Activation of MET via diverse exon 14 splicing alterations occurs in multiple tumor types and confers clinical sensitivity to MET inhibitors.

By G. Frampton, Siraj M. Ali, M. Rosenzweig, J. Chmielecki, Xinyuan Lu, T. Bauer, M. Akimov, J. Bufill, Carrie Lee, D. Jentz and 28 more. Cancer Discovery, 2015

714 citations recorded by the source corpus.

Subfields: Hepatology, Pulmonary and Respiratory Medicine, Surgery

View Paper: https://www.semanticscholar.org/paper/0b35633dd8a7619f6dd3d972ec32e9a8ac5080ba

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Hepatology

1. Lewis R. Roberts
2. J. D. Yang

In Pulmonary and Respiratory Medicine

1. Mark A. Rubin
2. J. Baselga
3. Marc Ladanyi
4. Gregory Riely
5. J. Luketich
6. Christine Lovly
7. Z. Du
8. M. Davis

In Surgery

1. A. Gimenez-Roqueplo
2. Karel Pacak
3. J. Luketich

Citations in the corpus

• Comprehensive Analysis of Alternative Splicing Across Tumors from 8,705 Patients (2018, background): “A prominent example for cis-acting mutations is found in the splice junctions ofMET leading to skipping of exon 14, resulting in activation of MET but also providing specific sensitivity to MET inhibitors (Frampton et al., 2015; Paik et al., 2015).”
• OncoKB: A Precision Oncology Knowledge Base (2017, background): “However, durable complete or partial responses to crizotinib and cabozantinib in patients with MET exon 14 altered lung cancers have been reported 15,19 .”