Choudhary Alka, Zachek Brittany, Lera Robert F, Zasadil Lauren M, Lasek Amber, Denu Ryan A, Kim Hyunjung, Kanugh Craig, Laffin Jennifer J, Harter Josephine M, Wisinski Kari B, Saha Sandeep, Weaver Beth A, Burkard Mark E
University of Wisconsin Carbone Cancer Center, University of Wisconsin, Madison, Wisconsin. Hematology/Oncology Division, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
University of Wisconsin Carbone Cancer Center, University of Wisconsin, Madison, Wisconsin. Department of Cell and Regenerative Biology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Mol Cancer Ther. 2016 Jan;15(1):48-59. doi: 10.1158/1535-7163.MCT-15-0527. Epub 2015 Nov 19.
Increased ploidy is common in tumors but treatments for tumors with excess chromosome sets are not available. Here, we characterize high-ploidy breast cancers and identify potential anticancer compounds selective for the high-ploidy state. Among 354 human breast cancers, 10% have mean chromosome copy number exceeding 3, and this is most common in triple-negative and HER2-positive types. Women with high-ploidy breast cancers have higher risk of recurrence and death in two patient cohorts, demonstrating that it represents an important group for improved treatment. Because high-ploidy cancers are aneuploid, rather than triploid or tetraploid, we devised a two-step screen to identify selective compounds. The screen was designed to assure both external validity on diverse karyotypic backgrounds and specificity for high-ploidy cell types. This screen identified novel therapies specific to high-ploidy cells. First, we discovered 8-azaguanine, an antimetabolite that is activated by hypoxanthine phosphoribosyltransferase 1 (HPRT1), suggesting an elevated gene-dosage of HPRT1 in high-ploidy tumors can control sensitivity to this drug. Second, we discovered a novel compound, 2,3-diphenylbenzo[g]quinoxaline-5,10-dione (DPBQ). DPBQ activates p53 and triggers apoptosis in a polyploid-specific manner, but does not inhibit topoisomerase or bind DNA. Mechanistic analysis demonstrates that DPBQ elicits a hypoxia gene signature and its effect is replicated, in part, by enhancing oxidative stress. Structure-function analysis defines the core benzo[g]quinoxaline-5,10 dione as being necessary for the polyploid-specific effects of DPBQ. We conclude that polyploid breast cancers represent a high-risk subgroup and that DPBQ provides a functional core to develop polyploid-selective therapy. Mol Cancer Ther; 15(1); 48-59. ©2015 AACR.
倍性增加在肿瘤中很常见,但针对具有额外染色体组的肿瘤的治疗方法尚不存在。在此,我们对高倍体乳腺癌进行了特征描述,并鉴定了对高倍体状态具有选择性的潜在抗癌化合物。在354例人类乳腺癌中,10%的肿瘤平均染色体拷贝数超过3,这在三阴性和HER2阳性类型中最为常见。在两个患者队列中,患有高倍体乳腺癌的女性复发和死亡风险更高,这表明它是需要改进治疗的重要群体。由于高倍体癌症是非整倍体,而非三倍体或四倍体,我们设计了一个两步筛选来鉴定选择性化合物。该筛选旨在确保在不同核型背景下的外部有效性以及对高倍体细胞类型的特异性。该筛选鉴定出了针对高倍体细胞的新型疗法。首先,我们发现了8-氮杂鸟嘌呤,一种由次黄嘌呤磷酸核糖基转移酶1(HPRT1)激活的抗代谢物,这表明高倍体肿瘤中HPRT1基因剂量的增加可控制对该药物的敏感性。其次,我们发现了一种新型化合物,2,3-二苯基苯并[g]喹喔啉-5,10-二酮(DPBQ)。DPBQ以多倍体特异性方式激活p53并触发细胞凋亡,但不抑制拓扑异构酶或结合DNA。机制分析表明,DPBQ引发缺氧基因特征,其作用部分通过增强氧化应激得以重现。结构-功能分析确定核心苯并[g]喹喔啉-5,10-二酮对于DPBQ的多倍体特异性作用是必需的。我们得出结论,多倍体乳腺癌代表一个高危亚组,并且DPBQ为开发多倍体选择性疗法提供了一个功能核心。《分子癌症治疗》;15(1);48 - 59。©2015美国癌症研究协会。