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Nonductal Neoplasms of the Pancreas

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Nonductal Neoplasms of the Pancreas Modern Pathology (2007) 20, S94–S112 & 2007 USCAP, Inc All rights reserved 0893-3952/07 $30.00 www.modernpathology.org Nonductal neoplasms of the pancreas David S Klimstra Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA Although the majority of pancreatic neoplasms are infiltrating ductal adenocarcinomas or other neoplasms with ductal differentiation, neoplasms with acinar, endocrine, mixed, or uncertain differentiation constitute a diverse and distinctive group. The most common and best-characterized nonductal neoplasms are pancreatic endocrine neoplasm, acinar cell carcinoma, pancreatoblastoma, and solid pseudopapillary neoplasm. This review details the clinical and pathologic features of these nonductal neoplasms, highlighting diagnostic criteria including the use of specific immunohistochemical stains to define the cellular differentiation of the neoplasms. Modern Pathology (2007) 20, S94–S112. doi:10.1038/modpathol.3800686 Keywords: pancreas; endocrine; acinar; pancreatoblastoma; solid pseudopapillary One of the most important features of pancreatic ‘pancreatic endocrine neoplasms’ (PENs). The neoplasms, on which their classification in large older term ‘islet cell tumor’ is now discouraged part is based, is the line(s) of cellular differentiation as PENs do not necessarily arise from non-neo- the neoplasm displays. Most pancreatic epithelial plastic islet cells and some produce peptide neoplasms recapitulate to some degree one or more hormones not encountered in normal islets. PENs of the normal epithelial cell types of the pancreas: are classified into three categories based on size ductal, acinar, and endocrine. The vast majority of and mitotic rate. PENs measuring less than 0.5 cm pancreatic neoplasms (490%) have ductal differ- are regarded to be biologically benign and are entiation, including the most common tumor, termed endocrine microadenomas. PENs measur- infiltrating ductal adenocarcinoma, as well as many ing 0.5 cm or more and having a relatively low of the cystic and intraductal neoplasms. The small mitotic rate of up to 10 mitoses per 10 high-power group of ‘nonductal’ pancreatic neoplasms includes fields (50 mitoses per 50 hpf) are termed well- endocrine and acinar neoplasms as well as those differentiated pancreatic endocrine neoplasms, with mixed or undetermined differentiation. These and it is this group that constitutes the majority include pancreatic endocrine neoplasms, acinar cell of PENs that come to clinical attention. Poorly carcinoma and related entities, pancreatoblastoma, differentiated endocrine carcinomas with more that and solid-pseudopapillary neoplasm. Many of these 10 mitoses per 10 hpf do arise in the pancreas but entities are highly distinctive pathologically and are very rare. clinically, and their features differ substantially As pancreatic endocrine microadenomas measure from the more commonly encountered ductal ade- less than 0.5 cm and are by definition nonfunctional, nocarcinoma. In addition, they all typically have a they rarely come to clinical attention.1,2 Patients solid, hypercellular appearance; thus, they all fall with multiple endocrine neoplasia, type 1 (MEN1) into the same differential diagnosis. Herein are typically have numerous endocrine microadenomas, presented the clinical and pathologic features of in addition to larger PENs. The prevalence of these uncommon neoplasms. sporadic microadenomas is estimated to be as high as 10% of the adult population at autopsy when numerous sections of the pancreas are examined; Pancreatic endocrine neoplasms the rate is lower (1%) when fewer sections are 3,4 Pancreatic neoplasms in which the predominant studied. Most microadenomas are identified in- line of differentiation is endocrine are designated cidentally in pancreata resected for other neoplasms or at autopsy. Endocrine microadenomas may occur at any age, but, most are found in adults as their Correspondence: Dr DS Klimstra, MD, Department of Pathology, detection usually depends upon resection of a Memorial Sloan Kettering Cancer Center, 1275 York Avenue, portion of the pancreas for some other reasons. New York, NY 10021, USA. E-mail: [email protected] Patients with MEN1 are younger when their PENs Received and accepted 3 August 2006 are detected.5 Nonductal neoplasms of the pancreas DS Klimstra S95 By contrast, cells expressing one peptide typically predominate in endocrine microadenomas. Because they share many of the histologic features of larger PENs, it is tempting to assume that microadenomas represent an earlier phase in the development of clinically relevant PENs. Certainly, all PENs must pass through a microadenoma stage as they grow to sizes greater than 0.5 