c-MET/Phospho-MET Protein Expression and MET Gene Copy Number in Non-small Cell Lung Carcinomas

Tsuta, Koji; Kozu, Yoshiki; Mimae, Takahiro; Yoshida, Akihiko; Kohno, Takashi; Sekine, Ikuo; Tamura, Tomohide; Asamura, Hisao; Furuta, Koh; Tsuda, Hitoshi

doi:10.1097/jto.0b013e318241655f

Cited by 134 publications

(117 citation statements)

References 32 publications

(49 reference statements)

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“…As a result, MET protein overexpression in unselected NSCLC cases has been reported to range from 20% to 70%. 137,138 An MA has found that MET expression by IHC in NSCLC is a negative prognostic factor in patients with surgically resected NSCLC. 107 A frequently used commercially available antibody, particularly in clinical trials, is the CONFIRM anti-total MET (SP44) rabbit monoclonal primary antibody (Ventana Medical Systems, Tucson, Arizona) directed against a membranous and cytoplasmic epitope of MET.…”

Section: Lung Cancer Molecular Testing Guideline Updatementioning

confidence: 99%

Analytical Validation of BRAF Mutation Testing from Circulating Free DNA Using the Amplification Refractory Mutation Testing System

Aung

Donald

Ellison

et al. 2014

The Journal of Molecular Diagnostics

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Context: In 2013, an evidence-based guideline was published by the College of American Pathologists, the International Association for the Study of Lung Cancer, and the Association for Molecular Pathology to set standards for the molecular analysis of lung cancers to guide treatment decisions with targeted inhibitors. New evidence has prompted an evaluation of additional laboratory technologies, targetable genes, patient populations, and tumor types for testing. Objective: To systematically review and update the 2013 guideline to affirm its validity; to assess the evidence of new genetic discoveries, technologies, and therapies; and to issue an evidence-based update. Design: The College of American Pathologists, the International Association for the Study of Lung Cancer, and the Association for Molecular Pathology convened an expert panel to develop an evidence-based guideline to help define the key questions and literature search terms, review abstracts and full articles, and draft recommendations. Results: Eighteen new recommendations were drafted. The panel also updated 3 recommendations from the 2013 guideline. Conclusions: The 2013 guideline was largely reaffirmed with updated recommendations to allow testing of cytology samples, require improved assay sensitivity, and recommend against the use of

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Section: Lung Cancer Molecular Testing Guideline Updatementioning

confidence: 99%

Analytical Validation of BRAF Mutation Testing from Circulating Free DNA Using the Amplification Refractory Mutation Testing System

Aung

Donald

Ellison

et al. 2014

The Journal of Molecular Diagnostics

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“…Moreover, it is notable that all three of these mechanisms of MET/MET dysregulation have been documented in non-small cell lung cancer (NSCLC; refs. [19][20][21][22]. Early studies established that MET can be overexpressed or activated [as measured by phosphorylation of the catalytic domain as well as juxtamembrane (JM) domain], or the gene mutated (in the semaphorin or JM domains) and/or amplified in lung cancer.…”

Section: Hfg/met In Lung Cancermentioning

confidence: 99%

MET in Lung Cancer: Biomarker Selection Based on Scientific Rationale

Salgia

2017

Molecular Cancer Therapeutics

130

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MET or hepatocyte growth factor (HGF) receptor pathway signaling mediates wound healing and hepatic regeneration, with pivotal roles in embryonic, neuronal, and muscle development. However, dysregulation of MET signaling mediates proliferation, apoptosis, and migration and is implicated in a number of malignancies. In non-small cell lung cancer (NSCLC), aberrant MET signaling can occur through a number of mechanisms that collectively represent a significant proportion of patients. These include MET or HGF protein overexpression, MET gene amplification, MET gene mutation or fusion/rearrangement, or aberrations in downstream signaling or regulatory components. Responses to MET tyrosine kinase inhibitors have been documented in clinical trials in patients with MET-amplified or METoverexpressing NSCLC, and case studies or case series have shown that MET mutation/deletion is a biomarker that is also predictive of response to these agents. However, other recent clinical data have highlighted an urgent need to elucidate optimal biomarkers based on genetic and/or protein diagnostics to correctly identify patients most likely to benefit in ongoing clinical trials of an array of MET-targeted therapies of differing class. The latest advances in the development of MET biomarkers in NSCLC have been reviewed, toward establishing appropriate MET biomarker selection based on a scientific rationale. Mol Cancer Ther; 16(4); 555-65.Ó2017 AACR.

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“…26 The oncogenic dysregulation of the HGF/c-MET pathway has been implicated in a wide range of human epithelial cancers including liver, lung, colorectal, breast, pancreatic, ovarian, prostate, hepatic, and gastric cancers. [27][28][29][30][31] This pathway results in cell survival and migration and tumor development and progression. 27,32 c-Met over-activation occurs via several molecular mechanisms, including gene amplification, 31 overexpression, 33 mutations, 34 or RTK transactivation or changes in ligandinduced autocrine or paracrine signaling; 35 all of them have been reported in several human tumor types.…”

Section: Aberrant C-met Signaling In Crcmentioning

confidence: 99%

The c-Met receptor: Implication for targeted therapies in colorectal cancer

et al. 2017

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c-Met (mesenchymal-epithelial transition factor) is a tyrosine kinase receptor activated by hepatocyte growth factor and regulates multiple biological processes, such as cell scattering, survival, and proliferation. Aberrant c-Met signaling has been implicated in a variety of cancer types, including colorectal cancer. c-Met is genetically altered through various mechanisms that is associated with colorectal cancer progression and metastasis. Especially, in colorectal cancer, preclinical evidence for the aberrant activation of the c-Met signaling exists. Accordingly, molecular targeting of c-Met receptor could be a promising strategy, in the treatment of colorectal cancer patients. Recently, it was also shown that crosstalk between c-Met and other cell surface receptors attributes to tumorigenesis and development of therapeutic resistance. Characterization of the molecular mechanisms through which c-Met crosstalks with other receptors in favor of tumor formation and progression remains to explore. This review will describe the mechanisms of aberrant c-Met signaling in colorectal cancer and discuss on additional roles for c-Met receptor through crosstalk with other tyrosine kinase receptors and cell surface proteins in colorectal cancer. Novel therapeutic approaches for c-Met pathway targeting will also be discussed.

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c-MET/Phospho-MET Protein Expression and MET Gene Copy Number in Non-small Cell Lung Carcinomas

Abstract: c-MET/phospho-MET expression and MET BISH positivity differed according to histological type. Among ADCs, c-MET expression and MET BISH positivity were more common in poorly differentiated cases. MET BISH positivity was an independent prognostic factor in nonsquamous NSCLCs.

Cited by 134 publications

References 32 publications

Analytical Validation of BRAF Mutation Testing from Circulating Free DNA Using the Amplification Refractory Mutation Testing System

Analytical Validation of BRAF Mutation Testing from Circulating Free DNA Using the Amplification Refractory Mutation Testing System

MET in Lung Cancer: Biomarker Selection Based on Scientific Rationale

The c-Met receptor: Implication for targeted therapies in colorectal cancer

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