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
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
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]
Citations
Cites
Comprehensive molecular profiling of lung adenocarcinoma
The Cancer Genome Atlas Research Network (2014) · Nature · doi:10.1038/nature13385 · Cited by 5,732
Somatic mutations affect key pathways in lung adenocarcinoma
Ding, L., Getz, G., Wheeler, D. A., Mardis, E. R., McLellan, M. D., Cibulskis, K., Sougnez, C., Greulich, H., Muzny, D. M., Morgan, M. B., et al. (2008) · Nature · doi:10.1038/nature07423 · Cited by 2,681
Frampton, G. M., Fichtenholtz, A., Otto, G. A., Wang, K., Downing, S. R., He, J., Schnall-Levin, M., White, J., Sanford, E. M., An, P., et al. (2013) · Nature Biotechnology · doi:10.1038/nbt.2696 · Cited by 2,157
Self-citationMapping the Hallmarks of Lung Adenocarcinoma with Massively Parallel Sequencing
Imielinski, M., Berger, A. H., Hammerman, P. S., Hernandez, B., Pugh, T. J., Hodis, E., Cho, J., Suh, J., Capelletti, M., Sivachenko, A., et al. (2012) · Cell · doi:10.1016/j.cell.2012.08.029 · Cited by 1,789
Self-citationCui, J. J., Tran‐Dubé, M., Shen, H., Nambu, M. D., Kung, P., Pairish, M., Jia, L., Meng, J. J., Funk, L. A., Botrous, I., et al. (2011) · Journal of Medicinal Chemistry · doi:10.1021/jm2007613 · Cited by 967
Use of Statins and the Risk of Death in Patients With Prostate Cancer
Yu, O. H. Y., Eberg, M., Benayoun, S., Aprikian, A. G., Batist, G., Suissa, S., & Azoulay, L. (2013) · Journal of Clinical Oncology · doi:10.1200/jco.2013.49.4757 · Cited by 661
The transcriptional landscape and mutational profile of lung adenocarcinomaPreprint
Seo, J., Ju, Y. S., Lee, W., Shin, J.-Y., Lee, J. J.-K., Bleazard, T., Lee, J., Jung, Y. J., Kim, J. O., Shin, J.-Y., et al. (2012) · Genome Research · doi:10.1101/gr.145144.112 · Cited by 603
Ma, P. C., Jagadeeswaran, R., Jagadeesh, S., Tretiakova, M., Nallasura, V., Fox, E. A., Hansen, M., SCHAEFER, E. M., Naoki, K., Lader, A. S., et al. (2005) · Cancer Research · doi:10.1158/0008-5472.can-04-2650 · Cited by 576
Self-citationSpigel, D. R., Ervin, T. J., Ramlau, R., Daniel, D. B., Goldschmidt, J. H., Blumenschein, G. R., Krzakowski, M. J., Robinet, G., Godbert, B., Barlési, F., et al. (2013) · Journal of Clinical Oncology · doi:10.1200/jco.2012.47.4189 · Cited by 491
Somatic Mutations Lead to an Oncogenic Deletion of Met in Lung Cancer
Kong-Beltran, M., Seshagiri, S., Zha, J., Zhu, W., Bhawe, K. M., Mendoza, N., Holcomb, T., Pujara, K., Stinson, J., Fu, L., et al. (2006) · Cancer Research · doi:10.1158/0008-5472.can-05-2749 · Cited by 491
Flagged first, then by citations
Cited by
Sorted by citations
Items 101–200 of 799
Falchook, G. S., Kurzrock, R., Amin, H. M., Xiong, W., Fu, S., Piha-Paul, S. A., Jankú, F., Eskandari, G., Catenacci, D. V. T., Klevesath, M., et al. (2019) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-19-2860 · Cited by 93
“Activated MET can drive tumorigenesis (7) and make tumors resistant to EGFR inhibitors, VEGF inhibitors, and antihuman EGFR-2 therapies (1).”
BackgroundLi, A., Yang, J., Zhang, X., Zhang, Z., Su, J., Gou, L.-Y., Bai, Y., Zhou, Q. H., Yang, Z., Han‐Zhang, H., et al. (2017) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-3273 · Cited by 91
“The National Comprehensive Cancer Network (NCCN) guidelines recommend crizotinib to NSCLC patients harboring high level MET amplification or MET exon 14 skipping mutation (5, 6, 14, 15).”
BackgroundJamme, P., Fernandes, M., Copin, M., Descarpentries, C., Escande, F., Morabito, A., Grégoire, V., Jamme, M., Baldacci, S., Tulasne, D., et al. (2020) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2020.01.027 · Cited by 91
An Accurate and Comprehensive Clinical Sequencing Assay for Cancer Targeted and Immunotherapies
Cao, J., Chen, L., Li, H., Chen, H., Yao, J., Mu, S., Liu, W., Zhang, P., Cheng, Y., Liu, B., et al. (2019) · The Oncologist · doi:10.1634/theoncologist.2019-0236 · Cited by 89
“However, given the wide heterogeneity of genomic abnormalities across and within tumor types, precisely matching a patient to an appropriate treatment turns out to be a pressing need and crucial to the success of the development of targeted and immunotherapies [5, 6].”
