Chromosomal analysis of Barrett's cells: demonstration of instability and detection of the metaplastic lineage involved

被引:49
作者
Chaves, Paula [1 ]
Crespo, Mateus [1 ]
Ribeiro, Catarina [1 ]
Laranjeira, Catia [1 ]
Pereira, A. Dias [1 ]
Suspiro, Alexandra [1 ]
Cardoso, Paula [1 ]
Leitao, C. Nobre [1 ]
Soares, Jorge [1 ]
机构
[1] Inst Portuges Oncol Francisco Gentil, Serv Anat Patol, Grp Estudo Esofago Barrett, EPE, P-1099023 Lisbon, Portugal
关键词
barrett's esophagus; cellular phenotype; chromosomal abnormality; metaplasia;
D O I
10.1038/modpathol.3800787
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Barrett's esophagus is lined by columnar and goblets cells with gastric and intestinal characteristics. Despite the association between goblet elements and malignancy, it was not demonstrated that other columnar cells lineages are not related to neoplasia. Chromosomal abnormalities were described in metaplasia adjacent to Barrett's neoplasia, but it is unknown which metaplastic lineages are involved. This work assessed the frequency and the type of chromosomal abnormalities in Barrett's esophagus without neoplasia and performed the identification of the metaplastic cells carrying chromosomal gains. Barrett's esophagus biopsies were collected and processed for short-term cell culture and cytogenetic analysis. Combined immunofluorescence/ fluorescence in situ hybridization was performed in cases exhibiting chromosomal gains by using antisera against intestinal (MUC2) and gastric (MUC5AC and MUC6) apomucins and chromosome pericentromeric alpha satellite DNA probes for the chromosomes involved. Each case was scored for the number of spots (0, 1, 2, 42) in 200 nonoverlapping nuclei. Columnar and goblet cells were separately assessed. Short-term cell cultures were achieved in 40/60 cases (67%). There were clonal abnormalities in 27/40 cases (68%) and tetraploid (4n) clones in 10/40 (25%). Structural alterations were detected in 14/40 (35%) with recurrent breakpoints at 1q21, 15q15 and 15q22. Numerical changes (trisomies 7 and 18 and loss of Y) occurred in 16/40 (40%). Gains of chromosomes 7 and 18 were more frequent in columnar than in goblet cells (9.8% vs 0.7% (P < 0.05)) and (7.9 vs 1.9% (P < 0.05)) respectively. These alterations were detected in cells exhibiting gastric as well as intestinal features and were more frequent in cells without apomucin production. Conclusions: (1) chromosomal instability is a common finding in Barrett's esophagus without neoplasia. (2) The two metaplastic populations are committed, chromosomal gains being more frequent in columnar nongoblet than in goblet cells. (3) The two metaplastic phenotypes, gastric and intestinal, are equally involved.
引用
收藏
页码:788 / 796
页数:9
相关论文
共 51 条
[1]   AMPLIFICATION AND OVER-EXPRESSION OF THE EGFR AND ERBB-2 GENES IN HUMAN ESOPHAGEAL ADENOCARCINOMAS [J].
ALKASSPOOLES, M ;
MOORE, JH ;
ORRINGER, MB ;
BEER, DG .
INTERNATIONAL JOURNAL OF CANCER, 1993, 54 (02) :213-219
[2]   Evolution of neoplastic cell lineages in Barrett oesophagus [J].
Barrett, MT ;
Sanchez, CA ;
Prevo, LJ ;
Wong, DJ ;
Galipeau, PC ;
Paulson, TG ;
Rabinovitch, PS ;
Reid, BJ .
NATURE GENETICS, 1999, 22 (01) :106-109
[3]   Chromosomal numerical aberrations are frequent in oesophageal and gastric adenocarcinomas:: a study using in-situ hybridization [J].
Beuzen, F ;
Dubois, S ;
Fléjou, JF .
HISTOPATHOLOGY, 2000, 37 (03) :241-249
[4]   RISING INCIDENCE OF ADENOCARCINOMA OF THE ESOPHAGUS AND GASTRIC CARDIA [J].
BLOT, WJ ;
DEVESA, SS ;
KNELLER, RW ;
FRAUMENI, JF .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1991, 265 (10) :1287-1289
[5]   Mucin gene expression in intestinal epithelial cells in Crohn's disease [J].
Buisine, MP ;
Desreumaux, P ;
Leteurtre, E ;
Copin, MC ;
Colombel, JF ;
Porchet, N ;
Aubert, JP .
GUT, 2001, 49 (04) :544-551
[6]   Epidemiology of columnar-lined esophagus and adenocarcinoma [J].
Cameron, AJ .
GASTROENTEROLOGY CLINICS OF NORTH AMERICA, 1997, 26 (03) :487-+
[7]   Gastric and intestinal differentiation in Barrett's metaplasia and associated adenocarcinoma [J].
Chaves, P ;
Cruz, C ;
Pereira, AD ;
Suspiro, A ;
de Almeida, JCM ;
Leitao, CN ;
Soares, J .
DISEASES OF THE ESOPHAGUS, 2005, 18 (06) :383-387
[8]  
CHAVES P, 2001, RECENT ADV DIS OESOP
[9]  
Devesa SS, 1998, CANCER, V83, P2049, DOI 10.1002/(SICI)1097-0142(19981115)83:10<2049::AID-CNCR1>3.0.CO
[10]  
2-2