/pdf/pathology-and-genetics-of-tumours-of-the-digestive-system-3xy9cwrc3c.pdf

Pathology and genetics of tumours of the digestive system

Pathology and genetics: Tumours of the digestive system

Solid-pseudopapillary tumor of the pancreas (SPT) has distinctive morphologic and biologic features but an unclear origin. It is classified among the pancreatic epithelial tumors, though many are reported to be negative for cytokeratin. Also unclear are its neuroendocrine differentiation, its capability to express alpha-1-antitrypsin (AAT) and, in view of the tumor's striking prevalence in women, its relationship with the female genital tract. To clarify these issues, the immunoprofiles of 59 SPTs were defined by applying a battery of antibodies against cytokeratin, vimentin, neuron-specific enolase (NSE), synaptophysin, chromogranin A, tyrosine hydroxylase (TH), AAT, LeuM1, Ki-M1P, smooth-muscle actin, CD34, alpha-inhibin, calretinin, placental alkaline phosphatase (PLAP), and progesterone and estrogen receptors. The most consistent markers with the strongest immunoreactivity were vimentin, AAT, NSE, and the progesterone receptor, which were each found in more than 90% of the tumors. Using immunocytochemical methods involving antigen retrieval, cytokeratin was demonstrated in almost 70% of the cases. Synaptophysin was found in 22% of the tumors, while chromogranin was absent and tyrosine hydroxylase was only present in a few tumors. None of the other markers tested were expressed by SPTs. This staining pattern fails to reveal a clear phenotypic relationship with any of the defined cell lineages of the pancreas. In view of the striking female preponderance of SPTs and the known close approximation of the genital ridges to the pancreatic anlage during embryogenesis, it is, however, hypothesized that SPTs might derive from genital ridge/ovarian anlage-related cells, which were attached to the pancreatic tissue during early embryogenesis.

Solid-pseudopapillary tumor of the pancreas: its origin revisited.

To clarify the neuroendocrine differentiation and CD10 expression in solid-pseudopapillary tumors (SPTs) of the pancreas, we performed immunohistochemical analysis in 19 such tumors, including one solid-pseudopapillary carcinoma (SPC), along with 20 pancreatic neuroendocrine tumors (PNTs), six acinar cell carcinomas (ACCs), and one pancreatoblastoma (PB). We used antisera directed against CD56, synaptophysin, protein gene product 9.5, the alpha-subunit of Go protein, chromogranin A, CD10, trypsin, chymotrypsin, various cytokeratins (CKs), CA19-9, vimentin, and alpha-1-antitrypsin (AAT). All SPTs exhibited immunoreactivity for CD56 and CD10, and 15 expressed other neuroendocrine markers focally with the exception of chromogranin A. Frequent clustering of synaptophysin-positive cells was noted. Two cases contained a peculiar nodule that cytomorphologically and immunohistochemically resembled PNT. CD10-positive cells were scarce in one SPC. PNTs were CD56-positive, but often with faint intensity, and staining for other neuroendocrine markers, including chromogranin A, was diffusely positive. CD10 was detected, mostly in a focal pattern, in five PNTs. Pan-CK, CK8, CK18, and CK19 were more frequently demonstrated in PNT than SPT. Vimentin and AAT were often identified in PNT as well and were not specific for SPT. ACCs were CD56-negative, with the exception of one case designated as a mixed acinar-endocrine carcinoma. PB was focally positive for CD56 at the periphery of the tumor nests. Four ACCs and one PB exhibited focal CD10 reactivity. This study demonstrated the unique immunohistochemical features of SPT. Our results also suggest that SPT exhibits, at least focally, neuroendocrine differentiation, and that these neuroendocrine markers and CD10 are diagnostically useful.

Solid-pseudopapillary tumor of the pancreas: immunohistochemical localization of neuroendocrine markers and CD10.

We report 3 cases of a hitherto undescribed ovarian tumor histologically and immunohistochemically identical to pancreatic solid pseudopapillary neoplasms. The patients were aged 17, 21, and 57 years of age. Two tumors involved the left ovary and 1 the right ovary. They ranged from 3 to 25.5 cm and were confined to the ovary. Radiologic investigations did not show an alternative primary site. Grossly the neoplasms were solid and cystic. On microscopic examination they had mostly diffuse and pseudopapillary growth patterns. Other patterns included nested and microcystic, including cysts filled with colloid-like material. The tumor cells were monotonous and the nuclei were round to oval with pale chromatin and occasional longitudinal nuclear grooves. Clear intracytoplasmic vacuoles were noted in 2 cases, and all 3 cases showed eosinophilic globules. Mitoses and atypia were virtually absent. Immunohistochemically, all 3 neoplasms showed intranuclear positivity for β-catenin and loss of E-cadherin reactivity. All 3 tumors were negative for chromogranin, inhibin, and calretinin, although both cases evaluated for thyroglobulin were found negative. One patient has been followed for 6 years and is free of disease. The other 2 cases are recent. The tumors likely to enter into the differential diagnosis include sex-cord stromal tumors, steroid cell tumors, and struma ovarii. The morphologic and immunohistochemical similarity to pancreatic solid pseudopapillary neoplasm facilitates the accurate diagnosis of this rare ovarian neoplasm.

Solid pseudopapillary neoplasm of the ovary: a report of 3 primary ovarian tumors resembling those of the pancreas

Solid and papillary neoplasm arising from an ectopic pancreas in the mesocolon.

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Solid and papillary neoplasm arising from an ectopic pancreas in the mesocolon.