BackgroundHayashi, T., Desmeules, P., Smith, R. S., Drilon, A., Somwar, R., & Ladanyi, M. (2018) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-17-2343 · Cited by 90
“It has become standard practice to profile non-small cell lung carcinomas (NSCLCs), especially adenocarcinomas, for recurrent targetable alterations such as mutant EGFR, MAP2K1, BRAF, NRAS, or rearranged ALK, RET, ROS1, NTRK1, NTRK2, NTRK3, or amplified ERBB2 or MET exon 14 skipping (3-9), which, as strong mitogenic d…”
BackgroundHuang, K. K., Huang, J., Wu, J., Lee, M., Tay, S. T., Kumar, V., Ramnarayanan, K., Padmanabhan, N., Xu, C., Tan, A. L. K., et al. (2021) · Genome biology · doi:10.1186/s13059-021-02261-x · Cited by 88
“Specifically, lung cancer patients with MET exon 14 skipping are responsive to MET inhibitors despite not having other activating alterations [39], while melanoma patients expressing a BRAF isoform lacking exons 4–8, which encodes for the RAS binding domain, exhibit resistance to BRAF inhibitors [40].”
BackgroundAntibody-drug conjugates: A promising novel therapeutic approach in lung cancer
Desai, A. P., Abdayem, P., Adjei, A. A., & Planchard, D. (2021) · Lung Cancer · doi:10.1016/j.lungcan.2021.12.002 · Cited by 93
Lee, G. D., Lee, S. E., Oh, D., Yu, D.-B., Jeong, H. M., Kim, J., Hong, S., Jung, H. S., Oh, E., Song, J., et al. (2017) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2017.04.031 · Cited by 88
“1% (18 of 873).(8,10,21,22) The lower detection rate of METex14 skipping in our study could be due to the methodologic difference between RT-PCR– and next-generation sequencing–based analyses rather than ethnic differences.”
ResultBahcall, M., Awad, M. M., Sholl, L. M., Wilson, F. H., Xu, M., Wang, S., Palakurthi, S. S., Choi, J., Ivanova, E. V., Leonardi, G. C., et al. (2018) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-18-0876 · Cited by 93
“Amino acid substitution at Y1003 or mutations or deletions inMETex14 or its flanking introns that cause in-frame skipping ofMETex14 eliminates the CBL-binding site and leads to increased MET protein stability and effector signaling (13, 16).”
BackgroundCapmatinib for the treatment of non-small cell lung cancer
Vansteenkiste, J., de Kerkhove, C. V., Wauters, E., & Mol, P. V. (2019) · Expert Review of Anticancer Therapy · doi:10.1080/14737140.2019.1643239 · Cited by 92
“MET mutations occur in 3–4% of adenocarcinomas and 1–2% of other histological subsets of NSCLC [38,41].”
BackgroundThe role of alternative splicing in cancer
Singh, B., & Eyras, E. (2016) · Transcription · doi:10.1080/21541264.2016.1268245 · Cited by 85
“Importantly, the skipping of this exon is sufficient for MET activation and tumors that harbor the event respond to MET-targeted therapies.(48,49) Although this splicing change in MET has been explained so far as a result of somatic mutations on exon 14 or on its splice-sites, it is conceivable that the same splicing…”
BackgroundReceptor tyrosine kinases: biological functions and anticancer targeted therapy
Zhang, N., & Li, Y. (2023) · MedComm · doi:10.1002/mco2.446 · Cited by 97
Davies, K. D., Ng, T. L., Estrada‐Bernal, A., Le, A. T., Ennever, P. R., Camidge, D. R., Doebele, R. C., & Aisner, D. L. (2017) · JCO Precision Oncology · doi:10.1200/po.17.00117 · Cited by 88
“Activation of HGFRmediated signaling—most commonly via MET amplification and/or MET mutations that result in exon 14 skipping—is well described inNSCLC, and crizotinib is currently being investigated in these settings.(10-12) Recently, gene fusions that involveMET have been described in various cancers, including NSCL…”
BackgroundCREB5 promotes invasiveness and metastasis in colorectal cancer by directly activating MET
Wang, S., Qiu, J., Liu, L., Su, C., Qi, L., Huang, C., Chen, X., Zhang, Y., Ye, Y., Ding, Y., et al. (2020) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-020-01673-0 · Cited by 86
Molecular characterization of pulmonary sarcomatoid carcinoma: analysis of 33 cases
Terra, S. B. S. P., Jang, J. S., Bi, L., Kipp, B. R., Jen, J., Yi, E. S., & Boland, J. M. (2016) · Modern Pathology · doi:10.1038/modpathol.2016.89 · Cited by 87
Wu, Y.-L. L. C., Soo, R. A., Locatelli, G., Stammberger, U. M., Scagliotti, G. V., & Park, K. (2017) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2017.10.003 · Cited by 83
MET Exon 14 Mutation Encodes an Actionable Therapeutic Target in Lung Adenocarcinoma
Lu, X., Peled, N., Greer, J., Wu, W., Choi, P. S., Berger, A. H., Wong, S., Jen, K., Seo, Y., Hann, B. C., et al. (2017) · Cancer Research · doi:10.1158/0008-5472.can-16-1944 · Cited by 88
“Several groups have reported off-label use of crizotinib in NSCLC harboring MET exon 14 mutations (4, 19, 24).”
