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Low expression of CD40L in tumor-free lymph node of oral cavity cancer related with poor prognosis

Background Recently, the genetic alterations associated with tumor progression and impaired host immunity against transformed cells draw increased attention. Here, we characterized the differential gene expression patterns and protein expression in tumor-free lymph node from recurrent and non-recurr...

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Bibliographic Details
Published in:International journal of clinical oncology 2018-10, Vol.23 (5), p.851-859
Main Authors: Rah, Yoon Chan, Ahn, Jae-Cheul, Jeon, Eun-Hui, Kim, Hyojin, Paik, Jin Ho, Jeong, Woo-Jin, Kwon, Soon-Young, Ahn, Soon-Hyun
Format: Article
Language:English
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Summary:Background Recently, the genetic alterations associated with tumor progression and impaired host immunity against transformed cells draw increased attention. Here, we characterized the differential gene expression patterns and protein expression in tumor-free lymph node from recurrent and non-recurrent tumors to identify independent prognostic markers for oral squamous cell carcinoma (OSCC). Methods A cDNA microarray analysis was performed to identify the differentially expressed genes in regional tumor-free lymph nodes from OSCC patients with and without recurrence. Then, the protein expression of the selected genes was analyzed by immunohistochemistry in 60 OSCC patients to determine their association with survival. Results Widespread down-regulation of genes involved in antigen processing and recognition in lymph nodes was a distinctive feature. In univariate Kaplan–Meier analysis, lower expression of CD40L and CD80 in tumor-free lymph nodes was significantly correlated with poorer survival. In multivariate Cox regression analysis, CD40L was identified as an independent prognostic marker of disease-free survival. Conclusion Our data indicate that impaired host immunity (decreased CD40L expression) along with the TNM staging might be an important factor determining the prognosis of OSCC.
ISSN:1341-9625
1437-7772
DOI:10.1007/s10147-018-1294-3