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Rsf‐1/HBXAP overexpression is associated with disease‐specific survival of patients with gallbladder carcinoma

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Chen T‐J, Huang S‐C, Huang H‐Y, Wei Y‐C, Li C‐F. Rsf‐1/HBXAP overexpression is associated with disease‐specific survival of patients with gallbladder carcinoma. APMIS 2011; 119: 808–14.

Dysregulated chromatin remodeling often leads to abnormal gene expression or silencing in cells, thereby implicating tumor development and progression. As a subunit of remodeling and spacing factor (RSF) complex, Rsf‐1, a novel nuclear protein with histone chaperon function, mediates ATPase‐dependent chromatin remodeling and confer tumor aggressiveness in common carcinomas. We aimed, for the first time, to evaluate the Rsf‐1 expression status and its associations with clinicopathological features and patient survival in a well characterized cohort of gallbladder carcinomas. Using tissue microarray‐based immunohistochemistry, we assessed Rsf‐1 expression in gallbladder carcinomas, yielding 88 cases undergoing surgical intervention with interpretable results. The Rsf‐1 overexpression, present in 61 cases (69.3%), was significantly associated with higher histological grades (p = 0.002) and vascular invasion (p = 0.037) and marginally with non‐papillary histotypes (p = 0.058). In univariate log‐rank analysis, Rsf‐1 overexpression was significantly predictive of disease‐specific survival (p = 0.0015), which remained prognostically independent [p = 0.0191, risk ratio (RR) = 2.683], along with American Joint Committee on Cancer stages II–IV (p = 0.0265, RR = 2.102). Our findings indicate that Rsf‐1 overexpression is common and associated with adverse prognosticators in gallbladder carcinomas. It may confer tumor aggressiveness through chromatin remodeling and represents a potential prognostic biomarker of gallbladder carcinomas.
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Document Type: Research Article

Affiliations: Department of Pathology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung

Publication date: November 1, 2011

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