Immunohistochemical and Molecular Analysis of Giant Cell Carcinoma of the Pancreas

Imai, Yasuo; Morishita, Shinji; Ikeda, Yusei; Toyoda, Mitsuyasu; Ashizawa, T.; Yamamoto, Keiichiro; Inoue, Tohru; Ishikawa, Takatoshi

doi:10.1097/00006676-199904000-00013

Cited by 40 publications

(28 citation statements)

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“…This finding confirmed a previous report that Dpc4 expression was not lost in undifferentiated carcinomas with osteoclastic-like giant cells. 23 In our study, one acinar cell carcinoma did not have any expression of Dpc4 in the neoplastic cells. However, the internal positive control (ie, the nonneoplastic stroma cells) also did not shown expression of Dpc4, and this case was excluded from our analysis.…”

Section: Resultscontrasting

confidence: 40%

Expression of novel markers of pancreatic ductal adenocarcinoma in pancreatic nonductal neoplasms: additional evidence of different genetic pathways

et al. 2005

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Solid pseudopapillary tumor, pancreatoblastoma, undifferentiated carcinoma with osteoclastic-like giant cells, and acinar cell carcinomas are rare pancreatic nonductal neoplasms. Compared to the significant advances in our understanding of the pathogenesis of pancreatic ductal adenocarcinomas in the last decades, the molecular mechanisms underlying pancreatic nonductal neoplasms are poorly understood. In order to elucidate their molecular pathogenesis, we constructed tissue microarrays to study the expression of some novel pancreatic ductal adenocarcinoma-associated tumor markers in these nonductal pancreatic neoplasms. We analyzed nine markers including tumor suppressor gene (14-3-3 sigma), proliferation marker (topoisomerase II alpha), epithelial markers (prostate stem cell antigen, mesothelin and cytokeratin 19), stromal markers (fascin, hsp47 and fibronectin), and gamma-synuclein whose function is not delineated. In addition, we included tumor suppressor gene DPC4 and oncogene Beta-catenin to further confirm their expression in pancreatic nonductal tumors. Our results showed that in contrast to pancreatic ductal adenocarcinomas that show loss of Dpc4 protein in 55% of cases, loss of Dpc4 expression is absent in pancreatic nonductal neoplasms. Expression of 14-3-3 sigma is frequently seen in both pancreatic nonductal neoplasms (25-100%) and ductal adenocarcinomas (89%). Aberrant nuclear expression of beta-catenin is common in pancreatic nonductal neoplasms, specifically in solid pseudopapillary tumors (88%) and pancreatoblastomas (100%) but is rarely seen in pancreatic ductal adenocarcinomas (o5%). Expression of topoisomerase II alpha is not seen in solid pseudopapillary tumors and undifferentiated carcinomas with osteoclastic-like giant cells but is focally seen in pancreatoblastomas (50%) and acinar cell carcinomas (85%). Expression of PSCA and mesothelin was observed in pancreatic nonductal neoplasms but their expression was seen less frequently (0-50%) and weaker than that in pancreatic ductal adenocarcinomas (60-100%). CK19, a marker of pancreatic ductal adenocarcinomas, is not expressed in pancreatic nonductal neoplasms. Expression of gamma-synuclein as well as stromal markers (fascin, hsp47 and fibronectin) is frequently seen in both. Our findings indicate pancreatic nonductal neoplasms have distinctive patterns of protein expression relative to pancreatic ductal adenocarcinomas and suggest that pancreatic nonductal neoplasms have different genetic pathways from the more common pancreatic ductal adenocarcinomas.

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Section: Resultscontrasting

confidence: 40%

Expression of novel markers of pancreatic ductal adenocarcinoma in pancreatic nonductal neoplasms: additional evidence of different genetic pathways

et al. 2005

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“…There are limited data available about the pathologic and immunohistochemical characteristics, as well as the clinical behavior of this pathological entity [2][3][4][5][6][7]. Giant cell carcinoma is a rare and aggressive neoplasm, which has been described in a number of organs including lung, ovary, pancreas, breast, kidney, liver, gall bladder, and prostate [6,[8][9][10][11][12][13][14][15][16][17][18][19][20][21][22]. In urinary bladder, pleomorphic giant cell carcinoma has been acknowledged in classic and more recent review articles on unusual variants of bladder cancer, including the WHO current classification of infiltrating urothelial tumors [1][2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Pleomorphic giant cell carcinoma of the urinary bladder

et al. 2009

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“…On the contrary, treatment of isolated and purified hamster islets with BOP produced tumors of giant cell morphology. Similarities between the human and hamster tumors exist also on immunohistochemical and biological levels, including the coexpression of the epithelial marker cytokeratin, mesenchymal marker, vimentin, 14,18,19 neuroepithelial marker, NSE, 13 the mutation of K-ras 18,19 and overexpression of p53.…”

Section: Discussionmentioning

confidence: 96%

In Vitro Induction of Giant Cell Tumors from Cultured Hamster Islets Treated with N-Nitrosobis(2-Oxopropyl)amine

Matsuzaki

Schmied

Ulrich

et al. 2000

The American Journal of Pathology

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It is generally believed that over 90% of pancreatic cancers originate from ductal/ductular cells. Studies of the hamster pancreatic cancer model, which in biological and morphological aspects mimics human tumors, [1][2][3] however, have shown that pancreatic ductal adenocarcinoma originates not only from ductal/ductular cells but primarily from within islets, most probably from precursor (stem) cells.

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Immunohistochemical and Molecular Analysis of Giant Cell Carcinoma of the Pancreas

Cited by 40 publications

References 0 publications

Expression of novel markers of pancreatic ductal adenocarcinoma in pancreatic nonductal neoplasms: additional evidence of different genetic pathways

Expression of novel markers of pancreatic ductal adenocarcinoma in pancreatic nonductal neoplasms: additional evidence of different genetic pathways

Pleomorphic giant cell carcinoma of the urinary bladder

In Vitro Induction of Giant Cell Tumors from Cultured Hamster Islets Treated with N-Nitrosobis(2-Oxopropyl)amine

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