Somma, Pasquale (2006) Studio dell’espressione dell’Homeobox gene CDX2 nella metaplasia intestinale e nelle lesioni neoplastiche e preneoplastiche dello stomaco e correlazioni clinico-patologiche con l’infezione da Helicobacter Pilory. [Tesi di dottorato] (Inedito)

[img]
Anteprima
PDF
Tesi_di_dottorato_Somma_Pasquale.pdf

Download (5MB) | Anteprima
Tipologia del documento: Tesi di dottorato
Lingua: Italiano
Titolo: Studio dell’espressione dell’Homeobox gene CDX2 nella metaplasia intestinale e nelle lesioni neoplastiche e preneoplastiche dello stomaco e correlazioni clinico-patologiche con l’infezione da Helicobacter Pilory
Autori:
AutoreEmail
Somma, Pasquale[non definito]
Data: 2006
Tipo di data: Pubblicazione
Numero di pagine: 24
Istituzione: Università degli Studi di Napoli Federico II
Dipartimento: Scienze biomorfologiche e funzionali
Dottorato: Morfologia clinica e patologica
Ciclo di dottorato: 17
Coordinatore del Corso di dottorato:
nomeemail
Montagnani, Stefania[non definito]
Tutor:
nomeemail
De Rosa, Gaetano[non definito]
Data: 2006
Numero di pagine: 24
Parole chiave: CDX2, Gastric cancer, Intestinal metaplasma
Settori scientifico-disciplinari del MIUR: Area 05 - Scienze biologiche > BIO/17 - Istologia
Area 06 - Scienze mediche > MED/05 - Patologia clinica
Area 11 - Scienze storiche, filosofiche, pedagogiche e psicologiche > M-EDF/02 - Metodi e didattiche delle attività sportive
Area 06 - Scienze mediche > MED/03 - Genetica medica
Area 06 - Scienze mediche > MED/36 - Diagnostica per immagini e radioterapia
Area 06 - Scienze mediche > MED/08 - Anatomia patologica
Area 06 - Scienze mediche > MED/46 - Scienze tecniche di medicina di laboratorio
Area 05 - Scienze biologiche > BIO/16 - Anatomia umana
Depositato il: 31 Lug 2008
Ultima modifica: 30 Apr 2014 19:24
URI: http://www.fedoa.unina.it/id/eprint/1027
DOI: 10.6092/UNINA/FEDOA/1027

Abstract

BACKGROUND: Gastric carcinoma can be divided into the intestinal and diffuse type, or the differentiated and indifferentiated type, on the basis of its tendency to gland formation. Intestinal metaplasia (IM), where intestinal-type carcinoma is thought to develop, is classified into incomplete and complete types. The latter, which resembles small-intestinal absorptive epithelium, has been considered a precancerous lesion, and its development is strongly associated with Helicobacter Pilory (HP) infection. The molecular mechanism underlying the onset of IM remain elusive. AIMS: To evaluate the evolution of the IM, and to study by immunohistochemistry the expression of the homeobox gene CDX2 in IM before and after the pharmacological treatment for the Helicobacter Pilory eradication, and in 10 cases of gastric carcinoma of intestinal type with associated precancerous lesions. MATERIALS AND METHODS: Formalin-fixed and paraffin embedded tissue from gastric biopsy of 30 patients with complete IM, and 10 cases of gastric carcinoma (pT2bN1Mx) of intestinal type were enrolled. HP infection was assessed by modified Giemsa staining and CDX2 expression by immunohistochemical staining. For each cases of IM we studied two biopsies (before and after HP treatment). 11 cases of gastric biopsy specimens from normal controls were used as control. RESULTS: CDX2 was expressed in a nuclear pattern in all cases of IM before and after the pharmacological treatment for HP. All but one gastric carcinoma were negative for CDX2, in one case we found a quickly CDX2 cytoplasmatic expression. CONCLUSION: Our data confirm that CDX2 represent a transcription factor which is involved in the different aspects of gastric pathogenesis. It may be of special importance in inflammatory condition resulting in the development of intestinal metaplasia. However, CDX2 expression is reduced in gastric carcinomas as compared with IM. On the other hand, it is associated with tumor progression in the subgroup of intestinal carcinoma. Our results, in according with the data reported in literature to date, indicate that CDX2 expression in gastric cancer tissues can be a novel prognostic marker for patient survival.

Actions (login required)

Modifica documento Modifica documento