BackgroundMethodInfluentialSelf-citationGuo, Y., Song, J., Wang, Y., Huang, L., Sun, L., Zhao, J., Zhang, S., Jing, W., Ma, J., & Han, C. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.610923 · Cited by 87
Cell-free DNA and next-generation sequencing in the service of personalized medicine for lung cancer
Bennett, C. W., Berchem, G., Kim, Y. J., & El‐Khoury, V. (2016) · Oncotarget · doi:10.18632/oncotarget.11717 · Cited by 83
“Based on recent studies, about 3 to 5% of NSCLC patients are expected to harbor MET exon 14 skipping, driving cancer progression and metastasis [53, 121, 123, 127].”
BackgroundEnabling Precision Oncology Through Precision Diagnostics
Brown, N. A., & Elenitoba‐Johnson, K. S. J. (2020) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathmechdis-012418-012735 · Cited by 84
“Still other molecular alterations have associated targeted therapies with promising early clinical data—including MET exon 14 skipping mutations (20, 21), high-level MET amplification (22), RET rearrangements (23–25), and ERBB2 (HER2) mutations (26)—leading to new treatment recommendations from the National Comprehens…”
BackgroundFujino, T., Suda, K., & Mitsudomi, T. (2021) · Lung Cancer Targets and Therapy · doi:10.2147/lctt.s269307 · Cited by 85
“In addition, they are reportedly mutually exclusive.(13) Although the coexistence of TP53 mutation is associated with reduced efficacy in EGFR-mutated NSCLCs treated with EGFR-TKIs,(65) we could not find evidence that showed the impact of TP53 or MDM2”
BackgroundMET exon 14 skipping defines a unique molecular class of non-small cell lung cancer
Zheng, D., Wang, R., Ye, T., Yu, S., Hu, H., Shen, X., Li, Y., Ji, H., Sun, Y., & Chen, H. (2016) · Oncotarget · doi:10.18632/oncotarget.9541 · Cited by 80
“This constitutive activity was sensitive to MET inhibitors in NIH-3T3 cells harboring MET exon 14 alterations [23].”
BackgroundImmunotherapy in Non-Small Cell Lung Cancer With Actionable Mutations Other Than EGFR
Seegobin, K., Majeed, U., Wiest, N. E., Manochakian, R., Lou, Y., & Zhao, Y. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.750657 · Cited by 83
“METex14 occurs in 3–4% of lung cancers and 8–30% of sarcomatoid lung cancers (51, 52).”
BackgroundEbisudani, T., Hamamoto, J., Togasaki, K., Mitsuishi, A., Sugihara, K., Shinozaki, T., Fukushima, T., Kawasaki, K., Seino, T., Oda, M., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.112212 · Cited by 81
Alternative splicing in lung cancer
Coomer, A. O., Black, F., Greystoke, A., Munkley, J., & Elliott, D. J. (2019) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2019.05.006 · Cited by 78
Ma, P., Fu, Y., Cai, M., Yan, Y., Jing, Y., Zhang, S., Chen, M., Wu, J., Shen, Y., Zhu, L. W., et al. (2017) · Nature Communications · doi:10.1038/s41467-017-00963-0 · Cited by 75
Biopsy-free circulating tumor DNA assay identifies actionable mutations in lung cancer
Villaflor, V., Won, B., Nagy, R., Banks, K., Lanman, R. B., Talasaz, A., & Salgia, R. (2016) · Oncotarget · doi:10.18632/oncotarget.11801 · Cited by 75
Self-citationValidation of a Targeted RNA Sequencing Assay for Kinase Fusion Detection in Solid Tumors
Reeser, J. W., Patacsil, D., Miya, J., Kautto, E. A., Lyon, E., Zhu, E. Y., Wing, M. R., Smith, A. M., Reeder, M., Samorodnitsky, E., et al. (2017) · Journal of Molecular Diagnostics · doi:10.1016/j.jmoldx.2017.05.006 · Cited by 77
“In addition to fulfilling an unmet clinical need, OSUSpARKFuse also enables discovery research and opens doors for future clinical applications that involve the cancer transcriptome, including exon skipping, resistance mutations, and alternative splicing (Figure 6).(51,52,55) Using a”
BackgroundThe promise of selective MET inhibitors in non-small cell lung cancer with MET exon 14 skipping
Salgia, R., Sattler, M., Scheele, J., Stroh, C., & Felip, E. (2020) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2020.102022 · Cited by 75
Self-citationRecent progress in targeted therapy for non-small cell lung cancer
Xiao, Y., Liu, P., Wei, J., Zhang, X., Guo, J., & Lin, Y. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1125547 · Cited by 79
“6%, and these mutations do not coexist with other NSCLC driver variations, like ALK or EGFR (Frampton et al., 2015; Heist et al., 2016).”
