Papillary epithelial neoplasm of pancreas in a child. Report of a case with electron microscopy.
01 Nov 1970-Cancer (Wiley Subscription Services, Inc., A Wiley Company)-Vol. 26, Iss: 5, pp 1126-1134
TL;DR: An asymptomatic tumor of the head of the pancreas observed in a 12‐year‐old girl was removed by radical excision and the cell of origin is demonstrated ultrastructurally to be other than islet or exocrine, and probably to have been derived from ductular epithelium.
Abstract: An asymptomatic tumor of the head of the pancreas observed in a 12-year-old girl was removed by radical excision. the cell of origin of the tumor is demonstrated ultrastructurally to be other than islet or exocrine, and probably to have been derived from ductular epithelium. the malignant or benign nature of this tumor is discussed and requires longer follow-up for clarification.
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TL;DR: It is hypothesized that SPTs might derive from genital ridge/ovarian anlage-related cells, which were attached to the pancreatic tissue during early embryogenesis, as well as progesterone and estrogen receptors.
Abstract: 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.
324 citations
Cites background from "Papillary epithelial neoplasm of pa..."
...As there may also be ultrastructural features, such as primitive cell junctions, small bundles of tonofilaments, and intermediate microfilaments reminiscent of ductal/ductular differentiation or myoepithelial differentiation [1, 23, 27], an origin from the duct cell compartment of the pancreas has been suggested [ 12 , 23, 25, 30]....
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TL;DR: The results of immunohistochemical staining and electromicroscopy support the hypothesis that the tumor originates from pleuripotential embryonic stem cells, and pancreatic embryonic tumors seems preferable to papillary cystic and solid tumor of the pancreas to delineate the origin of the tumor and to reflect some of its biologic characteristics.
306 citations
TL;DR: It is suggested that SPT exhibits, at least focally, neuroendocrine differentiation, and that these neuro endocrine markers and CD10 are diagnostically useful.
Abstract: 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.
285 citations
Journal Article•
TL;DR: The association of atypias and carcinomas in situ in the patients with Pancreas carcinoma implies that there may be a significant latent period between the appearance of carcinoma in situ and the grossly recognizable pancreas cancer.
Abstract: Summary The study of histological sections of 406 cases of nonendocrine pancreas carcinoma at Memorial Hospital indicated that morphological patterns of pancreas carcinoma could be delineated as follows: duct cell adenocarcinoma (76%), giant-cell carcinoma (5%), microadenocarcinoma (4%), adenosquamous carcinoma (4%), mucinous adenocarcinoma (2%), anaplastic carcinoma (2%), cystadenocarcinoma (1%), acinar cell carcinoma (1%), carcinoma in childhood (under 1%), unclassified (7%). In 195 cases of patients with pancreas carcinoma, search was made for changes in the pancreas duct epithelium and these were compared to duct epithelium in a control group of 100 pancreases from autopsies of patients with nonpancreatic cancer. The following incidences were found for pancreas cancer and nonpancreatic cancer, respectively: mucous cell hypertrophy, 39 versus 28%; pyloric gland metaplasia, 28 and 17%; epidermoid metaplasia, 6 and 12%; papillary hyperplasia, 42 and 12%; atypical duct hyperplasia, 14% and none; carcinoma in situ in 19% and none in the control group. Mucin in the majority of pancreas cancers suggested that the cell type of origin of the common pancreas cancer is the mucin-producing duct epithelium. The association of atypias and carcinomas in situ in the patients with pancreas carcinoma implies, by analogy to other organs, that there may be a significant latent period between the appearance of carcinoma in situ and the grossly recognizable pancreas cancer.
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