Literature DB >> 23802768

Impact of MET expression on outcome in BRAF(V600E/K) advanced melanoma.

Adrian M Jubb1, Antoni Ribas, Jeffrey A Sosman, Grant A McArthur, Yibing Yan, Sandra Rost, Sherry Zhao, Hartmut Koeppen.   

Abstract

AIMS: Preclinical data suggest that signalling through the HGF-MET pathway may confer resistance to BRAF inhibition in BRAF(V600E/K) melanoma. Therefore, blockade of HGF-MET signalling might be a valid therapeutic strategy, in combination with BRAF inhibition, in BRAF(V600E/K) melanoma. The aim of this study was to investigate the clinical relevance of these observations by evaluating the survival impact of MET expression in patients with BRAF(V600E/K) advanced melanoma treated with vemurafenib. METHODS AND
RESULTS: Formalin-fixed tissue blocks were obtained of tumours from patients enrolled in the BRIM2 (n = 59) and BRIM3 (n = 150) trials of vemurafenib in advanced BRAF(V600E/K) melanoma. Immunohistochemistry for MET (SP44 rabbit monoclonal antibody) was performed with a highly validated assay and clinically validated scoring system. Pretreatment MET expression was frequent at the ≥1 + cutoff (BRIM3, 31%; BRIM2, 49%), but relatively infrequent at the ≥2 + cutoff (BRIM3, 9%; BRIM2, 19%). Retrospective subset analyses showed that, irrespective of the cutoff used or the treatment arm, MET expression did not show prognostic significance, in terms of objective response rate, progression-free survival, or overall survival.
CONCLUSIONS: MET is expressed in a proportion of BRAF(V600E/K) advanced melanomas. Further analyses on appropriately powered subsets are needed to determine the prognostic and predictive significance of MET in vemurafenib-treated melanoma.
© 2013 John Wiley & Sons Ltd.

Entities:  

Keywords:  BRAF; HGF; MET; SP44; melanoma

Mesh:

Substances:

Year:  2013        PMID: 23802768     DOI: 10.1111/his.12169

Source DB:  PubMed          Journal:  Histopathology        ISSN: 0309-0167            Impact factor:   5.087


  6 in total

Review 1.  Resistance to Raf inhibition in cancer.

Authors:  H Eirik Haarberg; Keiran S M Smalley
Journal:  Drug Discov Today Technol       Date:  2014-03

2.  Hypoxia-Driven Mechanism of Vemurafenib Resistance in Melanoma.

Authors:  Yong Qin; Jason Roszik; Chandrani Chattopadhyay; Yuuri Hashimoto; Chengwen Liu; Zachary A Cooper; Jennifer A Wargo; Patrick Hwu; Suhendan Ekmekcioglu; Elizabeth A Grimm
Journal:  Mol Cancer Ther       Date:  2016-07-25       Impact factor: 6.261

3.  Exogenous growth factors bFGF, EGF and HGF do not influence viability and phenotype of V600EBRAF melanoma cells and their response to vemurafenib and trametinib in vitro.

Authors:  Izabela Zalesna; Marta Osrodek; Mariusz L Hartman; Michal Rozanski; Malgorzata Sztiller-Sikorska; Karolina Niewinna; Dariusz Nejc; Malgorzata Czyz
Journal:  PLoS One       Date:  2017-08-22       Impact factor: 3.240

Review 4.  HGF/c-MET Signaling in Melanocytes and Melanoma.

Authors:  Malgorzata Czyz
Journal:  Int J Mol Sci       Date:  2018-12-03       Impact factor: 5.923

5.  Hepatocyte growth factor renders BRAF mutant human melanoma cell lines resistant to PLX4032 by downregulating the pro-apoptotic BH3-only proteins PUMA and BIM.

Authors:  Leona Rohrbeck; Jia-Nan Gong; Erinna F Lee; Andrew J Kueh; Andreas Behren; Lin Tai; Guillaume Lessene; David C S Huang; Walter D Fairlie; Andreas Strasser; Marco J Herold
Journal:  Cell Death Differ       Date:  2016-09-30       Impact factor: 15.828

6.  Evaluation of stromal HGF immunoreactivity as a biomarker for melanoma response to RAF inhibitors.

Authors:  Cecilia Lezcano; Chung-Wei Lee; Allison R Larson; Alexander M Menzies; Richard F Kefford; John F Thompson; Martin C Mihm; Shuji Ogino; Georgina V Long; Richard A Scolyer; George F Murphy
Journal:  Mod Pathol       Date:  2014-01-17       Impact factor: 7.842

  6 in total

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