BackgroundRegulation of the MET oncogene: molecular mechanisms
Zhang, J. Y., & Babic, A. (2016) · Carcinogenesis · doi:10.1093/carcin/bgw015 · Cited by 75
Genetic Heterogeneity of MET-Aberrant NSCLC and Its Impact on the Outcome of Immunotherapy
Kron, A., Scheffler, M., Heydt, C., Ruge, L., Schaepers, C., Eisert, A., Merkelbach‐Bruse, S., Riedel, R. F., Nogová, L., Fischer, R. N., et al. (2020) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2020.11.017 · Cited by 71
The Unique Characteristics of MET Exon 14 Mutation in Chinese Patients with NSCLC
Liu, S. M., Gou, L.-Y., Li, A., Lou, N.-N., Gao, H., Su, J., Yang, J., Zhang, X., Shao, Y. W., Dong, Z., et al. (2016) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2016.05.016 · Cited by 73
“001).(17) For this situation, we consider”
BackgroundMET/HGF pathway activation as a paradigm of resistance to targeted therapies
Ko, B., He, T., Gadgeel, S. M., & Halmos, B. (2017) · Annals of Translational Medicine · doi:10.21037/atm.2016.12.09 · Cited by 71
“NGS has become a very powerful diagnostic tool in our diagnostic armamentarium for MET gene alterations, especially given the broad spectrum of mutations affecting the 5’ and 3’ splice sites of the MET gene that are hard to capture using other methodologies (62,63).”
MethodApproaches to Tumor Classification in Pulmonary Sarcomatoid Carcinoma
Baldovini, C., Rossi, G., & Ciarrocchi, A. (2019) · Lung Cancer Targets and Therapy · doi:10.2147/lctt.s186779 · Cited by 73
Molecular Pathology of Lung CancerPreprint
Saller, J. J., & Boyle, T. A. (2021) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a037812 · Cited by 83
Ding, N., You, A., Tian, W., Gu, L., & Deng, D. (2020) · International Journal of Biological Sciences · doi:10.7150/ijbs.45886 · Cited by 69
Kohsaka, S., Tatsuno, K., Ueno, T., Nagano, M., Shinozaki‐Ushiku, A., Ushiku, T., Takai, D., Ikegami, M., Kobayashi, H., Kage, H., et al. (2019) · Cancer Science · doi:10.1111/cas.13968 · Cited by 69
Wiesweg, M., Eberhardt, W., Reis, H., Ting, S. C., Savvidou, N., Skiba, C., Herold, T., Christoph, D. C., Meiler, J., Worm, K., et al. (2016) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2016.08.137 · Cited by 69
Santarpía, M., Massafra, M., Gebbia, V., d’Aquino, A., Garipoli, C., Altavilla, G., & Rosell, R. (2021) · Translational Lung Cancer Research · doi:10.21037/tlcr-20-1113 · Cited by 72
“Recently, additional actionable oncogenic alterations other than EGFR, ALK, ROS1 and BRAF, have emerged, including MET alterations, RET and NTRK rearrangements (6-13).”
BackgroundInfluentialThe multiple paths towards MET receptor addiction in cancer
Duplaquet, L., Kherrouche, Z., Baldacci, S., Jamme, P., Cortot, A. B., Copin, M., & Tulasne, D. (2018) · Oncogene · doi:10.1038/s41388-018-0185-4 · Cited by 76
Detection of Novel NRG1, EGFR, and MET Fusions in Lung Adenocarcinomas in the Chinese Population
Pan, Y., Zhang, Y., Ye, T., Zhao, Y., Gao, Z., Yuan, H., Zheng, D., Zheng, S., Li, H., Li, Y., et al. (2019) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2019.07.022 · Cited by 69
A Review of Papillary Renal Cell Carcinoma and MET Inhibitors
Smith, K. E. R., & Bilen, M. A. (2019) · Kidney Cancer · doi:10.3233/kca-190058 · Cited by 68
Bang, Y., Su, W., Schüler, M., Nam, D., Lim, W. T., Bauer, T. M., Azaro, A., Poon, R. T. P., Hong, D. S., Lin, C., et al. (2019) · Cancer Science · doi:10.1111/cas.14254 · Cited by 66
Self-citationMET targeting: time for a rematch
Koch, J. P., Aebersold, D. M., Zimmer, Y., & Medová, M. (2020) · Oncogene · doi:10.1038/s41388-020-1193-8 · Cited by 66
“Indeed, there is evidence for the efficacy of MET-targeting therapies in NSCLC cases exhibiting MET alterations [86].”
