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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“…in clinical trials for NSCLC patients with this mutation [51–58]; (i) It represents a targetable alteration in cancer, particularly in NSCLC [44,47,48]; (ii) it occurs in 2-4% of NSCLC and, with less frequency, in gastrointestinal carcinomas, gliomas, sarcomas, and cancers of unknown…”
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“Furthermore, in addition to gene amplification or protein overexpression, enhanced signalling of the MET pathway can be induced by mutations resulting in exon 14 skipping [7].”
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“Individuals whose tumors harbor a high MET gene copy number and/or ampli fi cation and/or MET ex14 skipping mutations have demonstrated therapeutic response to tyrosine kinase inhibitors such as crizotinib 6,7,9,15,16 and cabozantinib.”
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“Unlike the other rare mutations described above, which are mainly present in nonsquamous histology, MET mutations are harbored in 2% of squamous cell carcinoma histology [74,75].”
BackgroundhnRNPU-mediated pathogenic alternative splicing drives gastric cancer progression
Jin, G., Song, Y., Fang, S., Yan, M., Yang, Z., Shao, Y. W., Zhao, K., Liu, M., Wang, Z., Guo, Z., et al. (2025) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-024-03264-9 · Cited by 10
“Exon 14 splice site alterations in MET have been identified as drivers of tumorigenesis [43].”
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“METex14 is observed in about 3% of NSCLC cases [19–21], and while deletions of this exon can be the result of genomic deletion events, they are more commonly caused by mutations in splicing donor and acceptor sites or within the polypyrimidine tract [21–23].”
RNA splicing: Novel star in pulmonary diseases with a treatment perspective
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“Cohort studies also reported distinct mutation patterns coincident with driver mutations suggesting distinct molecular subtypes in NSCLC (23).”
BackgroundOkano, S., Yamashiro, Y., Onagi, H., Sasa, K., Hayashi, T., Takahashi, M., Sugimoto, K., Sakamoto, K., Yao, T., & Saito, T. (2023) · Histopathology · doi:10.1111/his.15015 · Cited by 10
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“Finally, another two prospective studies screened cancer patients for a specific genomic aberration, IDH mutations [24], and MET ex14 alterations [25].”
BackgroundMethodBoldig, C. M., Boldig, K., Mokhtari, S., & Etame, A. B. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25136961 · Cited by 11
Double Trouble: A Case Series on Concomitant Genetic Aberrations in NSCLC
Steen, N. V. D., Mentens, Y., Ramael, M., León, L. G., Germonpré, P. R., Ferri, J., Gandara, D. R., Giovannetti, E., Peters, G. J., Pauwels, P., et al. (2017) · Clinical Lung Cancer · doi:10.1016/j.cllc.2017.06.010 · Cited by 10
“Several case reports have been published on concomitant cMET amplification and exon 14 skipping.(4,40) Based on the read counts in sequencing, selective amplification of the mutant cMET allele occurs.”
BackgroundMethodMolecular characteristics of multifocal brain histiocytic sarcoma
Marguet, F., Piton, N., Adle‐Biassette, H., Renaud, F., Bohers, É., Boyer, T., Zaréa, A., Derrey, S., Sabourin, J., & Laquerrière, A. (2018) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12490 · Cited by 10
Lung cancer histology-driven strategic therapeutic approaches
Galli, G., & Rossi, G. (2020) · Shanghai Chest · doi:10.21037/shc.2020.01.03 · Cited by 11
“A significantly higher rate of c-MET skipping mutations in exon 14 and MET amplification have been reported in this rare histology (41,42).”
BackgroundImmunotherapy in oncogene addicted non-small cell lung cancer
McLean, L. S., Leal, J. L., Solomon, B., & John, T. (2021) · Translational Lung Cancer Research · doi:10.21037/tlcr-20-772 · Cited by 11
Yao, H., Tong, X., & Wang, M. (2021) · Therapeutic Advances in Medical Oncology · doi:10.1177/17588359211006957 · Cited by 10
Song, Y., Li, G., Ju, K., Ran, W., Zhao, H., Liu, X., Hou, M., He, Y., Chen, Y., Zang, G., et al. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.755031 · Cited by 10
“Usually, MET exon 14 skipping is mutually exclusive with other oncogenic driver genes, such as EGFR (19).”
