PMID- 9772903
OWN - NLM
STAT- MEDLINE
DCOM- 19981023
LR  - 20190816
IS  - 0165-4608 (Print)
IS  - 0165-4608 (Linking)
VI  - 106
IP  - 1
DP  - 1998 Oct 1
TI  - Interphase cytogenetics of esophageal adenocarcinoma and precursor lesions.
PG  - 11-7
AB  - Limited information is currently available on chromosomal abnormalities in 
      esophageal adenocarcinoma and associated premalignant lesions. In this study, 
      numeric changes affecting chromosomes 4, 6, 7, 8, 9, 10, 11, 12, 17, 18, X, and Y 
      were analyzed by using fluorescence in situ hybridization (FISH) with 
      chromosome-specific centromere DNA probes in 12 esophageal adenocarcinomas. In 
      addition, TP53 overexpression, measured by immunohistochemistry, and 
      amplification of HER-2/neu and C-MYC, detected by FISH, were analyzed within the 
      same tumors. The most common numeric abnormalities detected were gains of 
      chromosomes 12 (8 cases), 6 (7 cases), 7 (7 cases), and 11 (6 cases). The total 
      number of abnormal chromosomes varied from 0 to 10, with an average of 4.6 per 
      case. Overexpression of TP53 was present in 9 of 12 cases. No correlation was 
      noted between the degree of aneusomy and TP53 overexpression. In contrast, 
      HER-2/neu amplification was present in two cases, both with large numbers of 
      aneusomic chromosomes. Amplification of C-MYC was detected in only one case that 
      had a moderate number of numeric abnormalities. In a subset of cases in which 
      premalignant lesions were examined, aneusomy was found to be an early change, 
      frequently present in both Barrett's esophagus and dysplastic regions. In 
      contrast, gene amplification and TP53 overexpression were restricted to more 
      advanced areas of dysplasia and malignancy. Screening larger cohorts of patients 
      with Barrett's esophagus or dysplasia for numeric abnormalities of chromosomes 6, 
      7, 11, and 12 may determine whether any of these abnormalities are predictive 
      markers of progression to malignancy.
FAU - Persons, D L
AU  - Persons DL
AD  - Department of Pathology and Laboratory Medicine, University of Kansas Medical 
      Center, Kansas City 66160-7232, USA.
FAU - Croughan, W S
AU  - Croughan WS
FAU - Borelli, K A
AU  - Borelli KA
FAU - Cherian, R
AU  - Cherian R
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Cancer Genet Cytogenet
JT  - Cancer genetics and cytogenetics
JID - 7909240
RN  - 0 (Tumor Suppressor Protein p53)
SB  - IM
MH  - Adenocarcinoma/*genetics
MH  - Aneuploidy
MH  - Barrett Esophagus/genetics
MH  - *Chromosome Aberrations
MH  - Esophageal Neoplasms/*genetics
MH  - Gene Amplification
MH  - Genes, erbB-2
MH  - Genes, myc
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Interphase
MH  - Precancerous Conditions/*genetics
MH  - Tumor Suppressor Protein p53
EDAT- 1998/10/17 00:00
MHDA- 1998/10/17 00:01
CRDT- 1998/10/17 00:00
PHST- 1998/10/17 00:00 [pubmed]
PHST- 1998/10/17 00:01 [medline]
PHST- 1998/10/17 00:00 [entrez]
AID - S0165460898000363 [pii]
AID - 10.1016/s0165-4608(98)00036-3 [doi]
PST - ppublish
SO  - Cancer Genet Cytogenet. 1998 Oct 1;106(1):11-7. doi: 
      10.1016/s0165-4608(98)00036-3.