BackgroundCerasuolo, A., Buonaguro, L., Buonaguro, L., & Tornesello, M. L. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.00474 · Cited by 71
Hong, L., Zhang, J., Heymach, J. V., & Le, X. (2021) · Therapeutic Advances in Medical Oncology · doi:10.1177/1758835921992976 · Cited by 66
Molecular classifications of gastric cancers: Novel insights and possible future applications
Garattini, S. K., Basile, D., Cattaneo, M., Fanotto, V., Ongaro, E., Bonotto, M., Negri, F., Berenato, R., Ermacora, P., Cardellino, G. G., et al. (2017) · World Journal of Gastrointestinal Oncology · doi:10.4251/wjgo.v9.i5.194 · Cited by 66
Kim, S., Kim, T. M., Kim, D., Kim, S., Kim, M., Ahn, Y., Keam, B., & Heo, D. S. (2018) · Cancer Research and Treatment · doi:10.4143/crt.2018.052 · Cited by 66
“The selectivity of capmatinib is >10,000-fold for MET in human kinase assays [14].”
BackgroundLiquid Biopsy in Non-Small Cell Lung Cancer
Molina‐Vila, M. Á., Mayo‐de‐las‐Casas, C., Giménez-Capitán, A. A., Jordana‐Ariza, N., Garzón, M., Balada‐Bel, A., Villatoro, S., Teixidó, C., García‐Peláez, B., Aguado, C., et al. (2016) · Frontiers in Medicine · doi:10.3389/fmed.2016.00069 · Cited by 64
Casolino, R., Beer, P. A., Chakravarty, D., Davis, M. B., Malapelle, U., Mazzarella, L., Normanno, N., Pauli, C., Subbiah, V., Turnbull, C., et al. (2024) · CA A Cancer Journal for Clinicians · doi:10.3322/caac.21825 · Cited by 69
cMET Exon 14 Skipping: From the Structure to the Clinic
Steen, N. V. D., Giovannetti, E., Pauwels, P., Peters, G. J., Hong, D. S., Cappuzzo, F., Hirsch, F. R., & Rolfo, C. D. (2016) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2016.05.005 · Cited by 65
“A splice variant of cMET has also been discovered,(4,5) and in recent years it has been shown that this confers sensitivity to cMET small molecule inhibitors.(6,7) This splice variant is not restricted to NSCLC tumors but has also been detected in gastrointestinal malignancies.”
BackgroundHe, A. R., Cohen, R. B., Denlinger, C. S., Sama, A. R., Birnbaum, A. E., Hwang, J. J., Sato, T., Lewis, N. L., Mynderse, M., Niland, M., et al. (2019) · The Oncologist · doi:10.1634/theoncologist.2018-0411 · Cited by 65
Gastrointestinal malignancies harbor actionable MET exon 14 deletions
Lee, J., Ou, S. I., Lee, J. M., Kim, S. Y., Hong, M., Kim, S. Y., Kang, S. Y., Ahn, S., Kang, S. Y., Lee, S., et al. (2015) · Oncotarget · doi:10.18632/oncotarget.4721 · Cited by 64
Self-citationAnti-c-Met monoclonal antibody ABT-700 breaks oncogene addiction in tumors with MET amplification
Wang, J., Goetsch, L., Tucker, L. A., Zhang, Q. Y., Gonzalez, A., Vaidya, K. S., Oleksijew, A., Boghaert, E. R., Song, M., Sokolova, I., et al. (2016) · BMC Cancer · doi:10.1186/s12885-016-2138-z · Cited by 64
“Recently somatic splice site alterations at MET exon 14 (METex14) that result in exon skipping and MET activation were described in human cancers [27].”
BackgroundKim, E. K., Kim, K., Lee, C. Y., Kim, S., Chang, S. H., Cho, B. C., & Shim, H. S. (2018) · Clinical Lung Cancer · doi:10.1016/j.cllc.2018.10.004 · Cited by 63
Self-citationGlaenzel, U., Jin, Y., Hansen, R., Schroer, K., Rahmanzadeh, G., Pfaar, U., van Lier, J. J., Borell, H., Meissner, A., Camenisch, G., et al. (2020) · Drug Metabolism and Disposition · doi:10.1124/dmd.119.090324 · Cited by 63
“The pathway can also be activated via MET gene amplification, which occurs in about 1%–4% of newly diagnosed cases with epidermal growth factor receptor–wild-type non–small-cell lung cancer (NSCLC) (Cappuzzo et al., 2009; Kawakami et al., 2014; Schildhaus et al., 2015).”
