UNLABELLED: 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, >2) 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.
UNLABELLED: 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, >2) 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.
Authors: Cathy Bennett; Nimish Vakil; Jacques Bergman; Rebecca Harrison; Robert Odze; Michael Vieth; Scott Sanders; Laura Gay; Oliver Pech; Gaius Longcroft-Wheaton; Yvonne Romero; John Inadomi; Jan Tack; Douglas A Corley; Hendrik Manner; Susi Green; David Al Dulaimi; Haythem Ali; Bill Allum; Mark Anderson; Howard Curtis; Gary Falk; M Brian Fennerty; Grant Fullarton; Kausilia Krishnadath; Stephen J Meltzer; David Armstrong; Robert Ganz; Gianpaolo Cengia; James J Going; John Goldblum; Charles Gordon; Heike Grabsch; Chris Haigh; Michio Hongo; David Johnston; Ricky Forbes-Young; Elaine Kay; Philip Kaye; Toni Lerut; Laurence B Lovat; Lars Lundell; Philip Mairs; Tadakuza Shimoda; Stuart Spechler; Stephen Sontag; Peter Malfertheiner; Iain Murray; Manoj Nanji; David Poller; Krish Ragunath; Jaroslaw Regula; Renzo Cestari; Neil Shepherd; Rajvinder Singh; Hubert J Stein; Nicholas J Talley; Jean-Paul Galmiche; Tony C K Tham; Peter Watson; Lisa Yerian; Massimo Rugge; Thomas W Rice; John Hart; Stuart Gittens; David Hewin; Juergen Hochberger; Peter Kahrilas; Sean Preston; Richard Sampliner; Prateek Sharma; Robert Stuart; Kenneth Wang; Irving Waxman; Chris Abley; Duncan Loft; Ian Penman; Nicholas J Shaheen; Amitabh Chak; Gareth Davies; Lorna Dunn; Yngve Falck-Ytter; John Decaestecker; Pradeep Bhandari; Christian Ell; S Michael Griffin; Stephen Attwood; Hugh Barr; John Allen; Mark K Ferguson; Paul Moayyedi; Janusz A Z Jankowski Journal: Gastroenterology Date: 2012-04-24 Impact factor: 22.682
Authors: Santhoshi Bandla; Jeffrey H Peters; David Ruff; Shiaw-Min Chen; Chieh-Yuan Li; Kunchang Song; Kimberly Thoms; Virginia R Litle; Thomas Watson; Nikita Chapurin; Michal Lada; Arjun Pennathur; James D Luketich; Derick Peterson; Austin Dulak; Lin Lin; Adam Bass; David G Beer; Tony E Godfrey; Zhongren Zhou Journal: Ann Surg Date: 2014-07 Impact factor: 12.969
Authors: Stuart Jon Spechler; Rebecca C Fitzgerald; Ganapathy A Prasad; Kenneth K Wang Journal: Gastroenterology Date: 2010-01-18 Impact factor: 22.682