BackgroundMET Exon 14 Skipping Mutations
Davies, K. D., Ritterhouse, L. L., Snow, A. N., & Sidiropoulos, N. (2022) · Journal of Molecular Diagnostics · doi:10.1016/j.jmoldx.2022.04.005 · Cited by 10
Targeting Molecular Alterations in Non-Small-Cell Lung Cancer: What’s Next?
Castro, R. L., García-Peña, T., Mielgo-Rubio, X., Riudavets, M., Teixidó, C., Vilariño, N., Couñago, F., & Mezquita, L. (2022) · Personalized Medicine · doi:10.2217/pme-2021-0059 · Cited by 10
MET alterations in advanced non-small cell lung cancer
Chagas, G. C. L., Rangel, A. R., & Osta, B. E. E. (2024) · Current Problems in Cancer · doi:10.1016/j.currproblcancer.2024.101075 · Cited by 9
The MET Oncogene: An Update on Targeting Strategies
Gallo, S., Folco, C. B., & Crepaldi, T. (2024) · Pharmaceuticals · doi:10.3390/ph17111473 · Cited by 9
“…lung cancers, including lung adenocarcinomas (approximately 3%), lung squamous carcinomas (around 5%), and a substantial percentage of highly aggressive and chemoresistant lung sarcomatoid tumors (20-30%), a rare but notable subset (constituting approximately 1% of all lung malignancies) [37–40].”
Loss of DDX24 inhibits lung cancer progression by stimulating IKBKG splicing-mediated autophagy
Sun, S., Jing, X., Tong, G., Chen, C., Xie, S., Wang, C., Chen, D., Zhao, J., Qi, Y., Zhang, W., et al. (2025) · Theranostics · doi:10.7150/thno.102425 · Cited by 9
“For instance, in lung cancer, frequent mutations near the 5' and 3' splice sites of MET lead to exon 14 skipping, disrupting METΔ14 binding to CBL, thereby promoting MET protein stability and ultimately contributing to tumorigenesis [18, 19].”
L’épissage des ARN pré-messagers : quand le splicéosome perd pied
Dujardin, G., Daguenet, É., Bernard, D. G., Flodrops, M., Durand, S., Chauveau, A., Khoury, F. E., Jossic-Corcos, C. L., & Corcos, L. (2016) · médecine/sciences · doi:10.1051/medsci/20163212014 · Cited by 9
“Cependant, les sites d’épissage de l’exon 14 de l’oncogène MET sont souvent mutés dans les adénocarcinomes du poumon (3 %), conduisant à une exclusion de cet exon dans l’ARNm (Figure 4C) [21].”
Progress on treatment of MET signaling pathway in non-small cell lung cancer
Yu, X., Yu, S., & Fan, Y. (2020) · International Journal of Clinical Oncology · doi:10.1007/s10147-020-01702-0 · Cited by 9
Recurrent splice site mutations affect key diffuse large B-cell lymphoma genes
Andrades, Á., Álvarez-Pérez, J. C., Patiño-Mercau, J. R., Cuadros, M., Baliñas-Gavira, C., & Medina, P. P. (2022) · Blood · doi:10.1182/blood.2021011708 · Cited by 9
Fischer, A., Bankel, L., Hiltbrunner, S., Rechsteiner, M., Rüschoff, J. H., Rushing, E. J., Britschgi, C., & Fontecedro, A. C. (2022) · Targeted Oncology · doi:10.1007/s11523-022-00918-6 · Cited by 9
“However, several studies, including one large NGS-based study [11], reported that MET exon 14 skipping alterations are mutually exclusive with other oncogenic mutations, except for MET amplification and MDM2 amplification [11, 12, 40].”