BackgroundInfluentialTherapeutic strategies in METex14 skipping mutated non-small cell lung cancer
Drusbosky, L. M., Dawar, R., Rodríguez, E., & Ikpeazu, C. V. (2021) · Journal of Hematology & Oncology · doi:10.1186/s13045-021-01138-7 · Cited by 62
Heigener, D. F., & Reck, M. (2018) · Recent results in cancer research/Recent Results in Cancer Research · doi:10.1007/978-3-319-91442-8_4 · Cited by 64
Yu, Y., Zhou, J., Li, X., Goto, K., Min, X., Nishino, K., Cui, J., Wu, L., Sakakibara, J., Shu, Y., et al. (2023) · EClinicalMedicine · doi:10.1016/j.eclinm.2023.101952 · Cited by 62
Gow, C., Hsieh, M., Wu, S., & Shih, J. (2016) · Lung Cancer · doi:10.1016/j.lungcan.2016.12.001 · Cited by 63
Pruis, M. A., Geurts-Giele, W. R. R., von der, T. J. H., Meijssen, I. C., Dinjens, W. N. M., Aerts, J. G. J. V., Dingemans, A. C., Lolkema, M. P., Paats, M. S., & Dubbink, H. J. (2019) · Lung Cancer · doi:10.1016/j.lungcan.2019.11.010 · Cited by 62
HSP90 inhibitors in lung cancer: promise still unfulfilled.
Chatterjee, S., Bhattacharya, S., Socinski, M. A., & Burns, T. F. (2016) · PubMed · Cited by 60
Poirot, B., Doucet, L. S., Benhenda, S., Champ, J., Meignin, V., & Lehmann‐Che, J. (2017) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2017.07.026 · Cited by 61
“METex14mutations reported only in patients with lung cancer were extracted from Frampton et al.9 (Supplementary Data), Awad et al.,10 Liu et al.,11 Paik et al.,12 and Tong et al.13 or identified in our laboratory.”
InfluentialDong, H., Li, P., Wu, C., Zhou, X., Lu, H., & Zhou, T. (2016) · Lung Cancer · doi:10.1016/j.lungcan.2016.11.006 · Cited by 64
New Targets in Lung Cancer (Excluding EGFR, ALK, ROS1)
Russo, A., Lopes, A. R., McCusker, M. G., Garrigues, S. G., Ricciardi, G. R. R., Arensmeyer, K. E., Scilla, K. A., Mehra, R., & Rolfo, C. D. (2020) · Current Oncology Reports · doi:10.1007/s11912-020-00909-8 · Cited by 65
Ligand-receptor interaction atlas within and between tumor cells and T cells in lung adenocarcinoma
Chen, Z., Yang, X., Bi, G., Liang, J., Hu, Z., Zhao, M., Li, M., Lu, T., Zheng, Y., Sui, Q., et al. (2020) · International Journal of Biological Sciences · doi:10.7150/ijbs.42080 · Cited by 58
“More recent investigations focusing on MET exon 14 alterations and MET amplification have been notable for meaningful clinical responses to MET inhibitor therapy in a substantial proportion of patients [48, 49].”
BackgroundGuyard, A., Danel, C. J., Théou–Anton, N., Debray, M., Gibault, L., Mordant, P., Castier, Y., Crestani, B., Zalcman, G., Blons, H., et al. (2017) · Respiratory Research · doi:10.1186/s12931-017-0605-y · Cited by 61
“Case reports have demonstrated responses to MET-inhibitors in ADC patients with METex14 alterations [26].”
BackgroundLaguna, J. C., García-Pardo, M., Alessi, J. V., Barrios, C. H., Singh, N., Al-Shamsi, H. O., Loong, H. H.-F., Ferriol, M., Recondo, G., & Mezquita, L. (2024) · Therapeutic Advances in Medical Oncology · doi:10.1177/17588359241231260 · Cited by 60
Advances in the Development of Molecularly Targeted Agents in Non-Small-Cell Lung Cancer
Dolly, S. O., Collins, D. C., Sundar, R., Popat, S., & Yap, T. A. (2017) · Drugs · doi:10.1007/s40265-017-0732-2 · Cited by 59
“More recently, MET exon 14 skipping alterations were identified in approximately 4% of patients with NSCLC [116], which appear to sensitize such patients to bona fide MET inhibitors, such as crizotinib, cabozantinib (Cabometyx ; Ipsen), and capmitinib (INC280; Incyte) [116].”
