PMID- 26097886
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150623
LR  - 20200930
IS  - 2331-4737 (Print)
IS  - 2331-4737 (Electronic)
IS  - 2331-4737 (Linking)
VI  - 2
IP  - 5
DP  - 2015
TI  - Retrospective Review of MET Gene Mutations.
PG  - 533-41
AB  - C-MET proto-oncogene is a tyrosine kinase situated on chromosome 7. C-MET and its 
      ligand hepatocyte growth factor/scatter factor (HGF/SF) play a role in 
      proliferation, differentiation and organ development. C-MET genetic aberrations 
      are found associated with driving tumorigenesis. In this retrospective study, we 
      reviewed molecular analysis data gathered from a cancer institute during a 
      two-year period (2010-2012). Upon detection of tumors harboring c-MET mutations, 
      we determined the status of the other mutations tested and evaluated c-MET 
      expression by fluorescent in-situ hybridization (FISH). Our search resulted in 
      identification of 134 c-MET mutations, 44% of which had mutations of at least one 
      of the other genes tested. No c-MET expression aberrancy was detected in this 
      subset by FISH. Survival amongst the patients with surgically resected metastatic 
      colorectal cancers (CRC) was slightly better in those with only a c-MET mutation 
      compared to those with no mutation detected, although the difference was not 
      statistically significant. When c-MET inhibition becomes an integrated part of 
      chemotherapy practice, our observed frequency of co-mutations will be an argument 
      for utilizing c-MET targeted treatment in combination with other targeted drugs 
      and therapeutic strategies. Larger studies can aid to further parse out c-MET 
      prognostic and therapeutic significance.
FAU - Zenali, Maryam
AU  - Zenali M
AD  - Department of Pathology and Laboratory Medicine, University of Texas MD Anderson 
      Cancer Center, Houston, Texas.
FAU - deKay, James
AU  - deKay J
AD  - Department of Pathology and Laboratory Medicine, University of Vermont Medical 
      Center, Burlington, Vermont.
FAU - Liu, Zesheng
AU  - Liu Z
AD  - Institute of Personalized Cancer Therapy, University of Texas MD Anderson Cancer 
      Center, Houston, Texas.
FAU - Hamilton, Stanley
AU  - Hamilton S
AD  - Department of Pathology and Laboratory Medicine, University of Texas MD Anderson 
      Cancer Center, Houston, Texas.
FAU - Zuo, Zhuang
AU  - Zuo Z
AD  - Department of Molecular Pathology, University of Texas MD Anderson Cancer Center, 
      Houston, Texas.
FAU - Lu, Xinyan
AU  - Lu X
AD  - Department of Hematopathology, University of Texas MD Anderson Cancer Center, 
      Houston, Texas.
FAU - Bakkar, Rania
AU  - Bakkar R
AD  - Department of Pathology, University of New Mexico, Albuquerque, New Mexico.
FAU - Mills, Gordon
AU  - Mills G
AD  - Institute of Personalized Cancer Therapy, University of Texas MD Anderson Cancer 
      Center, Houston, Texas.
FAU - Broaddus, Russell
AU  - Broaddus R
AD  - Department of Pathology and Laboratory Medicine, University of Texas MD Anderson 
      Cancer Center, Houston, Texas.
LA  - eng
GR  - P50 CA083639/CA/NCI NIH HHS/United States
PT  - Journal Article
DEP - 20150514
PL  - United States
TA  - Oncoscience
JT  - Oncoscience
JID - 101636666
PMC - PMC4468339
OTO - NOTNLM
OT  - C-MET
OT  - FISH
OT  - co-mutations
OT  - targeted therapy
COIS- CONFLICT OF INTEREST The authors have nothing to disclose.
EDAT- 2015/06/23 06:00
MHDA- 2015/06/23 06:01
PMCR- 2015/05/14
CRDT- 2015/06/23 06:00
PHST- 2015/02/18 00:00 [received]
PHST- 2015/05/05 00:00 [accepted]
PHST- 2015/06/23 06:00 [entrez]
PHST- 2015/06/23 06:00 [pubmed]
PHST- 2015/06/23 06:01 [medline]
PHST- 2015/05/14 00:00 [pmc-release]
AID - 161 [pii]
AID - 10.18632/oncoscience.161 [doi]
PST - epublish
SO  - Oncoscience. 2015 May 14;2(5):533-41. doi: 10.18632/oncoscience.161. eCollection 
      2015.