BackgroundLandscape of the clinical development of China innovative anti-lung cancer drugs
Shi, Y. (2022) · Cancer Pathogenesis and Therapy · doi:10.1016/j.cpt.2022.10.003 · Cited by 11
Acquired EGFR Mutation as the Potential Resistance Driver to Crizotinib in a MET-Mutated Tumor
Benderra, M., Aspeslagh, S., Postel-Vinay, S. C., Bigot, L., de Baère, T., Loriot, Y., Lacroix, L., Massard, C., Vassal, G., André, F., et al. (2015) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2015.08.001 · Cited by 9
“MET exon14 alterations (4% of adenocarcinomas of the lung(5)) lead to crizotinib sensitivity.(6)”
BackgroundInhibition du récepteur MET : un espoir dans la lutte contre les résistances aux thérapies ciblées ?
Hochart, A., Leblond, P., Bourhis, X. L., Meignan, S., & Tulasne, D. (2016) · Bulletin du Cancer · doi:10.1016/j.bulcan.2016.10.014 · Cited by 9
Lapère, C., Cortot, A. B., Grégoire, V., Cockenpot, V., Tulasne, D., & Copin, M. (2017) · The American Journal of Surgical Pathology · doi:10.1097/pas.0000000000000810 · Cited by 9
An update on biomarkers for kinase inhibitor response in non-small-cell lung cancer
Ku, B. M., Sun, J., Lee, S.-H., Ahn, J. S., Park, K., & Ahn, M. (2017) · Expert Review of Molecular Diagnostics · doi:10.1080/14737159.2017.1372196 · Cited by 10
“capmatinib was reported in patients with advanced lung cancers with MET exon 14 alterations, prompting drug development focused on MET exon 14 alterations [67,69].”
BackgroundTan, X., Dai, L., Wang, Y., Liang, G., Yang, N., & Chen, M. (2017) · Medicine · doi:10.1097/md.0000000000008744 · Cited by 9
Narrative review: mesenchymal-epithelial transition inhibitors—meeting their target
Safi, D., Hejleh, T. A., & Furqan, M. (2021) · Translational Lung Cancer Research · doi:10.21037/tlcr-20-588 · Cited by 9
Deveaux, A. E., Allen, T. A., Abo, M. A., Qin, X., Zhang, D., Patierno, B. M., Gu, L., Gray, J. E., Pecot, C. V., Dressman, H. K., et al. (2021) · Lung Cancer · doi:10.1016/j.lungcan.2021.01.015 · Cited by 9
“Inhibition of MET in the presence of either MET exon 14 splice site alterations or MET amplification is an emerging therapeutic option for NSCLC (53).”
BackgroundFarooq, H., Bien, H., Chang, V. T.-S., Becker, D. J., Park, Y.-H., & Bates, S. E. (2022) · Seminars in Oncology · doi:10.1053/j.seminoncol.2022.06.008 · Cited by 9
MET in the Driver's Seat: Exon 14 Skipping Mutations as Actionable Targets in Lung Cancer
Sattler, M., & Salgia, R. (2016) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2016.07.003 · Cited by 9
“in three METex14-positive patients.(8,11) Larger clinical trials focused on METex14 alterations are expected to give a much clearer picture of the true response in a bigger cohort.”
BackgroundResultSelf-citationTargeting MET Exon 14 Skipping Alterations: Has Lung Cancer MET Its Match?
Yap, T. A., & Popat, S. (2016) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2016.10.019 · Cited by 9
Shabana, S. M., Neamatallah, M., Said, M. A., Othman, A. I., Ammar, O. A.-A., Amer, M. A., & El-Missiry, M. A. (2024) · Revista Brasileira de Farmacognosia · doi:10.1007/s43450-024-00538-3 · Cited by 8
“Inhibition of c-MET expression has shown promising results in the inhibition of cancer cell growth (Frampton et al. 2015).”
