in several previous reports (1-5).”
BackgroundGu, L., Zhao, Y., Wen, F., Zhang, D., Cai, J., & Chen, Z. (2023) · Anti-Cancer Drugs · doi:10.1097/cad.0000000000001495 · Cited by 1
Precision medicine in immunotherapy and lung cancer
Sánchez‐Céspedes, M. (2023) · Anales de la Real Academia Nacional de Farmacia · doi:10.53519/analesranf.2023.89.01.01
Alternative Splicing Changes As Drivers Of Cancer
Climente-González, H., Porta‐Pardo, E., Godzik, A., & Eyras, E. (2017) · Zenodo (CERN European Organization for Nuclear Research) · doi:10.5281/zenodo.793565 · Cited by 1
Strickland, M. R., & Janne, P. A. (2020) · Annals of Translational Medicine · doi:10.21037/atm-20-4253 · Cited by 1
“They argue that expression analysis could represent a useful prescreening tool as current DNA-based assay approaches risk not fully capturing the heterogeneous landscape of over 120 mutations associated with METex14 (12).”
BackgroundMethodResultInfluentialSomatic Mutation But Not Aneuploidy Differentiates Lung Cancer in Never-Smokers and SmokersPreprint
Moorthi, S., Paguirigan, A. L., Ko, M., Pettinger, M. B., Hoge, A. C. H., Nag, A., Patel, N. A., Wu, F., Sather, C. L., Fitzgibbon, M., et al. (2023) · SSRN Electronic Journal · doi:10.1101/2023.01.05.522947 · Cited by 1
Malapelle, U., Tabbò, F., & Muscarella, L. A. (2023) · Frontiers in Oncology · doi:10.3389/fonc.2023.1239304 · Cited by 1
“NSCLC, oncogene driver, co-occurrent mutations, targeted therapy, prognosis Editorial on the Research Topic Concomitant pathogenic mutations in oncogene-driven subgroups: when next generation biology meets targeted therapy in NSCLC Starting from the Epidermal Growth Factor Receptor (EGFR) (1) and Anaplastic Lymphoma K…”
BackgroundEstevam, G. O., Linossi, E. M., Macdonald, C. B., Espinoza, C. A., Michaud, J. M., Coyote‐Maestas, W., Collisson, E. A., Jura, N., & Fraser, J. S. (2023) · eLife · doi:10.7554/elife.91619.1 · Cited by 2
Self-citationMoro‐Sibilot, D., Duruisseaux, M., Levra, M. G., Sakhri, L., & Toffart, A. (2015) · Revue des Maladies Respiratoires Actualités · doi:10.1016/s1877-1203(16)30033-7
Biomarkers for Lung Cancer: Focusing on Targeted Drug Resistance
Yano, S. (2016) · Haigan · doi:10.2482/haigan.56.55
La génétique somatique des tumeurs solides, un incontournable à l’ère de la médecine de précision
Lehmann‐Che, J., Poirot, B., Boyer, J. C., & Evrard, A. (2017) · Therapies · doi:10.1016/j.therap.2016.09.009
Optimizing Sequencing in Patients with NSCLC and Actionable Mutations | PER
Reckamp, K. L. (2017) · American Journal of Hematology / Oncology®
MET ex14-Positive NSCLC: Time to Take the Therapy to the Target to Aim for a Cure?
Zhu, V. W., & Ou, S. I. (2017) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2017.06.009
Self-citationMutation Testing of Lung Cancer Biomarkers (Excluding IHC and NGS)
Portier, B. P. (2017) · Molecular pathology library · doi:10.1007/978-3-319-62941-4_7
Role of crizotinib in c-mesenchymal-epidermal transition-positive nonsmall cell lung cancer patients
Batra, U., Jain, A., Sharma, M., Bajaj, R., & Suryavanshis, M. (2017) · Indian Journal of Cancer · doi:10.4103/0019-509x.219592
Large-scale study of rna processing alterations in multiple cancers
Singh, B. (2017) · LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas)
Nichtkleinzelliges Lungenkarzinom – Pathologie und Biologie
Wittersheim, M., Schallenberg, S., & Büttner, R. (2018) · Der Onkologe · doi:10.1007/s00761-018-0461-5
Targeted RNA NextGenSeq profiling in oncology using single molecule molecular inversion probesPreprint
Lenting, K., van den Heuvel, C. N. A. M., van Ewijk, A., Tindall, E. A., Ge, W., Küsters, B., Dorsthorst, M. T., ter Laan, M., Huynen, M. A., & Leenders, W. P. J. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/440065
“For instance, MET overexpression may lead to inclusion of patients for treatment with MET-inhibitors, whereas such treatment can lead to rapid selection of subclones that overexpress rescue kinases, or overexpress inhibitors of phosphatases [52–54].”
BackgroundInfluentialFrontline Systemic Therapy Options in Nonsmall Cell Lung Cancer
Ramalingam, S. S., Pillai, R. N., Reinmuth, N., & Reck, M. (2018) · Elsevier eBooks · doi:10.1016/b978-0-323-52357-8.00044-5
Systemic Options for Second-Line Therapy and Beyond
Goss, G. D., & Mok, T. S. K. (2018) · Elsevier eBooks · doi:10.1016/b978-0-323-52357-8.00045-7
Nichtkleinzelliges Lungenkarzinom – Pathologie und Biologie
Wittersheim, M., Schallenberg, S., & Büttner, R. (2019) · Wiener klinisches Magazin · doi:10.1007/s00740-019-0277-y
Prioritizing mutational profiling for targeted therapy of lung adenocarcinoma
Sinjab, A. F., & Tfayli, A. (2019) · Journal of Thoracic Disease · doi:10.21037/jtd.2019.02.29
“Indeed, novel MET inhibitors (crizotinib, cabozantinib, and more recently, capmatinib) are currently being investigated in advanced stage lung cancers, targeting a number of MET genetic lesions such as exon 14 skipping mutations and METamp (11,12).”
