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BMC Cancer  2007 

Expression of CD80 and CD86 costimulatory molecules are potential markers for better survival in nasopharyngeal carcinoma

DOI: 10.1186/1471-2407-7-88

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Abstract:

Expression of CD80, CD86, HLA-DR, S-100 protein and the presence of infiltrating lymphocytes and follicular dendritic reticulum cells were immunohistochemically examined on the paraffin-embedded tissue blocks from newly diagnosed NPC patients (n = 50). The results were correlated with clinical outcome of patients.CD80 and CD86 were each expressed in 10 of 50 cases in which they co-expressed in 9 cases. Univariate analysis revealed that patients with CD80/CD86 expression had significantly better overall survival than those without it (P = 0.017), but after adjustment for stage, nodal status, and treatment, the expression of CD80/CD86 did not significantly correlate with overall survival. Expression of HLA-DR and the presence of infiltrating lymphocytes and dendritic cells did not appear to have impact on the survival of patients.Expression of CD80 and CD86 costimulatory molecules appears to be a marker of better survival in patient with NPC.Nasopharyngeal carcinoma (NPC) is a neoplasm with high incidence in Southeast Asia, the Mediterranean basin, and North Africa. Early-stage NPC is usually treated with radiotherapy alone, and combination of chemotherapy is effective in the more advanced-stages of NPC [1-4]. Identification of a pathobiological correlate of clinical behavior of NPC represents a challenge. The development of such a test may improve the outcome of treatment as high-risk patients could benefit from early intervention and aggressive treatment.B7 Costimulatory molecules are membrane-bound molecules which play a decisive role in the activation of T cells. This costimulatory pathway involves the interaction of two distinct B7 molecules, B7-1 (CD80) and B7-2 (CD86), which are transmembrane glycoprotein members of the Ig superfamily [5-7] expressed on antigen-presenting cells with their T cell counter receptors CD28 and CTLA-4 [8]. Interaction of B7:CD28 has been shown to provide a critical signal for T cell activation, while the absence of this signal result

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