Koji Domori1, Ken Nishikura, Yoichi Ajioka, Yutaka Aoyagi. 1. Division of Molecular and Diagnostic Pathology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan, doumori-nii@umin.ac.jp.
Abstract
BACKGROUND: Gastric neuroendocrine neoplasia has been classified as neuroendocrine tumor (NET), a less-malignant type, and neuroendocrine carcinoma (NEC), a more-malignant type. We investigated phenotypic expression profiles to clarify the differences between NET and NEC in terms of histopathology and carcinogenesis. METHODS: We assayed 86 cases of gastric neuroendocrine neoplasms (NET G1, n = 25; NET G2, n = 9; NEC, n = 52), using six exocrine markers (MUC5AC, human gastric mucin, MUC6, M-GGMC-1, MUC2, and CDX2). RESULTS: NEC frequently coexisted with adenocarcinomatous components (75 %; 39 of 52) and the majority (71.8 %; 28 of 39) showed intraglandular endocrine cell hyperplasia, although no cases of NET showed adenocarcinomatous components. Mucin phenotype significantly differed between NET and NEC; none of NET cases expressed any exocrine markers other than CDX2, although the majority of NEC (86.5 %; 45 of 52) expressed at least one or more exocrine markers with various positive rates for each marker (range, 8.2-74.0 %). Each NEC component showed only the phenotype expressed in the adenocarcinomatous component in the same tumor. Furthermore, double immunohistochemistry revealed dual expression of CDX2 and chromogranin A in half the NEC cases (23 of 46). CONCLUSIONS: These data suggest that gastric NETs (G1 and G2) and NECs have different processes of carcinogenesis, and gastric NECs may be generated from preceding adenocarcinomas.
BACKGROUND: Gastric neuroendocrine neoplasia has been classified as neuroendocrine tumor (NET), a less-malignant type, and neuroendocrine carcinoma (NEC), a more-malignant type. We investigated phenotypic expression profiles to clarify the differences between NET and NEC in terms of histopathology and carcinogenesis. METHODS: We assayed 86 cases of gastric neuroendocrine neoplasms (NET G1, n = 25; NET G2, n = 9; NEC, n = 52), using six exocrine markers (MUC5AC, humangastric mucin, MUC6, M-GGMC-1, MUC2, and CDX2). RESULTS: NEC frequently coexisted with adenocarcinomatous components (75 %; 39 of 52) and the majority (71.8 %; 28 of 39) showed intraglandular endocrine cell hyperplasia, although no cases of NET showed adenocarcinomatous components. Mucin phenotype significantly differed between NET and NEC; none of NET cases expressed any exocrine markers other than CDX2, although the majority of NEC (86.5 %; 45 of 52) expressed at least one or more exocrine markers with various positive rates for each marker (range, 8.2-74.0 %). Each NEC component showed only the phenotype expressed in the adenocarcinomatous component in the same tumor. Furthermore, double immunohistochemistry revealed dual expression of CDX2 and chromogranin A in half the NEC cases (23 of 46). CONCLUSIONS: These data suggest that gastric NETs (G1 and G2) and NECs have different processes of carcinogenesis, and gastric NECs may be generated from preceding adenocarcinomas.
Authors: Y Takenaka; T Tsukamoto; T Mizoshita; N Ogasawara; N Hirano; T Otsuka; H Ban; T Nakamura; Y Yamamura; M Kaminishi; M Tatematsu Journal: Histol Histopathol Date: 2007-03 Impact factor: 2.303
Authors: James C Yao; Manal Hassan; Alexandria Phan; Cecile Dagohoy; Colleen Leary; Jeannette E Mares; Eddie K Abdalla; Jason B Fleming; Jean-Nicolas Vauthey; Asif Rashid; Douglas B Evans Journal: J Clin Oncol Date: 2008-06-20 Impact factor: 44.544
Authors: G Rindi; G Klöppel; H Alhman; M Caplin; A Couvelard; W W de Herder; B Erikssson; A Falchetti; M Falconi; P Komminoth; M Körner; J M Lopes; A-M McNicol; O Nilsson; A Perren; A Scarpa; J-Y Scoazec; B Wiedenmann Journal: Virchows Arch Date: 2006-09-12 Impact factor: 4.064