Papillary Cystic Tumor of the Pancreas: <i>A Clinicopathologic Study of 20 Cases with Cytologic, Immunohistochemical, Ultrastructural, and Flow Cytometric Observations, and a Review of the Literature</i>

Pettinato, Guido; Jc, Manivel; Ravetto, C; Terracciano, Luigi; Ew, Gould; A, di Tuoro; Jaszcz, W; Albores‐Saavedra, Jorge

doi:10.1093/ajcp/98.5.478

Cited by 199 publications

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“…Of the five cases with the most chromosomal alterations (five or more, cases [8][9][10][11][12], all (100%) had indicators of aggressive behavior: four had aggressive histologic features and one was a 9.9 cm tumor (Tables 1 and 2). Statistical analysis demonstrated a significant correlation between the presence of one or more aggressive feature and the frequency of chromosomal abnormalities (P ¼ 0.024, Mann-Whitney U-test).…”

Section: Resultsmentioning

confidence: 99%

“…Both aneuploid and diploid tumors have been detected by flow cytometry. 3,6,[8][9][10][11] Various chromosomal abnormalities have also been reported, primarily using cytogenetic techniques. [12][13][14][15][16] Two studies using comparative genomic hybridization (CGH) found no chromosomal gains or losses, 11,17 while in another study of one case using the more sensitive array CGH technique, two alterations were detected: loss of heterozygosity for HRAS in chromosome band 11p15.5 and a less significant loss of the short arm of chromosome 16.…”

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confidence: 99%

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Array comparative genomic hybridization analysis of solid pseudopapillary neoplasms of the pancreas

et al. 2008

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Solid pseudopapillary neoplasms of the pancreas are low-grade malignancies, but their biological behavior cannot be stratified solely on the basis of histopathologic criteria. Aside from mutations in b-catenin and lack of genetic changes common to pancreatic ductal adenocarcinomas, little is known about the chromosomal alterations in solid pseudopapillary neoplasms. We applied array comparative genomic hybridization to a series of 12 patients. The average age was 31 years (range 12-52 years) with 10 female and 2 male patients. The average tumor size was 7.3 cm (range 2-24 cm) with five lesions greater than 5 cm. All cases had 'bland' cytology without significant pleomorphism or high nuclear grade, but seven cases demonstrated at least one of these potentially aggressive histopathologic features: size 45 cm, tumor necrosis, lymphovascular invasion, perineural invasion and peripancreatic invasion. Clinically, one lesion demonstrated aggressive behavior. By array comparative genomic hybridization, chromosomal losses and/or gains were identified in eight cases; five cases had multiple (five or more) alterations. The most common alterations were gains at 13q, 17q, 1q and 8q. Six of the seven cases with at least one aggressive feature had genetic alterations, while only two cases without adverse features had genetic alterations (P ¼ 0.024). The single clinically aggressive tumor exhibited seven chromosomal gains and four aggressive histopathologic features. Our study demonstrates that genetic alterations detected by array comparative genomic hybridization are common in solid pseudopapillary neoplasms of the pancreas. Additional study and longer follow-up are needed to determine if these genetic abnormalities could help predict clinical behavior in these neoplasms.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

Array comparative genomic hybridization analysis of solid pseudopapillary neoplasms of the pancreas

et al. 2008

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“…Microscopically, the tumor cells in 'solid' areas are uniform, arranged in sheets and cords around fibrovascular septa; whereas those in 'pseudopapillary' areas show degenerative changes in the cells away from the vasculature. [4][5][6][7][8] Despite its characteristic microscopic appearance and recent studies of this type of tumor for molecular changes, 9 the immunophenotype of markers is not specific and does not define a line of differentiation corresponding to any normal pancreatic cell type.…”