Felip, E., Metro, G., Tan, D. S.-W., Wolf, J., Mark, M. T., Boyer, M. J., Hughes, B. G. M., Bearz, A., Moro‐Sibilot, D., Le, X., et al. (2024) · Lung Cancer · doi:10.1016/j.lungcan.2024.107820 · Cited by 8
Rivas, S., Sepúlveda, R. V., Tapia, I., Estay, C., Soto, V. H., Blanco, A., González, E., & Armisén, R. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252413715 · Cited by 8
Advances in clinical research of MET exon 14 skipping mutations in non-small cell lung cancer
Wang, M., Zhang, S., Yi, D., Ou, Y., Xie, S., Zeng, C., Qin, X., Zhao, L., Wang, Z., Kong, F., et al. (2025) · Journal of Cancer Research and Clinical Oncology · doi:10.1007/s00432-025-06115-y · Cited by 8
“…drugs, METex14 patients show remarkable response rates to MET-targeting tyrosine kinase inhibitors (MET-TKIs) and become the target of personalized therapy (Tong et al. 2016), showing a high potential in the treatment of lung cancer (Cancer Genome Atlas Research N 2014; Frampton et al. 2015).”
The actionable transcriptome: a framework for incorporating RNA sequencing into precision oncology
Johnson, A., Shen, Y., Zheng, X., Su, F., Zeng, J., Uzunparmak, B., Breuer, E.-K. Y., Holla, V. R., Kahle, M., Kim, S.-H., et al. (2026) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-025-01110-1 · Cited by 12
“For example, MET exon 14-skipping mutations confer constitutive activity to the receptor tyrosine kinase MET, which drives oncogenic processes such as cell survival and proliferation 127 .”
Self-citationDeng, F., Ma, W., & Wei, S. (2026) · Cancers · doi:10.3390/cancers18020207 · Cited by 8
“[90].”
The contributions of extrachromosomal DNA elements in neoplasm progression.
Hong, J., Zheng, S., & Jiang, D. (2021) · PubMed Central · Cited by 8
Liu, Z., Xiao, Y., Liu, X., Li, Q., Liu, T., Zhu, F., Wu, G., & Zhang, L. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.755893 · Cited by 8
“There are some published cases showing favorable response with targeting RAS/MAPK pathway by trametinib (MEK1/2 inhibitor) (5), crizotinib (MET and ALK inhibitor) (11), and vemurafenib (BRAF inhibitor) (12).”
BackgroundWeng, Y., Qian, H., Hong, L., Zhao, S., Deng, X., & Shen, B. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2022.1089008 · Cited by 8
Advances in Non-Small Cell Lung Cancer (NSCLC) Treatment—A Paradigm Shift in Oncology
Ali, A. (2024) · Pharmaceuticals · doi:10.3390/ph17020246 · Cited by 8
“…against the diverse genomic landscape in NSCLC include anaplastic lymphoma kinase (ALK) inhibitors for gene rearrangements [2] and mutations in MET [3], ROS1 [4], BRAF [5] and KRAS [6], which have led to the development of targeted inhibitors, including crizotinib, alectinib, entrectinib,…”
BackgroundRecording and classifying MET receptor mutations in cancers
Guérin, C., & Tulasne, D. (2024) · eLife · doi:10.7554/elife.92762 · Cited by 8
“The vast majority of MET mutations recorded in lung cancer, in contrast to renal cancer, lead to exon 14 skipping: about 160 different mutations having been recorded (; Ma et al., 2003 ; Schrock et al., 2016 ; Frampton et al., 2015 ; Lee et al., 2017 ).”
BackgroundInfluentialYang, M., Zheng, G., Chen, F., Tang, H., Liu, Y., Gao, X., Huang, Y., Lv, Z., Li, B., Yang, M., et al. (2025) · BMC Cancer · doi:10.1186/s12885-024-13410-3 · Cited by 8
“Only one patient harbored a MET frameshift loss, which was distinct from the typical MET exon 14 skipping mutation [50, 51].”
