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Prognostic impact of CXCR4 and CXCR7 expression in pancreatic adenocarcinoma
Author(s) -
Gebauer Florian,
Tachezy Michael,
Effenberger Katharina,
von Loga Katharina,
Zander Hilke,
Marx Alexander,
Kaifi Jussuf T.,
Sauter Guido,
Izbicki Jakob R,
Bockhorn Maximilian
Publication year - 2011
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21957
Subject(s) - cxcr4 , medicine , chemokine receptor , pathological , tissue microarray , immunohistochemistry , chemokine , adenocarcinoma , carcinogenesis , pathology , cancer research , receptor , oncology , cancer
Background Chemokines and their receptors are known to play important roles in the tumorigenesis of many malignancies. The aim of this study was to evaluate the prognostic impact of the expression of the chemokine receptors CXCR4 and CXCR7 in patients with pancreatic adenocarcinoma (PAC). Methods Expression of CXCR4 and CXCR7 in specimens from 249 patients with PAC was evaluated by immunohistochemistry on a tissue microarray and matched with clinicopathological parameters and overall survival. Results Expression of CXCR4 was detected in 215 patients (86.4%) and CXCR7 in 47 patients (18.9%). No association between CXCR4 and CXCR7 expression was evident, although all the CXCR7 positive tumors were also CXCR4 positive. pT1/2 tumors showed a higher frequency of CXCR7 expression than pT3/4 tumors ( P  = 0.018), while more dedifferentiated tumors had elevated CXCR7 expression ( P  = 0.036). Overall and disease‐free survival revealed no association with either CXCR4 or CXCR7 expression. Conclusion CXCR7 is associated with tumor grade and inversely associated with tumor size and may play a potential role in tumor progression and differentiation. In contrast to previously reported data our results revealed no significant association between CXCR4 expression and clinical or pathological data. J. Surg. Oncol. 2011;104:140–145. © 2011 Wiley‐Liss, Inc.

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