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食管鳞状细胞癌中白细胞浸润及热休克蛋白70表达的免疫组织化学研究

Immunohistochemical study of leukocyte infiltration and expression of hsp70 in esophageal squamous cell carcinoma.

作者信息

Takeno S, Noguchi T, Kikuchi R, Wada S, Sato T, Uchida Y

机构信息

Department of Surgery II, Oita Medical University, Hasama-machi, Oita 879-5593, Japan.

出版信息

Oncol Rep. 2001 May-Jun;8(3):585-90. doi: 10.3892/or.8.3.585.

DOI:10.3892/or.8.3.585
PMID:11295085
Abstract

It is reported that macrophages and CD4+ or CD8+ cytotoxic T cells have an important role in the suppression of cancer progression. The aim of this study was to clarify these immune responses in patients with esophageal cancer. We enrolled 28 patients with pT2 esophageal cancer that had been resected without preoperative adjuvant therapy. The correlations between the numbers of infiltrating CD4+, CD8+ and CD68+ cells, the expression of heat shock protein 70 (hsp70) and a variety of clinicopathologic factors were analyzed. The numbers of CD8+ T cells and CD68+ macrophages showed a significant positive correlation with tumor diameter (p = 0.01, p = 0.037) and the expression of hsp70 (p = 0.01, p = 0.02) and a negative correlation with lymph node metastasis (p = 0.0079, p < 0.0001). The expression of hsp70 exhibited a negative correlation with lymph node metastasis (p = 0.023). CD8+ T cells and CD68+ macrophages might have a suppressive function against esophageal cancer progression. Our results suggested that hsp70 might play an important role in the presentation of tumor specific antigens.

摘要

据报道,巨噬细胞以及CD4+或CD8+细胞毒性T细胞在抑制癌症进展中发挥着重要作用。本研究的目的是阐明食管癌患者的这些免疫反应。我们纳入了28例未经术前辅助治疗而接受手术切除的pT2期食管癌患者。分析了浸润的CD4+、CD8+和CD68+细胞数量、热休克蛋白70(hsp70)的表达与各种临床病理因素之间的相关性。CD8+ T细胞和CD68+巨噬细胞的数量与肿瘤直径(p = 0.01,p = 0.037)以及hsp70的表达(p = 0.01,p = 0.02)呈显著正相关,与淋巴结转移呈负相关(p = 0.0079,p < 0.0001)。hsp70的表达与淋巴结转移呈负相关(p = 0.023)。CD8+ T细胞和CD68+巨噬细胞可能对食管癌进展具有抑制作用。我们的结果表明,hsp70可能在肿瘤特异性抗原的呈递中发挥重要作用。

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Cell Stress Chaperones. 2006 Spring;11(1):34-43. doi: 10.1379/csc-159r.1.
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World J Gastroenterol. 2005 Nov 14;11(42):6689-93. doi: 10.3748/wjg.v11.i42.6689.