预处理自然杀伤抗原密度与长期皮下注射重组白细胞介素-2和重组干扰素- α的肿瘤患者的临床反应相关。

Molecular biotherapy Pub Date : 1992-12-01
S Duensing, M Hadam, A Körfer, A Schomburg, T Menzel, J Grosse, H Kirchner, H Poliwoda, J Atzpodien
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引用次数: 0

摘要

我们评估了47例晚期肾癌患者循环NK细胞中自然杀伤(NK)细胞相关CD56抗原的密度。患者接受低剂量皮下重组白介素-2 (il -2)和重组干扰素- α (rifn - α)联合治疗作为家庭治疗。治疗前完全或部分缓解的患者的CD56抗原密度比在治疗中出现疾病进展的患者高2.2倍(P < 0.005)。治疗周期6周后,治疗应答者的NK细胞显著表达(2.1倍;P < 0.005)无反应患者的CD56抗原高于NK细胞。这些结果表明,治疗前和治疗后NK抗原密度水平的潜在作用与治疗反应具有生物学相关性。
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Pretreatment natural killer antigen density correlates to clinical response in tumor patients receiving long-term subcutaneous recombinant interleukin-2 and recombinant interferon-alpha.

We evaluated density of the natural killer (NK) cell-associated CD56 antigen on circulating NK cells of 47 patients with advanced renal cell carcinoma. Patients received a combination of low-dose subcutaneous recombinant interleukin-2 (rIL-2) and recombinant interferon-alpha (rIFN-alpha) as home therapy. Antigen density of CD56 before therapy was 2.2-fold higher (P < 0.005) in patients who subsequently achieved a complete or partial remission when compared with patients who presented with progressive disease on therapy. After a 6-week treatment cycle, NK cells of treatment responders expressed significantly (2.1-fold; P < 0.005) more CD56 antigens than NK cells in nonresponding patients. These results suggested a potential role of both pre- and posttreatment NK antigen density levels as a biologic correlate to treatment response.

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Innovation in science. Pretreatment natural killer antigen density correlates to clinical response in tumor patients receiving long-term subcutaneous recombinant interleukin-2 and recombinant interferon-alpha. The role of cytokines in tumor immunotherapy. Report on the 2nd Frankfurt International Cytokine Symposium 25-27 June 1992, Frankfurter Hof, Frankfurt, Germany. Relation between the biologic activities and chemical structures of synthetic microbial lipopeptide analogs in mice. Antitumor effect of recombinant human tumor necrosis factor-alpha analog combined with desmuramyl dipeptides LK-409 or LK-410 on sarcoma in mice.
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