BackgroundMignard, X., Ruppert, A.-M., Antoine, M., Vasseur, J., Girard, N., Mazières, J., Moro‐Sibilot, D., Fallet, V., Rabbe, N., Thivolet-Béjui, F., et al. (2018) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2018.08.008 · Cited by 58
“As MET amplification and exon 14 mutations are potential targets for TKIs in NSCLCs, and particularly in LSCs, these abnormalities must be diagnosed as efficiently as possible.(4,5) In this study, c-MET IHC could not be considered as a screening test either for MET amplification or MET exon 14 mutations, as sensitivit…”
Combination of HGF/MET-targeting agents and other therapeutic strategies in cancer
Moosavi, F., Giovannetti, E., Peters, G. J., & Firuzi, O. (2021) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2021.103234 · Cited by 58
Li, S. D., Ma, M., Li, H., Waluszko, A., Sidorenko, T., Schadt, E. E., Zhang, D. Y., Chen, R., & Ye, F. (2017) · Genome Medicine · doi:10.1186/s13073-017-0478-1 · Cited by 58
Cortot, A. B., Le, X., Smit, E. F., Viteri, S., Kato, T., Sakai, H., Park, K., Camidge, D. R., Berghoff, K., Vlassak, S., et al. (2022) · Clinical Lung Cancer · doi:10.1016/j.cllc.2022.01.003 · Cited by 57
Hughes, P. E., Rex, K. L., Caenepeel, S. R., Yang, Y., Zhang, Y., Broome, M. A., Kha, H. T., Burgess, T. L., Amore, B. M., Kaplan‐Lefko, P. J., et al. (2016) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-15-0871 · Cited by 56
“More recently, treatment with crizotinib or the investigational selective MET inhibitor INC 280 (capmatinib) demonstrated clinical activity in patients with tumors harboring MET exon 14 splicing alterations (16, 17).”
BackgroundConcordance between Comprehensive Cancer Genome Profiling in Plasma and Tumor Specimens
Müller, J. N., Falk, M., Talwar, J., Neemann, N., Mariotti, E., Bertrand, M., Zacherle, T., Lakis, S., Menon, R., Gloeckner, C., et al. (2017) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2017.07.014 · Cited by 57
Faiella, A., Riccardi, F., Cartenì, G., Chiurazzi, M., & Onofrio, L. (2022) · Journal of Oncology · doi:10.1155/2022/5179182 · Cited by 56
Parizadeh, S. M., Esfehani, R. J., Fazilat‐Panah, D., Hassanian, S. M., Shahidsales, S., Khazaei, M., Parizadeh, S. M. R., Ghayour‐Mobarhan, M., Ferns, G. A., & Avan, A. (2019) · IUBMB Life · doi:10.1002/iub.2063 · Cited by 55
“Deletion of the juxtamembrane domain is responsible for this downregulation delay (30).”
BackgroundMET Exon 14 Alterations in Lung Cancer: Exon Skipping Extends Half-Life
Drilon, A. E. D. C. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-0229 · Cited by 54
“It is important to note that genomic alterations that affect the Y1003 residue such asMETY1003F orMET exon14deletion can result in a similar biology without affecting splicing (5, 7).”
BackgroundInfluentialTowards quantitative and multiplexed in vivo functional cancer genomics
Winters, I. P., Murray, C. W., & Winslow, M. M. (2018) · Nature Reviews Genetics · doi:10.1038/s41576-018-0053-7 · Cited by 54
Clinical feasibility of NGS liquid biopsy analysis in NSCLC patients
Papadopoulou, E., Τσούλος, Ν., Tsantikidi, K., Metaxa-Mariatou, V., Stamou, P. E., Kladi-Skandali, A., Kapeni, E., Tsaousis, G., Pentheroudakis, G. E., Petrakis, D., et al. (2019) · PLoS ONE · doi:10.1371/journal.pone.0226853 · Cited by 55
Chu, Q. S.-C. (2020) · Therapeutic Advances in Medical Oncology · doi:10.1177/1758835919895756 · Cited by 56
Recent Progress in Rare Oncogenic Drivers and Targeted Therapy For Non-Small Cell Lung Cancer
Guo, Y., Cao, R., Zhang, X., Huang, L., Sun, L., Zhao, J., Ma, J., & Han, C. (2019) · OncoTargets and Therapy · doi:10.2147/ott.s230309 · Cited by 54
“These effects activate downstream signaling pathways, including RAS/RAF/ MAPK, PI3K/AKT/mTOR, WNT/β-catenin, and STAT, that play important roles in cell growth, apoptosis, motility, and invasiveness.(56,57) In NSCLC, several mechanisms of MET activation have been identified, including mutation, rearrangement or amplif…”
BackgroundImpaired c-Met Receptor Degradation Mediated by MET Exon 14 Mutations in Non–Small-Cell Lung Cancer
Awad, M. M. (2016) · Journal of Clinical Oncology · doi:10.1200/jco.2015.64.2777 · Cited by 56
Lategahn, J., Keul, M., & Rauh, D. (2017) · Angewandte Chemie International Edition · doi:10.1002/anie.201710398 · Cited by 52
Wu, Y.-L. L. C., Smit, E. F., & Bauer, T. M. (2021) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2021.102173 · Cited by 51
Self-citationVenkataramany, A. S., Schieffer, K. M., Lee, K., Cottrell, C. E., Wang, P. Y., Mardis, E. R., Cripe, T. P., & Chandler, D. S. (2022) · Annals of Oncology · doi:10.1016/j.annonc.2022.03.011 · Cited by 57
Tumor educated platelet: the novel BioSource for cancer detection
Ding, S., Dong, X., & Song, X. (2023) · Cancer Cell International · doi:10.1186/s12935-023-02927-5 · Cited by 53
Pilotto, S., Γκουντάκος, Α., Carbognin, L., Scarpa, A., Tortora, G., & Bria, E. (2017) · Annals of Translational Medicine · doi:10.21037/atm.2016.12.33 · Cited by 50
“Moreover, as described in lung cancer (24), MET exon 14 skipping mutations occur mutually exclusively with other validated drivers, thus supporting its oncogenic implication and defining a distinct molecular subgroup of gastrointestinal malignancies (29).”
