PMID- 10797290
OWN - NLM
STAT- MEDLINE
DCOM- 20000608
LR  - 20211203
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 86
IP  - 5
DP  - 2000 Jun 1
TI  - Synchronous multiple primary gastrointestinal cancer exhibits frequent 
      microsatellite instability.
PG  - 678-83
AB  - Colorectal (CRC) and gastric cancers (GC), the most common gastrointestinal 
      malignancies, have been known to develop occasionally in a same patient. Previous 
      studies have focused on the etiology of patients with multiple primary gastric 
      and colorectal cancer (MPGCC); however, the carcinogenic process of MPGCC remains 
      unclear. In this study, we have examined the genetic alterations in MPGCC in 
      order to clarify the carcinogenic pathway. Twenty patients with sporadic MPGCC 
      were examined for microsatellite instability (MSI) and frameshift mutations of 
      target genes such as TGFbetaRII, BAX and IGFIIR. In 10 (50%) of 20 patients with 
      MPGCC, MSI was present at least at 1 lesion of GC or CRC. Four (50%) of 8 cases 
      with synchronous MPGCC displayed MSI in both GC and CRC, while only 1 (8%) of 12 
      cases of metachronous MPGCC exhibited MSI in both organs. Carcinogenic process of 
      MPGCC was fairly associated with the MSI pathway, particularly in cases of 
      synchronous MPGCC. MSI was found in 5 (25%) of 20 GCs and in 10 (50%) of 20 CRCs. 
      MSI was involved more closely in CRC than in GC among MPGCC. Although most 
      frameshift mutations at target genes were found in the MSI-positive MPGCC, 
      infrequent mutations were observed in the genes. Frameshift mutation was found in 
      only 1 of 5 cases of MSI-positive GC at TGFbetaRII. Only 2 of 10 cases of CRC 
      with MSI showed mutation at TGFbetaRII, and 1 case also showed mutation at BAX 
      and IGFIIR. Our findings suggest that TGFbetaRII, BAX and IGFIIR are not the main 
      target genes for carcinogenesis in MSI-positive MPGCC.
CI  - Copyright 2000 Wiley-Liss, Inc.
FAU - Ohtani, H
AU  - Ohtani H
AD  - First Department of Surgery, Osaka City University Medical School, Osaka, Japan.
FAU - Yashiro, M
AU  - Yashiro M
FAU - Onoda, N
AU  - Onoda N
FAU - Nishioka, N
AU  - Nishioka N
FAU - Kato, Y
AU  - Kato Y
FAU - Yamamoto, S
AU  - Yamamoto S
FAU - Fukushima, S
AU  - Fukushima S
FAU - Hirakawa-Ys Chung, K
AU  - Hirakawa-Ys Chung K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (BAX protein, human)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (G-T mismatch-binding protein)
RN  - 0 (MSH3 protein, human)
RN  - 0 (Multidrug Resistance-Associated Proteins)
RN  - 0 (MutS Homolog 3 Protein)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Receptor, IGF Type 2)
RN  - 0 (Receptors, Transforming Growth Factor beta)
RN  - 0 (bcl-2-Associated X Protein)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.30 (Receptor, Transforming Growth Factor-beta Type II)
RN  - Y49M64GZ4Q (multidrug resistance-associated protein 1)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - DNA-Binding Proteins/genetics
MH  - Female
MH  - Frameshift Mutation
MH  - Gastrointestinal Neoplasms/*genetics
MH  - Humans
MH  - Loss of Heterozygosity
MH  - Male
MH  - *Microsatellite Repeats
MH  - Middle Aged
MH  - *Multidrug Resistance-Associated Proteins
MH  - MutS Homolog 3 Protein
MH  - Neoplasms, Multiple Primary/*genetics
MH  - Protein Serine-Threonine Kinases
MH  - Proto-Oncogene Proteins/genetics
MH  - *Proto-Oncogene Proteins c-bcl-2
MH  - Receptor, IGF Type 2/genetics
MH  - Receptor, Transforming Growth Factor-beta Type II
MH  - Receptors, Transforming Growth Factor beta/genetics
MH  - bcl-2-Associated X Protein
EDAT- 2000/05/08 09:00
MHDA- 2000/06/10 09:00
CRDT- 2000/05/08 09:00
PHST- 2000/05/08 09:00 [pubmed]
PHST- 2000/06/10 09:00 [medline]
PHST- 2000/05/08 09:00 [entrez]
AID - 10.1002/(SICI)1097-0215(20000601)86:5<678::AID-IJC12>3.0.CO;2-O [pii]
AID - 10.1002/(sici)1097-0215(20000601)86:5<678::aid-ijc12>3.0.co;2-o [doi]
PST - ppublish
SO  - Int J Cancer. 2000 Jun 1;86(5):678-83. doi: 
      10.1002/(sici)1097-0215(20000601)86:5<678::aid-ijc12>3.0.co;2-o.