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SETting OP449 into the PP2A-activating drug family.将OP449归入PP2A激活药物家族。
Clin Cancer Res. 2014 Apr 15;20(8):2026-8. doi: 10.1158/1078-0432.CCR-14-0166. Epub 2014 Mar 14.
2
Antagonism of SET using OP449 enhances the efficacy of tyrosine kinase inhibitors and overcomes drug resistance in myeloid leukemia.使用OP449拮抗SET可增强酪氨酸激酶抑制剂的疗效并克服髓系白血病中的耐药性。
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3
Targeting inhibitors of the tumor suppressor PP2A for the treatment of pancreatic cancer.靶向肿瘤抑制因子PP2A的抑制剂用于治疗胰腺癌。
Mol Cancer Res. 2014 Jun;12(6):924-39. doi: 10.1158/1541-7786.MCR-13-0542. Epub 2014 Mar 25.
4
Combined targeting of SET and tyrosine kinases provides an effective therapeutic approach in human T-cell acute lymphoblastic leukemia.联合靶向SET和酪氨酸激酶为人类T细胞急性淋巴细胞白血病提供了一种有效的治疗方法。
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本文引用的文献

1
Antagonism of SET using OP449 enhances the efficacy of tyrosine kinase inhibitors and overcomes drug resistance in myeloid leukemia.使用OP449拮抗SET可增强酪氨酸激酶抑制剂的疗效并克服髓系白血病中的耐药性。
Clin Cancer Res. 2014 Apr 15;20(8):2092-103. doi: 10.1158/1078-0432.CCR-13-2575. Epub 2014 Jan 16.
2
PP2A-activating drugs selectively eradicate TKI-resistant chronic myeloid leukemic stem cells.PP2A 激活剂药物选择性根除 TKI 耐药性慢性髓性白血病干细胞。
J Clin Invest. 2013 Oct;123(10):4144-57. doi: 10.1172/JCI68951. Epub 2013 Sep 3.
3
Antagonistic activities of the immunomodulator and PP2A-activating drug FTY720 (Fingolimod, Gilenya) in Jak2-driven hematologic malignancies.免疫调节剂和 PP2A 激活药物 FTY720（芬戈莫德，Gilenya）在 Jak2 驱动的血液系统恶性肿瘤中的拮抗作用。
Blood. 2013 Sep 12;122(11):1923-34. doi: 10.1182/blood-2013-03-492181. Epub 2013 Aug 7.
4
Protein phosphatase 2A: a target for anticancer therapy.蛋白磷酸酶 2A：抗癌治疗的靶点。
Lancet Oncol. 2013 May;14(6):e229-38. doi: 10.1016/S1470-2045(12)70558-2.
5
A potential therapeutic application of SET/I2PP2A inhibitor OP449 for canine T-cell lymphoma.SET/I2PP2A抑制剂OP449在犬T细胞淋巴瘤中的潜在治疗应用。
J Vet Med Sci. 2013;75(3):349-54. doi: 10.1292/jvms.12-0366. Epub 2012 Nov 5.
6
Overexpression of SET is a recurrent event associated with poor outcome and contributes to protein phosphatase 2A inhibition in acute myeloid leukemia.SET 的过表达是与不良预后相关的复发性事件，并导致急性髓系白血病中蛋白磷酸酶 2A 的抑制。
Haematologica. 2012 Apr;97(4):543-50. doi: 10.3324/haematol.2011.050542. Epub 2011 Dec 1.
7
Apolipoprotein E and peptide mimetics modulate inflammation by binding the SET protein and activating protein phosphatase 2A.载脂蛋白E和肽模拟物通过结合SET蛋白并激活蛋白磷酸酶2A来调节炎症。
J Immunol. 2011 Feb 15;186(4):2535-42. doi: 10.4049/jimmunol.1002847.
8
Chronic myeloid leukemia: mechanisms of blastic transformation.慢性髓细胞白血病：细胞性白血病转化的机制。
J Clin Invest. 2010 Jul;120(7):2254-64. doi: 10.1172/JCI41246. Epub 2010 Jul 1.
9
Essential requirement for PP2A inhibition by the oncogenic receptor c-KIT suggests PP2A reactivation as a strategy to treat c-KIT+ cancers.致癌受体 c-KIT 对蛋白磷酸酶 2A（PP2A）抑制的基本要求提示 PP2A 的再激活可作为治疗 c-KIT+癌症的一种策略。
Cancer Res. 2010 Jul 1;70(13):5438-47. doi: 10.1158/0008-5472.CAN-09-2544. Epub 2010 Jun 15.
10
FTY720, a new alternative for treating blast crisis chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphocytic leukemia.FTY720，一种治疗急变期慢性粒细胞白血病和费城染色体阳性急性淋巴细胞白血病的新选择。
J Clin Invest. 2007 Sep;117(9):2408-21. doi: 10.1172/JCI31095.

将OP449归入PP2A激活药物家族。

SETting OP449 into the PP2A-activating drug family.

作者信息

Neviani Paolo, Perrotti Danilo

机构信息

Authors' Affiliations: The Ohio State University Comprehensive Cancer Center, Columbus, Ohio; and Department of Medicine, The Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland.

出版信息

Clin Cancer Res. 2014 Apr 15;20(8):2026-8. doi: 10.1158/1078-0432.CCR-14-0166. Epub 2014 Mar 14.

DOI:10.1158/1078-0432.CCR-14-0166
PMID:24634375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4286336/
Abstract

The protein phosphatase 2A (PP2A) tumor suppressor is inactivated in different leukemias through the activity of its endogenous inhibitors (e.g., SET), which are aberrantly regulated by oncogenic tyrosine kinases. Like other effective and nontoxic PP2A-activating drugs (PAD), OP449 inhibits SET and impairs leukemogenesis. This further supports the immediate use of PADs in patients with leukemia.

摘要

蛋白磷酸酶2A（PP2A）肿瘤抑制因子在不同白血病中通过其内源性抑制剂（如SET）的活性而失活，这些抑制剂受到致癌酪氨酸激酶的异常调控。与其他有效且无毒的PP2A激活药物（PAD）一样，OP449抑制SET并损害白血病发生。这进一步支持了在白血病患者中立即使用PAD。