赫赛汀耐药性乳腺癌细胞的发展。

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Kute T,缺乏厘米,威林汉M, Bishwokama B,威廉姆斯H,巴雷特K,米切尔T,沃恩JP

赫赛汀耐药性乳腺癌细胞的发展。

血细胞计数a . 2004年2月,57 (2):86 - 93。

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14750129 (在PubMed

]

文摘

背景:赫赛汀,her - 2的人源化抗体,现在用于转移性乳腺癌治疗的诊所。her - 2 +的患者只有30%的反应率和耐药机制被称为。赫赛汀行动的机制也未知但一直与细胞周期抑制有关。方法:赫赛汀和其他抗体治疗的影响取决于细胞计数和细胞周期分析。her - 2和p27表达水平进行了分析通过流式细胞术和AKT激活水平相比,免疫印迹分析。免疫荧光细胞her - 2和p27表达测定。结果:赫赛汀治疗bt - 474细胞,导致细胞生长的抑制和逮捕在G1期。增长的功效被逮捕并不是直接相关的her - 2抗体的亲和力。我们实验室已经开发了耐赫赛汀治疗的细胞系。在耐药细胞株,绑定的抗体不受阻。 However, Herceptin has completely lost the ability to inhibit cell proliferation. Yet, the mouse isotype 4D5 maintains significant inhibitory activity upon Herceptin-resistant clones. CONCLUSIONS: Herceptin binds effectively to Her-2 on the cell surface of Herceptin-resistant cell lines and the level of Her-2 expression on the cell surface is not downregulated. Herceptin resistance is not due to downregulation of levels of AKT protein expression, although, phosphorylation of AKT is enhanced in resistant lines and could have a role in resistance. Resistance appears to correlate with the loss of nuclear expression of the cyclin-dependent kinase inhibitor, p27, as defined by immunofluorescence and flow cytometry studies and cdk-2 binding studies.

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