PMID- 16050800
OWN - NLM
STAT- MEDLINE
DCOM- 20050927
LR  - 20191109
IS  - 0731-8898 (Print)
IS  - 0731-8898 (Linking)
VI  - 24
IP  - 3
DP  - 2005
TI  - Role of c-MET in upper aerodigestive malignancies--from biology to novel 
      therapies.
PG  - 149-62
AB  - Overactivation and defective downregulation of receptor tyrosine kinase (RTK) 
      pathways have been implicated in human carcinogenesis. RTKs represent an 
      important class of anticancer novel therapeutic target. Some RTKs are known to be 
      protooncogenes that can mediate signal transduction, alteration of reactive 
      oxygen species (ROS), cellular proliferation, cell motility and migration, 
      apoptosis, and survival. c-MET is a unique RTK that regulates a wide variety of 
      cellular functions. c-MET has been shown to be overexpressed or mutated in a 
      variety of human malignancies. Stimulation of c-MET via its natural ligand 
      hepatocyte growth factor/ scatter factor (HGF/SF) leads to a plethora of 
      biological and biochemical effects in the cell. Activation of c-MET signaling can 
      lead to cell motility and scattering, angiogenesis, proliferation, branching 
      morphogenesis, invasion, and eventual metastasis. This review summarizes the 
      structure and functions of c-MET, with particular emphasis on its role in upper 
      aerodigestive malignancies. The unique biological functions altered by c-MET and 
      its mutations are discussed as well. Finally, c-MET, when mutated or 
      overexpressed in malignant cells, serves as an important therapeutic target, and 
      the most recent data with respect to its inhibition are also summarized in this 
      review.
FAU - Dietrich, Sascha
AU  - Dietrich S
AD  - Section of Hematology/Oncology, Department of Medicine, Pritzker School of 
      Medicine, The University of Chicago, Chicago, Illinois 60637, USA.
FAU - Uppalapati, Radha
AU  - Uppalapati R
FAU - Seiwert, Tanguy Y
AU  - Seiwert TY
FAU - Ma, Patrick C
AU  - Ma PC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - J Environ Pathol Toxicol Oncol
JT  - Journal of environmental pathology, toxicology and oncology : official organ of 
      the International Society for Environmental Toxicology and Cancer
JID - 8501420
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
SB  - IM
MH  - Animals
MH  - Carcinoma, Non-Small-Cell Lung/genetics/*metabolism/therapy
MH  - Carcinoma, Small Cell/genetics/*metabolism/therapy
MH  - Carcinoma, Squamous Cell/genetics/*metabolism/therapy
MH  - Disease Models, Animal
MH  - Esophageal Neoplasms/genetics/*metabolism/therapy
MH  - Humans
MH  - Lung Neoplasms/genetics/*metabolism/therapy
MH  - Mice
MH  - Mutation
MH  - Proto-Oncogene Proteins c-met/antagonists & inhibitors/genetics/*metabolism
MH  - Signal Transduction
RF  - 59
EDAT- 2005/07/30 09:00
MHDA- 2005/09/28 09:00
CRDT- 2005/07/30 09:00
PHST- 2005/07/30 09:00 [pubmed]
PHST- 2005/09/28 09:00 [medline]
PHST- 2005/07/30 09:00 [entrez]
AID - 3514f0af2eca0266,5251600349524a03 [pii]
AID - 10.1615/jenvpathtoxoncol.v24.i3.20 [doi]
PST - ppublish
SO  - J Environ Pathol Toxicol Oncol. 2005;24(3):149-62. doi: 
      10.1615/jenvpathtoxoncol.v24.i3.20.