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| Mismatch repair proteins and microsatellite instability in solid pseudopapillary neoplasm of the pancreas |
| Claudia Covelli a , ∗, Paola Parente a , Francesco Pepe b , Pasquale Pisapia b , Fabiola Fiordelisi a , Umberto Malapelle b |
a UOC di Anatomia Patologica, Fondazione Casa Sollievo della Sofferenza, Viale Cappuccini 1, 71013 San Giovanni Rotondo, FG, Italy
b Department of Public Health, University of Naples Federico II, Via Pansini 5, 80131 Napoli, Italy
∗ Corresponding author.
E-mail address: c.covelli@operapadrepio.it (C. Covelli). |
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Abstract Solid pseudopapillary neoplasms (SPNs) are rare solid pancreatic tumors mainly affecting young women. Despite the high percentage of favorable prognosis, they are considered as low grade malignant neoplasms, and metastases occur in 5%−15% of patients. Almost all SPNs (95%) have somatic activating mutations in the β-catenin gene [1] . β-catenin plays a crucial role in cell proliferation and differentiation via Wnt signaling pathway and interacts with E-cadherin and α-catenin for the regulation of cell adhesion and growth [2] . Another relevant genetic alteration in pancreatic neoplasms is represented by the DNA mismatch repair deficiency (dMMR). dMMR is strongly associated with a microsatellite instability (MSI) status as a result of an alteration in the lengths of microsatellites due to deletion/insertion of repeating units in tumor DNA [3] . dMMR was observed in approximately 1%−2% of patients with pancreatic adenocarcinoma [4] . To date, the “gold standard” for the evaluation of protein integrity of MMR is immunohistochemistry (IHC), showing an analytical sensitivity > 90%, specificity of 100% and predictive value of 97% for microsatellite stability (MSS) and 100% for MSI [5] . The study aimed to investigate the expression of MMR proteins and the MSI status in pancreatic SPNs.
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2019, Vol. 18 
