Clinical and immunohistochemical features of 34 solid pseudopapillary tumors of the pancreas
Article first published online: 25 JAN 2011
© 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd
Journal of Gastroenterology and Hepatology
Volume 26, Issue 2, pages 267–274, February 2011
How to Cite
Nguyen, N. Q., Johns, A. L., Gill, A. J., Ring, N., Chang, D. K., Clarkson, A., Merrett, N. D., Kench, J. G., Colvin, E. K., Scarlett, C. J. and Biankin, A. V. (2011), Clinical and immunohistochemical features of 34 solid pseudopapillary tumors of the pancreas. Journal of Gastroenterology and Hepatology, 26: 267–274. doi: 10.1111/j.1440-1746.2010.06466.x
- Issue published online: 25 JAN 2011
- Article first published online: 25 JAN 2011
- Accepted manuscript online: 12 AUG 2010 10:49AM EST
- Accepted for publication 26 July 2010.
- solid pseudopapillary tumors
Background and Aim: Clinicopathological data regarding pancreatic solid pseudopapillary tumors (SPT) in a multiethnic country are limited. The aim of the present study was to characterize pancreatic SPT in Australia.
Methods: Clinicopathological features, treatment, immunohistochemical findings and outcome data of 34 patients (79% Caucasian, 12% Asian, 6% South Pacific Islander and 3% African) with pancreatic SPT were reviewed.
Results: The most presenting complaint was abdominal pain. Median diameter of tumors was 60 mm (range: 20–220); predominantly located in the pancreatic tail (tail : body : head = 23:3:8). All tumors were resected and patients underwent surgery, including a liver resection for metastasis, all patients were alive after a median follow up of 70 months (IQR: 48–178). Two patients underwent repeated surgery for local recurrences with liver metastases after 8 and 18 months, which were successfully managed by surgical resection. Completeness of excision, perineural spread, vascular space invasion, mitotic rate and cellular atypia did not predict recurrence. In all cases, there was aberrant nuclear staining of beta-catenin and a loss of membranous expression of E-cadherin with aberrant nuclear localization of the cytoplasmic domain. Most pancreatic SPT were also strongly positive for CD10 (96%), progesterone receptor (79%), cytokeratin (28%), synapthophysin (26%) and chromogranin (15%).
Conclusions: Pancreatic SPT occur in all races and are uniformly indolent. Given complete resection of a pancreatic SPT is usually curative and recurrences can be treated with re-operation, correct diagnosis is important.