Synchronous primary lung adenocarcinomas harboring distinct MET Exon 14 splice site mutations
Wang, S. X. Y., Lei, L., Guo, H. H., Shrager, J. B., Kunder, C. A., & Neal, J. W. (2018) · Lung Cancer · doi:10.1016/j.lungcan.2018.06.019 · Cited by 8
Giménez‐Xavier, P., Pros, E., Aza, A., Morán, S., Tonda, R., Esteve‐Codina, A., Dabad, M., & Sánchez‐Céspedes, M. (2018) · Oncotarget · doi:10.18632/oncotarget.25862 · Cited by 8
Wang, F., Lu, J., Wu, X., Feng, Y., Shao, Q., An, X., & Wang, H.-Y. (2019) · Cancer Management and Research · doi:10.2147/cmar.s200263 · Cited by 8
“More recent studes have focused on MET mutations and amplifications for favorable clinical responses to METinhibitor therapy.(6,7) In addition, antibodies targeting PD1 have shown unprecedented durable clinical responses in lung cancer.”
BackgroundShimokawa, M., Nosaki, K., Seto, T., Ohashi, K., Morise, M., Horinouchi, H., Sakakibara, J., Murakami, H., Yano, S., Satouchi, M., et al. (2020) · Trials · doi:10.1186/s13063-020-4221-7 · Cited by 8
Oncogenic Genetic Alterations in Non-Small-Cell Lung Cancer (NSCLC) in Southwestern China
Ma, Y., Li, Q., Du, Y., Chen, W., Zhao, G., Liu, X., Li, H., Liu, J., Shen, Z., Ma, L., et al. (2020) · Cancer Management and Research · doi:10.2147/cmar.s266069 · Cited by 8
Piton, N., Lanic, M., Marguet, F., Lamy, A., Blanchard, F., Guisier, F., Viennot, M., Salaün, M., Thiberville, L., Jardin, F., et al. (2021) · Laboratory Investigation · doi:10.1038/s41374-021-00536-2 · Cited by 8
“This figure is adapted from [34] and [50].”
BackgroundUntangling the KRAS mutated lung cancer subsets and its therapeutic implications
Kulshrestha, R., Kumar, P., Singh, A., Nupur, K., Spalgias, S., Mrigpuri, P., & Rajkumar (2021) · Molecular Biomedicine · doi:10.1186/s43556-021-00061-0 · Cited by 8
Claerhout, S., Lehnert, S., Borght, S. V., Spans, L., Dooms, C., Wauters, E., Vansteenkiste, J., Weynand, B., Deraedt, K., Bourgain, C., et al. (2022) · Lung Cancer · doi:10.1016/j.lungcan.2022.02.013 · Cited by 8
Saigí, M., Carcereny, E., Morán, T., Cucurull, M., Doménech, M., Hernández, A., Martínez‐Cardús, A., Pros, E., & Sánchez‐Céspedes, M. (2022) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2022.102430 · Cited by 8
Comprehensive analysis of MET mutations in NSCLC patients in a real-world setting
Ai, X., Yu, Y., Zhao, J., Sheng, W., Bai, J., Fan, Z., Liu, X., Ji, W., Chen, R., & Lü, S. (2022) · Therapeutic Advances in Medical Oncology · doi:10.1177/17588359221112474 · Cited by 8
Das, R., Jakubowski, M. A., Spildener, J., & Cheng, Y. (2022) · Cancers · doi:10.3390/cancers14194814 · Cited by 8
“Among them, METex14 is the most widely reported, 4–40% of which can occur concurrently with MET amplification [3,14,15].”
BackgroundFrom targeted therapy to a novel way: Immunogenic cell death in lung cancer
Xu, J., Xiong, Y., Xu, Z., Xing, H., Zhou, L., & Zhang, X. (2022) · Frontiers in Medicine · doi:10.3389/fmed.2022.1102550 · Cited by 10
Wolf, J., Souquet, P.-J., Goto, K., Cortot, A. B., Baik, C. S., Heist, R. S., Kim, T. M., Han, J., Neal, J. W., Mansfield, A. S., et al. (2023) · Clinical Lung Cancer · doi:10.1016/j.cllc.2023.08.011 · Cited by 8
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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