合成寄生虫衍生肽GK1增加临床前小鼠黑色素瘤模型的存活率。

Cancer biotherapy & radiopharmaceuticals Pub Date : 2013-11-01 Epub Date: 2013-07-10 DOI:10.1089/cbr.2012.1438
Armando Pérez-Torres, Jesús Vera-Aguilera, Juan Carlos Hernaiz-Leonardo, Eduardo Moreno-Aguilera, Diego Monteverde-Suarez, Carlos Vera-Aguilera, Daniel Estrada-Bárcenas
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引用次数: 11

摘要

目的:在小鼠黑色素瘤模型中评估一种合成寄生虫衍生肽GK1的治疗效果,GK1是一种免疫反应增强剂。这种黑色素瘤模型与人类IIb期黑色素瘤相关,这种黑色素瘤通过广泛的手术切除治疗;采用手术治疗的平行研究作为指导目的进行。实验设计:C57BL/6小鼠侧腹皮下注射2×10(5) B16-F10小鼠黑色素瘤细胞。当肿瘤达到20mm3时,将小鼠分成两组;GK1组每周在瘤周注射GK1 (10 μg/100 μL无菌生理盐水),对照组每周在瘤周注射无菌生理盐水100 μL,不作进一步干预。每天监测所有小鼠的临床表现、肿瘤大小和存活率。当肿瘤大小为20 mm3 (A组)、500 mm3 (B组)和>500 mm3 (C组)时并行手术治疗。结果:GK1肽有效延长平均生存时间9.05天,相当于增加42.58%,并在治疗第3天至第12天显著延缓肿瘤生长。此外,肿瘤坏死明显增加(pp结论:GK1肽在小鼠黑色素瘤模型中显示出治疗特性,治疗导致治疗动物的平均生存时间显着增加(42.58%)。GK1作为实验性和人类癌症化疗鸡尾酒疗法的主要或辅助成分的潜力仍有待确定,手术切除对于小鼠模型黑色素瘤的任何新的实验性治疗仍然是一个挑战。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The synthetic parasite-derived peptide GK1 increases survival in a preclinical mouse melanoma model.

The synthetic parasite-derived peptide GK1 increases survival in a preclinical mouse melanoma model.

The synthetic parasite-derived peptide GK1 increases survival in a preclinical mouse melanoma model.

The synthetic parasite-derived peptide GK1 increases survival in a preclinical mouse melanoma model.

Purpose: The therapeutic efficacy of a synthetic parasite-derived peptide GK1, an immune response booster, was evaluated in a mouse melanoma model. This melanoma model correlates with human stage IIb melanoma, which is treated with wide surgical excision; a parallel study employing a surgical treatment was carried out as an instructive goal.

Experimental design: C57BL/6 mice were injected subcutaneously in the flank with 2×10(5) B16-F10 murine melanoma cells. When the tumors reached 20 mm3, mice were separated into two different groups; the GK1 group, treated weekly with peritumoral injections of GK1 (10 μg/100 μL of sterile saline solution) and the control group, treated weekly with an antiseptic peritumoral injection of 100 μL of sterile saline solution without further intervention. All mice were monitored daily for clinical appearance, tumor size, and survival. Surgical treatment was performed in parallel when the tumor size was 20 mm3 (group A), 500 mm3 (group B), and >500 mm3 (group C).

Results: The GK1 peptide effectively increased the mean survival time by 9.05 days, corresponding to an increase of 42.58%, and significantly delayed tumor growth from day 3 to 12 of treatment. In addition, tumor necrosis was significantly increased (p<0.05) in the treated mice. The overall survival rates obtained with surgical treatment at 6 months were 83.33% for group A, 40% for group B, and 0% for group C, with significant differences (p<0.05) among the groups.

Conclusions: The GK1 peptide demonstrated therapeutic properties in a mouse melanoma model, as treatment resulted in a significant increase in the mean survival time of the treated animals (42.58%). The potential for GK1 to be used as a primary or adjuvant component of chemotherapeutic cocktails for the treatment of experimental and human cancers remains to be determined, and surgical removal remains a challenge for any new experimental treatment of melanoma in mouse models.

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