NDLI: HGF/c-Met overexpressions, but not met mutation, correlates with progression of non-small cell lung cancer.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gumustekin, Mukaddes Kargi, Aydanur Bulut, Gulay Gozukizil, Aysim Ulukus, Cagnur Oztop, Ilhan Atabey, Nese
Description	Country affiliation: Turkey Author Affiliation: Gumustekin M ( Department of Pharmacology, Dokuz Eylul University Medical School, Inciralti, 35340, Izmir, Turkey.)
Abstract	Hepatocyte Growth Factor (HGF) and its receptor c-Met are suggested to play an important role in progression of solid organ tumors by mediating cell motility, invasion and metastasis. Overexpression of HGF and c-Met have been shown in non-small-cell lung cancer (NSCLC). However, their role in tumor progression is not clearly defined. The aim of this study is to determine the role of HGF/c-Met pathway and its association with invasion related markers and clinicopathologic parameters in NSCLC. Immunohistochemical analysis was performed on 63 paraffin-embedded NSCLC tumor sections. The expressions of invasion related markers such as Matrix Metalloproteinases (MMPs) 2 and 9, Tissue Inhibitor Metalloproteinase (TIMP) 1 and 3 and RhoA were also examined. Co-expression of HGF/c-Met was significantly associated with lymph node invasion and TIMP-3 and RhoA overexpressions. There were positive correlation between TIMP-3 overexpression and advanced stage and negative correlation between RhoA overexpression and survival. DNA sequencing for Met mutations in both nonkinase and tyrosine kinase (TK) domain was established. A single nucleotide polymorphism (SNP) in sema domain and two SNPs in TK domain of c-Met were found. There was no statistically significant correlation between the presence of c-Met alterations and clinicopathologic parameters except shorter survival time in cases with two SNPs in TK domain. These results suggest that HGF/c-Met might exert their effects in tumor progression in association with RhoA and probably with TIMP-3. The blockade of the HGF/c-Met pathway with RhoA and/or TIMP-3 inhibitors may be an effective therapeutic target for NSCLC treatment.
File Format	HTM / HTML
ISSN	12194956
Issue Number	2
Volume Number	18
e-ISSN	15322807
Journal	Pathology & Oncology Research
Language	English
Publisher	Springer
Publisher Date	2012-04-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Subject Keyword	Discipline Oncology Carcinoma, Non-small-cell Lung Genetics Metabolism Mutation Proto-oncogene Proteins C-met Tissue Inhibitor Of Metalloproteinase-3 Rhoa Gtp-binding Protein Adenocarcinoma Mortality Blotting, Western Carcinoma, Large Cell Carcinoma, Squamous Cell Disease Progression Female Humans Immunoenzyme Techniques Lung Neoplasms Male Middle Aged Polymorphism, Single Nucleotide Prognosis Rna, Messenger Real-time Polymerase Chain Reaction Retrospective Studies Reverse Transcriptase Polymerase Chain Reaction Survival Rate Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cancer Research Pathology and Forensic Medicine Oncology

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