PMID- 16685384
OWN - NLM
STAT- MEDLINE
DCOM- 20070308
LR  - 20190606
IS  - 1021-335X (Print)
IS  - 1021-335X (Linking)
VI  - 15
IP  - 6
DP  - 2006 Jun
TI  - Relation of DNA ploidy to genetic aberrations detected by chromosomal CGH and 
      FISH in gastric adenocarcinomas.
PG  - 1491-6
AB  - We analyzed DNA copy number aberrations (DCNAs) by chromosomal comparative 
      genomic hybridization (CGH) in 93 consecutive sporadic gastric adenocarcinomas. 
      In addition, numerical aberrations in chromosomes 7, 11, 17, and 18 were 
      evaluated by fluorescence in situ hybridization (FISH). Gastric cancers were 
      divided on the basis of nuclear DNA content measured by laser scanning cytometry 
      (LSC) into two groups, 36 DNA diploid (1.0 <or= DNA index (DI) < 1.2) and 57 
      aneuploid (DI >or= 1.2) cancers. The most frequent gain and loss of DNA copy 
      number were found at 8q21-23 and 19p13.3, respectively, in both diploid and 
      aneuploid cancers. Diploid cancers were further divided on the basis of genetic 
      aberrations into major type and subtype cancers. The diploid cancer group 
      included nine subtype cancers that showed large numbers of DCNAs; the mean number 
      of DCNAs detected by CGH was 26.7 per tumor. This value was much larger in these 
      diploid subtype cancers than diploid major type cancers (mean, 5.2 per tumor, 
      p<0.0001). These nine cancers were also characterized by large intercellular 
      variations in chromosome copy numbers that were not detected in the 27 major 
      diploid type cancers. The aneuploid cancer group included only three subtype 
      tumors that showed only a small number of DCNAs (mean, 3 per tumor) and minimal 
      intercellular variations in chromosomal copy number. These data indicate that 
      gastric adenocarcinomas can be divided into three types; aneuploid, major diploid 
      type and diploid subtype cancers. Large-scale studies are necessary to clarify 
      the differences in biological characteristics and underlying genetic mechanisms 
      between these types.
FAU - Furuya, Tomoko
AU  - Furuya T
AD  - Department of Pathology, Yamaguchi University School of Medicine, Ube 755-8505, 
      Japan.
FAU - Uchiyama, Tetsuji
AU  - Uchiyama T
FAU - Adachi, Atsushi
AU  - Adachi A
FAU - Chochi, Yasuyo
AU  - Chochi Y
FAU - Oga, Atsunori
AU  - Oga A
FAU - Kawauchi, Shigeto
AU  - Kawauchi S
FAU - Ishiglo, Kimio
AU  - Ishiglo K
FAU - Sasaki, Kohsuke
AU  - Sasaki K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (DNA, Neoplasm)
SB  - IM
MH  - Adenocarcinoma/*genetics
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - *Chromosome Aberrations
MH  - DNA, Neoplasm/genetics
MH  - Female
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Male
MH  - Middle Aged
MH  - Nucleic Acid Hybridization
MH  - *Ploidies
MH  - Stomach Neoplasms/*genetics
EDAT- 2006/05/11 09:00
MHDA- 2007/03/09 09:00
CRDT- 2006/05/11 09:00
PHST- 2006/05/11 09:00 [pubmed]
PHST- 2007/03/09 09:00 [medline]
PHST- 2006/05/11 09:00 [entrez]
AID - 10.3892/or.15.6.1491 [doi]
PST - ppublish
SO  - Oncol Rep. 2006 Jun;15(6):1491-6. doi: 10.3892/or.15.6.1491.