Expression and prognosis value of SHP2 in patients with pancreatic ductal adenocarcinoma
- 242 Downloads
SHP2 is an src homology (SH) 2 domain-containing protein tyrosine phosphatase (PTP). SHP2 implicitly contributes to tumorigenesis, but the role of SHP2 in pancreatic ductal adenocarcinoma is still unknown. The purpose of this study was to evaluate the prognostic significance and associated expression of SHP2 in pancreatic ductal adenocarcinoma (PDAC) patients. We used immunohistochemistry to assess the protein expression levels of SHP2 in 79 PDAC specimens. The correlations between SHP2 expression and various clinicopathological features were evaluated by Pearson’s chi-square (χ 2) test, Fisher’s exact test, and Spearman’s rank. Univariate and multivariate Cox regression analyses were used to identify correlations between the immunohistochemical data for SHP2 expression and the clinicopathologic characteristics in PDAC. Kaplan-Meier survival analysis was used to demonstrate the relation between overall survival and the expression of SHP2. Immunohistochemistry revealed significantly higher rates of high SHP2 expression in PDAC tissues (55.7 %) versus adjacent non-cancer tissues (10.1 %) (P < 0.05). Expression of SHP2 was only significantly correlated with histological differentiation (P = 0.033) and vital status (P = 0.025). Patients with high SHP2 expression had shorter overall survival times compared to those with low SHP2 expression (P = 0.000). Multivariate Cox regression analysis revealed that SHP2 overexpression was an independent prognostic factor in PDAC (P = 0.012). Our study demonstrated for the first time that higher expression of SHP2 might be involved in the progression of pancreatic ductal adenocarcinoma, suggesting that SHP2 may be a potential prognostic marker and target for therapy.
KeywordsSHP2 Pancreatic ductal adenocarcinoma Prognosis Survival
Compliance with ethical standards
This study was approved by the Ethics Review Committee of the Fuzhou General Hospital of Nanjing Military Command, and each patient signed an informed consent form before enrollment into the study.
Conflicts of interest
This work was funded by grants from the National Natural Science Foundation of China (No. 81302067 and No. 81302164).
- 26.Leibowitz MS, Srivastava RM, Andrade FP, Egloff AM, Wang L, Seethala RR, et al. SHP2 is overexpressed and inhibits pSTAT1-mediated APM component expression, T-cell attracting chemokine secretion, and CTL recognition in head and neck cancer cells. Clin Cancer Res. 2013;19:798–808.CrossRefPubMedPubMedCentralGoogle Scholar
- 30.Tempero MA, Arnoletti JP, Behrman S, Ben-Josef E, Benson AR, Berlin JD, et al. Pancreatic adenocarcinoma. J Natl Compr Cancer Netw. 2010;8:972–1017.Google Scholar
- 32.Aceto N, Sausgruber N, Brinkhaus H, Gaidatzis D, Martiny-Baron G, Mazzarol G, et al. Tyrosine phosphatase SHP2 promotes breast cancer progression and maintains tumor-initiating cells via activation of key transcription factors and a positive feedback signaling loop. Nat Med. 2012;18:529–37.CrossRefPubMedGoogle Scholar