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confidence: 99%

Loss of cell-adhesion molecule complexes in solid pseudopapillary tumor of pancreas

et al. 2007

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Solid pseudopapillary tumor of pancreas (SPT) is a rare neoplasm that occurs most often in young females with the two distinct features, the 'solid-cystic' gross appearance, and the 'solid-pseudopapillary' microscopic pattern. It has been reported that almost all SPT tumors contain a mutation in the b-catenin gene; however, the histogenetic origin of this tumor remains largely a mystery. E-cadherin is a cell adhesion molecule that links to catenins to form cell adhesion junctions, which is associated with the cytoskeleton formation. In this study, we examined the expression of E-cadherin and b-catenin from SPT in an attempt to determine the molecular basis for the unusual morphology of this tumor. Nine cases of SPT were retrieved from Surgical Pathologic Archives of three institutions, including one male and eight females. H&E slides of each case were reviewed to confirm the diagnosis. The b-catenin gene was sequenced in one case. E-cadherin and b-catenin immunostains, were performed on all nine cases. Sequencing analysis on one case showed a point mutation of the b-catenin gene, confirming previous findings that almost all SPT tumors contain mutation in the b-catenin gene. Immunostains showed that, in both solid and pseudopapillary areas, all the tumor cells lost expression of E-cadherin, and bcatenin nuclear expression was observed in all cases. Our findings suggest that loss of cytoplasmic b-catenin protein in the cell adhesion complex due to b-catenin gene mutation, results in instability of the complex, loss of E-cadherin in cell membrane, and eventually dissociation of the tumor cells to form the pseudopapillary pattern. Modern Pathology (2007) 20, 509-513.

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“…The solid pseudopapillary tumor of the pancreas is still an enigma (42); it is a rare tumor of uncertain histogenesis and undetermined differentiation (8) and with low malignant potential. The tumor is likely derived from a pluripotent indifferent stem cell capable of both endocrine and exocrine differentiation.…”

Section: Discussionmentioning

confidence: 99%

“…Flow cytometric analyses have shown that most tumors are diploid (3,8,44), although focal aneuploidy may be found after extensive sampling (44). Two tumors with metastatic disease were DNA aneuploid (3,4).…”

Section: Discussionmentioning

confidence: 99%

Deregulated Expression of Cell Cycle–Associated Proteins in Solid Pseudopapillary Tumor of the Pancreas

2001

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Solid pseudopapillary tumor of the pancreas was studied in a 20-year-old woman and a 54-year-old woman. In the younger patient, the tumor had metastasized to the liver 8 years after distal pancreatectomy. In both neoplasms, the distinct histologic pattern of solid, pseudopapillary, and degenerative cystic areas was present. Analysis by means of immunohistochemistry revealed a diffuse expression for vimentin, neuron-specific enolase, and a focal positivity for ␣1-antitrypsin, whereas epithelial markers were negative in the tumor of the older patient and only focally expressed in the tumor of the younger patient. Immunohistochemical analysis of cell cycle-associated proteins provided an overexpression of cyclin D1 and cyclin D3 in both tumors, although to varying degrees. In addition, the cyclin-dependent kinase inhibitors p21, and to a lesser extent p27, were up-regulated just as mdm2. There was no accumulation of p53 protein, and Ki67-positive cells were extremely scarce. Analysis of the liver metastases showed an immunoreactive profile similar to that of the primary tumor. The results show a deregulation of the cell cycle with overexpression of cell cycle-activating proteins D1 and D3 and a probably counterbalancing upregulation of the cyclin-dependent kinase inhibitors p21 and p27. The findings may explain the low pool of Ki67-reactive tumor cells and the generally good clinical outcome of these tumors. Whether a more profound dysbalance of the cell cycle regulation is responsible for the development of metastatic disease remains to be clarified.

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Papillary Cystic Tumor of the Pancreas: A Clinicopathologic Study of 20 Cases with Cytologic, Immunohistochemical, Ultrastructural, and Flow Cytometric Observations, and a Review of the Literature

Cited by 199 publications

References 0 publications

Array comparative genomic hybridization analysis of solid pseudopapillary neoplasms of the pancreas

Array comparative genomic hybridization analysis of solid pseudopapillary neoplasms of the pancreas

Loss of cell-adhesion molecule complexes in solid pseudopapillary tumor of pancreas

Deregulated Expression of Cell Cycle–Associated Proteins in Solid Pseudopapillary Tumor of the Pancreas

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