鉴定整合素连接激酶（ILK）作为急性和慢性髓系白血病的新型治疗靶点。
Identification of ILK as a novel therapeutic target for acute and chronic myeloid leukemia.
作者信息
de la Puente Pilar, Weisberg Ellen, Muz Barbara, Nonami Atsushi, Luderer Micah, Stone Richard M, Melo Junia V, Griffin James D, Azab Abdel Kareem
机构信息
Department of Radiation Oncology, Cancer Biology Division, Washington University in Saint Louis School of Medicine, St. Louis, MO, USA.
Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
出版信息
Leuk Res. 2015 Sep 9. doi: 10.1016/j.leukres.2015.09.005.
Current treatment options as well as clinical efficacy are limited for chronic myelogenous leukemia (CML), Ph+ acute lymphoblastic leukemia (ALL), and acute myeloid leukemia (AML). In response to the pressing need for more efficacious treatment approaches and strategies to override drug resistance in advanced stage CML, Ph+ ALL, and AML, we investigated the effects of inhibition of ILK as a potentially novel and effective approach to treatment of these challenging malignancies. Using the small molecule ILK inhibitor, Cpd22, and ILK knockdown, we investigated the importance of ILK in the growth and viability of leukemia. Our results suggest that the ILK inhibition may be an effective treatment for CML, Ph+ ALL, and AML as a single therapy, with ILK expression levels positively correlating with the efficacy of ILK inhibition. The identification of ILK as a novel target for leukemia therapy warrants further investigation as a therapeutic approach that could be of potential clinical benefit in both acute and chronic myeloid leukemias.
目前，慢性粒细胞白血病（CML）、Ph+急性淋巴细胞白血病（ALL）和急性髓系白血病（AML）的治疗选择及临床疗效都很有限。为了应对晚期CML、Ph+ ALL和AML中对更有效治疗方法及克服耐药性策略的迫切需求，我们研究了抑制整合素连接激酶（ILK）作为治疗这些具有挑战性恶性肿瘤的潜在新方法的效果。使用小分子ILK抑制剂Cpd22和ILK基因敲低技术，我们研究了ILK在白血病生长和存活中的重要性。我们的结果表明，抑制ILK可能作为单一疗法对CML、Ph+ ALL和AML有效，且ILK表达水平与ILK抑制疗效呈正相关。将ILK鉴定为白血病治疗的新靶点，作为一种可能对急性和慢性髓系白血病都有潜在临床益处的治疗方法，值得进一步研究。
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