PMID- 10626794
OWN - NLM
STAT- MEDLINE
DCOM- 20000124
LR  - 20120605
IS  - 0008-5472 (Print)
IS  - 0008-5472 (Linking)
VI  - 59
IP  - 24
DP  - 1999 Dec 15
TI  - Deletion of the carboxyl-terminal exons of K-sam/FGFR2 by short homology-mediated
      recombination, generating preferential expression of specific messenger RNAs.
PG  - 6080-6
AB  - The K-sam gene was first identified as an amplified gene from human gastric
      cancer cell line KATOIII, and its product is identical to fibroblast growth
      factor receptor 2. The K-sam gene is located on human chromosome 10q26 and is
      preferentially amplified in the poorly differentiated types, especially in the
      scirrhous type, of gastric cancers. During the course of studies on the
      structural characterization of the amplification units, we found that the
      carboxyl-terminal exons of K-sam were deleted in three of four of the scirrhous
      type of gastric cancer cell lines. These deletions generate preferential
      expression of mRNAs encoding K-sam proteins lacking the carboxyl-terminal region 
      containing the tyrosine residues at positions 780, 784, and 813. The
      carboxyl-terminal region has been reported to have a sequence required for the
      inhibition of NIH3T3 transformation, indicating that cells with amplification of 
      the truncated K-sam gene have a growth advantage during the carcinogenic process 
      for the scirrhous type of gastric cancers. This is the first report showing the
      deletion of the carboxyl-terminal exons of the receptor-type of the protein
      tyrosine kinase gene. Sequence analysis of the DNA sequences surrounding the
      deletion junctions shows the presence of unique sequences and indicates the
      involvement of short homology-mediated recombination in the generation of these
      deletions.
FAU - Ueda, T
AU  - Ueda T
AD  - Genetics Division, National Cancer Center Research Institute, Tokyo, Japan.
FAU - Sasaki, H
AU  - Sasaki H
FAU - Kuwahara, Y
AU  - Kuwahara Y
FAU - Nezu, M
AU  - Nezu M
FAU - Shibuya, T
AU  - Shibuya T
FAU - Sakamoto, H
AU  - Sakamoto H
FAU - Ishii, H
AU  - Ishii H
FAU - Yanagihara, K
AU  - Yanagihara K
FAU - Mafune, K
AU  - Mafune K
FAU - Makuuchi, M
AU  - Makuuchi M
FAU - Terada, M
AU  - Terada M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Fibroblast Growth Factor)
RN  - EC 2.7.10.1 (FGFR2 protein, human)
RN  - EC 2.7.10.1 (Fgfr2 protein, mouse)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 2)
SB  - IM
MH  - 3T3 Cells
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Cell Line
MH  - Exons
MH  - *Gene Deletion
MH  - Humans
MH  - Mice
MH  - Molecular Sequence Data
MH  - RNA, Messenger/biosynthesis
MH  - Receptor Protein-Tyrosine Kinases/biosynthesis/*genetics
MH  - Receptor, Fibroblast Growth Factor, Type 2
MH  - Receptors, Fibroblast Growth Factor/biosynthesis/*genetics
MH  - Recombination, Genetic
MH  - Sequence Analysis
MH  - Sequence Homology, Nucleic Acid
MH  - Tumor Cells, Cultured
EDAT- 2000/01/08 00:00
MHDA- 2000/01/08 00:01
CRDT- 2000/01/08 00:00
PHST- 2000/01/08 00:00 [pubmed]
PHST- 2000/01/08 00:01 [medline]
PHST- 2000/01/08 00:00 [entrez]
PST - ppublish
SO  - Cancer Res. 1999 Dec 15;59(24):6080-6.