BackgroundInfluentialSplice Variants of the RTK Family: Their Role in Tumour Progression and Response to Targeted Therapy
Fayçal, C. A., Hatat, A., Gazzéri, S., & Eymin, B. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18020383 · Cited by 55
“MET Skipping of exon 14 Activation of MET kinase activity Oncogenic transformation [20]”
BackgroundThe METeoric rise of MET in lung cancer
Friedlaender, A., Drilon, A. E. D. C., Banna, G. L., Peters, S., & Addeo, A. (2020) · Cancer · doi:10.1002/cncr.33159 · Cited by 51
“3).(6,11,12) Exon 14 alterations tend to be mutually exclusive with other primary oncogenic drivers except for MET amplifications, copy number variants, and MDM2 amplifications.”
BackgroundBiological therapies in nonsmall cell lung cancer
Zugazagoitia, J., Molina‐Pinelo, S., López‐Ríos, F., & Paz-Ares, L. G. (2017) · European Respiratory Journal · doi:10.1183/13993003.01520-2016 · Cited by 49
Lee, J., Madison, R. W., Classon, A., Gjoerup, O. V., Rosenzweig, M. R., Frampton, G. M., Alexander, B. M., Oxnard, G. R., Venstrom, J. M., Awad, M. M., et al. (2021) · JCO Precision Oncology · doi:10.1200/po.21.00122 · Cited by 49
“This could be due to a number of reasons including (1) for our TTD analysis, seven patients still remained on MET TKI at the time of data cutoff, (2) patients treated in the RW setting likely had worse performance status on average, and (3) differences between TTD and PFS as noted below.”
ResultInfluentialSelf-citationSaffroy, R., Fallet, V., Girard, N., Mazières, J., Moro‐Sibilot, D., Lantuéjoul, S., Rouquette, I., Thivolet-Béjui, F., Vieira, T., Antoine, M., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.16403 · Cited by 48
“In our study, we have constructed a multiplex panel gathering all the gene abnormalities described by Frampton et al. [1].”
InfluentialHave Clinical Trials Properly Assessed c-Met Inhibitors?
Hughes, V. S., & Siemann, D. W. (2017) · Trends in cancer · doi:10.1016/j.trecan.2017.11.009 · Cited by 48
“Exon 14 skipping was not found in female reproductive, colorectal, or pancreatic tumors [7].”
BackgroundEmerging MET tyrosine kinase inhibitors for the treatment of non-small cell lung cancer
Fujino, T., Suda, K., & Mitsudomi, T. (2020) · Expert Opinion on Emerging Drugs · doi:10.1080/14728214.2020.1791821 · Cited by 49
Passaro, A., Attili, I., Rappa, A., Vacirca, D., Ranghiero, A., Fumagalli, C., Guarize, J., Spaggiari, L., de Marinis, F., Barberis, M. C. P., et al. (2021) · Cancers · doi:10.3390/cancers13092172 · Cited by 46
Catenacci, D. V. T., Ang, A. L., Liao, W., Shen, J., O’Day, E., Loberg, R. D., Cecchi, F., Hembrough, T., Ruzzo, A., & Graziano, F. (2016) · Cancer · doi:10.1002/cncr.30437 · Cited by 46
Management of Non-small Cell Lung Cancer Patients with MET Exon 14 Skipping Mutations
Huang, C., Zou, Q., Liu, H., Qiu, B., Li, Q., Lin, Y., & Liang, Y. (2020) · Current Treatment Options in Oncology · doi:10.1007/s11864-020-0723-5 · Cited by 46
Xu, Z., Li, H., Dong, Y., Cheng, P., Luo, F., Fu, S., Gao, M., Kong, L., & Che, N. (2020) · OncoTargets and Therapy · doi:10.2147/ott.s241231 · Cited by 46
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