cm. However, there are a number of findings including their prevalence, their peptide cell constitution, and their molecular profile that suggest that most microadenomas are not simply smaller versions of PENs. Importantly, it appears likely that most microadenomas do not progress beyond the stage of a small, biologically benign endocrine neoplasm. Well-differentiated pancreatic endocrine neo- plasms constitute one of the more interesting Figure 1 Endocrine microadenoma. This 2 mm endocrine neo- families of pancreatic neoplasms owing to the plasm is circumscribed but not encapsulated and consists of variety of paraneoplastic syndromes with which ribbons and nests of uniform cells. they may be associated. They are subclassified as functional or nonfunctional depending upon the presence or absence of such a paraneoplastic The endocrine microadenomas that are recog- syndrome. Functional PENs include insulinomas, nized grossly are circumscribed but unencapsulated glucagonomas, somatostatinomas, gastrinomas, VI- soft tan nodules averaging 1–2 mm. Microscopically, Pomas (vasoactive intestinal polypeptide-omas), endocrine microadenomas usually have a nesting serotonin secreting tumors, and other rare ectopic or trabecular architecture with minimal fibrous hormone-producing and mixed hormone-producing stroma between the neoplastic lobules (Figure 1), entities. A PEN not associated with a clinical although hyalinized amyloid-like material may syndrome is designated a nonfunctional PEN.Itis be found. The cells closely resemble normal islet important to recognize that the designation func- cells, and mitotic figures usually are not identified. tional PEN only applies to those neoplasms asso- By immunohistochemistry, microadenomas express ciated with a corresponding clinical syndrome.1 general endocrine markers including chromogranin, Many other PENs ‘function’, in the sense that they synaptophysin, and CD56. Most label for only one or produce peptide hormones that may be detected two of the four normal islet peptides, and it is in the serum or in the neoplastic cells by immuno- common to find either glucagon or PP labeling in the histochemistry;9,10 however, these ‘nonsyndromic’ majority of the cells.4 Labeling for ectopic peptides PENs are still categorized with the nonfunctional such as VIP or gastrin is uncommon. group. An exception to this rule, for historical The differential diagnosis of endocrine micro- reasons, is the PP cell PEN or PPoma,11,12 a PEN adenomas includes acinar cell nodules as well as that is demonstrated to produce predominantly PP non-neoplastic islets of Langerhans that are either by immunohistochemistry. Most such PENs also enlarged (islet hyperplasia) or distorted owing to have serum elevations of PP, but there are no chronic pancreatitis (islet aggregation). Acinar cell specific symptoms attributable to PP, so PPomas nodules6,7 are small, circumscribed collections of are technically nonsyndromic PENs, despite being cytologically altered acinar cells. Careful examina- traditionally classified with the functional group. tion reveals basal polarization of the nuclei and PENs constitute 1–2% of pancreatic neoplasms.1 apical cytoplasmic zymogen granules, distinguish- The prevalence of PENs in the general population ing acinar cell nodules from endocrine microade- is about one in 100 000.13 Although functional nomas. Because normal non-neoplastic islets vary PENs were overrepresented in older studies, non- considerably in size, occasional islets may overlap functional PENs currently comprise more than half in size with microadenomas. Furthermore, in of surgically resected cases.9 Among the functional chronic pancreatitis there is aggregation of islets variants,1 insulinomas make up 42%, gastrinomas as the exocrine elements atrophy, resulting in 24%, glucagonomas 14%, VIPomas 10%, somato- nodular collections of distorted islets and simulat- statinomas 6%, and the remaining ectopic and ing a neoplasm.8 Non-neoplastic islets retain their multiple hormone-producing neoplasms are rare.14–16 heterogeneous population of different peptide PENs are most common between the ages of 40 and cell types, and immunohistochemical labeling of 60 (mean ¼ 58)4,17 and are rare in childhood. Overall, non-neoplastic islets for the normal islet peptides both men and women develop PENs with an (insulin, glucagon, somatostatin, and pancreatic equal frequency, although there are some differences polypeptide (PP)) reveals the presence of all cell in the male-to-female ratio among the different types, in roughly normal numbers and distribution. functional types. The presenting clinical features Modern Pathology (2007) 20, S94–S112 Nonductal neoplasms of the pancreas DS Klimstra S96 depend upon the presence and type of any endo- crine paraneoplastic syndrome. A detailed descrip- tion
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