BackgroundInfluentialMET as a Therapeutic Target: Have Clinical Outcomes Been “MET” in Lung Cancer?
Nam, A., & Salgia, R. (2019) · Current cancer research · doi:10.1007/978-3-030-17832-1_5
Self-citationHeat Shock Protein 90 Inhibitors in Lung Cancer Therapy
Chatterjee, S., & Burns, T. F. (2019) · Heat shock proteins · doi:10.1007/978-3-030-03952-3_19
Martinez, F. J. (2019) · American Journal of Biomedical Science & Research · doi:10.34297/ajbsr.2019.06.001002
“The MET oncogene has been shown to be a sufficient cause of carcinoma exclusive of other oncogenic drivers including EGFR, KRAS, and BRAF mutations in addition to being exclusive to ALK ROS-1 and RET gene rearrangements [8].”
BackgroundImmunhistochemische und molekularpathologische Diagnostik von Lungenkarzinomen
Wagner, B. J., & Buettner, R. (2020) · Wiener klinisches Magazin · doi:10.1007/s00740-020-00341-5
“MET-Alterationen Für den Membranrezeptor MET (Ligand: „hepatocyte growth factor“) sind 4 wichtige genetische Aberrationen bekannt: 1) Deletionen in Intronbereichen um Exon 14, die zu Spleissvarianten ohne Exon 14 und zu längerem Verweilen von MET in der Zellmembran führen („exon14 skipping mutations“), 2) Amplifikatio…”
BackgroundTargeting Co-Occurring Genomic Alterations in MET Exon 14 Skipping Mutation-Positive NSCLC
Yasuda, H. (2020) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2020.02.014
Metadata
- Authors
- Frampton, G. M., Ali, S. M., Rosenzweig, M., Chmielecki, J., Lu, X., Bauer, T. M., Akimov, M., Bufill, J. A., Lee, C., Jentz, D., Hoover, R., Ou, S.-H. I., Salgia, R., Brennan, T., Chalmers, Z. R., Jaeger, S., Huang, A., Elvin, J. A., Erlich, R., Fichtenholtz, A., Gowen, K. A., Greenbowe, J., Johnson, A., Khaira, D., McMahon, C., Sanford, E. M., Roels, S., White, J., Greshock, J., Schlegel, R., Lipson, D., Yelensky, R., Morosini, D., Ross, J. S., Collisson, E., Peters, M., Stephens, P. J., & Miller, V. A.
- Affiliations
- Foundation Medicine (United States) (US)
- University of California, San Francisco (US)
- Tennessee Oncology (US)
- Novartis (Switzerland) (CH)
- 5Michiana Hematology-Oncology, PC, Mishawaka, Indiana.
- University of North Carolina at Chapel Hill (US)
- South Bend Medical Foundation (US)
- University of California, Irvine (US)
- University of Chicago (US)
- 1Foundation Medicine Inc., Cambridge, Massachusetts.
- Corresponding author
- Frampton, Garrett M.
- ORCID
- Frampton, Garrett M.
- Ali, Siraj M.
- Rosenzweig, Mark
- Chmielecki, Juliann
- Lu, Xinyuan
- Bauer, Todd M.
- Akimov, Mikhail
- Lee, Carrie
- Ou, Sai-Hong Ignatius
- Salgia, Ravi
- Chalmers, Zachary R.
- Huang, Alan
- Elvin, Julia A.
- Johnson, Adrienne
- Sanford, Eric M.
- Roels, Steven
- Greshock, Joel
- Lipson, Doron
- Yelensky, Roman
- Ross, Jeffrey S.
- Collisson, Eric
- Miller, Vincent A.
- Venue
- Cancer Discovery
- Published
- 2015-08-01
- Volume
- 5
- Issue
- 8
- Pages
- 850-859
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- OpenAlex
- W2160212814
- Cited by
- 796
- References
- 41
- Citations by year
- 2026: 26 · 2025: 47 · 2024: 69 · 2023: 83 · 2022: 73 · 2021: 97 · 2020: 91 · 2019: 71 · 2018: 71 · 2017: 86 · 2016: 65 · 2015: 13
- FWCI
- 62.31
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cancer Discovery (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (P30CA016086)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Mechanisms and Therapy
- Keywords
- MET activation, MET inhibitors, exon skipping, lung adenocarcinoma, glioma, histiocytic sarcoma, targeted therapy sensitivity, oncogenic transformation, comprehensive genomic profiling, tumor genomic profiles
- MeSH terms
- Aged, Aged, 80 and over, Antineoplastic Agents, Exons, Female, Humans, Immunohistochemistry, Male, Mutation, Neoplasm Staging, Neoplasms, Tomography, X-Ray Computed, Cluster Analysis, Alternative Splicing, Drug Resistance, Neoplasm, Proto-Oncogene Proteins c-met, Gene Expression Profiling, Genomics, Protein Kinase Inhibitors
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