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TOPOIIα and HER-2/neu overexpression/amplification in Barrett’s oesophagus, dysplasia and adenocarcinoma

Rossi E, Villanacci V, Bassotti G, Donato F, Festa A, Cengia G, Grisanti S & Cestari R (2010) Histopathology57, 81–89 TOPOIIα and HER-2/neu overexpression/amplification in Barrett’s oesophagus, dysplasia and adenocarcinoma AIMS: Topoisomerase IIα (TOPOIIα) and HER-2/neu are chromosome 17q genes...

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Detalles Bibliográficos
Autores principales: Rossi, Elisa, Villanacci, Vincenzo, Bassotti, Gabrio, Donato, Francesco, Festa, Andrea, Cengia, Gianpaolo, Grisanti, Salvatore, Cestari, Renzo
Formato: Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2916224/
https://www.ncbi.nlm.nih.gov/pubmed/20557373
http://dx.doi.org/10.1111/j.1365-2559.2010.03580.x
Descripción
Sumario:Rossi E, Villanacci V, Bassotti G, Donato F, Festa A, Cengia G, Grisanti S & Cestari R (2010) Histopathology57, 81–89 TOPOIIα and HER-2/neu overexpression/amplification in Barrett’s oesophagus, dysplasia and adenocarcinoma AIMS: Topoisomerase IIα (TOPOIIα) and HER-2/neu are chromosome 17q genes coamplified in various cancers; no data exist for Barrett’s oesophagus (BO) and BO adenocarcinoma (ADC). The aim was to investigate gene amplification and protein overexpression of TopoIIα and Her-2/neu in non-dysplastic BO, dysplastic BO, Barrett ADC, and chromosome 17 aneusomy. METHODS AND RESULTS: Forty-four patients [18 BO, 13 BO with dysplasia (five low-grade dysplasia, eight high-grade dysplasia) and 13 ADC in BO] were evaluated by immunohistochemistry and fluorescence in situ hybridization (FISH). Genes (HER-2/neu and TOPOIIα) and chromosome 17 were evaluated by FISH. Patients with BO, dysplasia and ADC were compared. A significant association was found between TOPOIIα protein overexpression and TopoIIα gene amplification, chromosome 17 aneusomy, HER-2/neu gene amplification and HER-2 protein overexpression as well as between HER-2 protein and HER-2/neu gene, TopoIIα gene and aneusomy for chromosome17, and between the genes TOPOIIα and HER-2/neu. Gene amplification (HER-2/neu, TOPOIIα), protein overexpression (HER-2/TOPOIIα), and chromosome 17 aneusomy were associated with dysplasia or ADC. Most BO patients showed no amplification/overexpression/aneusomy for the above genes, proteins and chromosome, with no differences between dysplasia and ADC. CONCLUSIONS: HER-2/neu and TOPOIIα amplification/overexpression might discriminate between BO and dysplasia/ADC. Chromosome 17 aneusomy is associated with dysplasia or ADC in BO.