Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
p16(INK4a) alterations in chronic pancreatitis-indicator for high-risk lesions for pancreatic cancer
Autore:
Gerdes, B; Ramaswamy, A; Kersting, M; Ernst, M; Lang, S; Schuermann, M; Wild, A; Bartsch, DK;
Indirizzi:
Univ Marburg, Dept Gen Surg, D-35033 Marburg, Germany Univ Marburg Marburg Germany D-35033 Gen Surg, D-35033 Marburg, Germany Univ Marburg, Dept Pathol, D-35033 Marburg, Germany Univ Marburg MarburgGermany D-35033 pt Pathol, D-35033 Marburg, Germany Univ Marburg, Dept Internal Med, D-35033 Marburg, Germany Univ Marburg Marburg Germany D-35033 ernal Med, D-35033 Marburg, Germany Gen Hosp Neubrandenburg, Dept Gen Surg, Neubrandenburg, Germany Gen Hosp Neubrandenburg Neubrandenburg Germany Neubrandenburg, Germany
Titolo Testata:
SURGERY
fascicolo: 4, volume: 129, anno: 2001,
pagine: 490 - 497
SICI:
0039-6060(200104)129:4<490:PAICPF>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
K-RAS MUTATIONS; LUNG-CANCER; PROLIFERATIVE LESIONS; GENE; ADENOCARCINOMA; TUMORS; CDKN2; P16; METHYLATION; CARCINOMAS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Gerdes, B Univ Marburg, Dept Gen Surg, Baldingerstr, D-35033 Marburg, Germany Univ Marburg Baldingerstr Marburg Germany D-35033 burg, Germany
Citazione:
B. Gerdes et al., "p16(INK4a) alterations in chronic pancreatitis-indicator for high-risk lesions for pancreatic cancer", SURGERY, 129(4), 2001, pp. 490-497

Abstract

Background. p16INK4a alterations are considered to be an early event in pancreatic tumorigenesis and have been described in duct lesions adjacent to pancreatic cancers. This study evaluates whether duct lesions in chronic pancreatitis tissues of patients without pancreatic cancer also harbor genetic alterations in the p16INK4a tumor-suppressor gene, and thus represent high-risk precursors for pancreatic cancer. Methods. Tissues were obtained from 20 pancreatic specimens taken from patients operated on for histologically verified chronic pancreatitis. Pancreatic intraductal neoplasias (PanIN) were identified in hematoxylin-and-eosin-stained slides. p16 protein expression was investigated immunohistochemically in all specimens. DNA from PanIN and non-PanIN tissue was analyzed genetically for p16INK4a mutations by single-strand conformation variation analysis and direct sequencing of the encoding region. Additionally, p16INK4a promoter methylation was analyzed by a methylation specific polymerase test. Results. PanIN-1a lesions were identified in 10 of the 20 chronic pancreatitis specimens. Four of these 10 PanIn-1a specimens (40%), but none of the 20 non-PanIN tissues, revealed a loss of p16 expression in immunohistochemistry. The mutational analysis of the p16INK4a gene showed 1 known polymorphism (c.442G > A; A148T) but no mutations. Two of the 10 specimens with PanIN revealed an inactivating hypermethylation of the p16INK4a promoter. Conclusions. This study shows for the first time that p16INK4a alterationscan be observed in a considerable number of PanIN1 in chronic pancreatitistissues not associated with pancreatic cancer. Therefore, p16INK4a alterations, especially promoter methylation, might indicate high-risk precursors in chronic pancreatitis that might progress to cancer.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 15:54:18