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本文引用的文献

1
Characterization of the Menin-MLL Interaction as Therapeutic Cancer Target.作为治疗性癌症靶点的Menin-MLL相互作用的特征分析
Cancers (Basel). 2020 Jan 14;12(1):201. doi: 10.3390/cancers12010201.
2
A Menin-MLL Inhibitor Induces Specific Chromatin Changes and Eradicates Disease in Models of MLL-Rearranged Leukemia.一种 Menin-MLL 抑制剂可诱导特定的染色质变化，并消除 MLL 重排白血病模型中的疾病。
Cancer Cell. 2019 Dec 9;36(6):660-673.e11. doi: 10.1016/j.ccell.2019.11.001.
3
Genomic Profiling of Childhood Tumor Patient-Derived Xenograft Models to Enable Rational Clinical Trial Design.对儿童肿瘤患者衍生异种移植模型进行基因组分析，以实现合理的临床试验设计。
Cell Rep. 2019 Nov 5;29(6):1675-1689.e9. doi: 10.1016/j.celrep.2019.09.071.
4
Menin regulates the serine biosynthetic pathway in Ewing sarcoma.Menin 调节尤文肉瘤中的丝氨酸生物合成途径。
J Pathol. 2018 Jul;245(3):324-336. doi: 10.1002/path.5085. Epub 2018 May 28.
5
Polycomb and Trithorax Group Genes in .中的多梳蛋白和三胸节复合体基因
Genetics. 2017 Aug;206(4):1699-1725. doi: 10.1534/genetics.115.185116.
6
Tumorigenicity of Ewing sarcoma is critically dependent on the trithorax proteins MLL1 and menin.尤因肉瘤的致瘤性严重依赖于三胸蛋白MLL1和Menin。
Oncotarget. 2017 Jan 3;8(1):458-471. doi: 10.18632/oncotarget.13444.
7
The Bromodomain BET Inhibitor JQ1 Suppresses Tumor Angiogenesis in Models of Childhood Sarcoma.溴结构域BET抑制剂JQ1在儿童肉瘤模型中抑制肿瘤血管生成。
Mol Cancer Ther. 2016 May;15(5):1018-28. doi: 10.1158/1535-7163.MCT-15-0567. Epub 2016 Feb 23.
8
Pharmacologic inhibition of the Menin-MLL interaction blocks progression of MLL leukemia in vivo.对Menin-MLL相互作用的药理学抑制可阻断MLL白血病在体内的进展。
Cancer Cell. 2015 Apr 13;27(4):589-602. doi: 10.1016/j.ccell.2015.02.016. Epub 2015 Mar 26.
9
Overexpression of HOX genes is prevalent in Ewing sarcoma and is associated with altered epigenetic regulation of developmental transcription programs.HOX基因的过表达在尤因肉瘤中普遍存在，并且与发育转录程序的表观遗传调控改变有关。
Epigenetics. 2014 Dec;9(12):1613-25. doi: 10.4161/15592294.2014.988048.
10
Menin promotes hepatocellular carcinogenesis and epigenetically up-regulates Yap1 transcription.Menin 促进肝细胞癌发生，并通过表观遗传上调 Yap1 转录。
Proc Natl Acad Sci U S A. 2013 Oct 22;110(43):17480-5. doi: 10.1073/pnas.1312022110. Epub 2013 Oct 7.

儿科临床前测试联盟评估 menin-MLL1 抑制剂 VTP-50469 治疗尤文肉瘤异种移植模型。

Evaluation of VTP-50469, a menin-MLL1 inhibitor, against Ewing sarcoma xenograft models by the pediatric preclinical testing consortium.

机构信息

UT Health San Antonio, Greehey Children's Cancer Research Institute, San Antonio, Texas.

Syndax Pharmaceuticals, Waltham, Massachusetts.

出版信息

Pediatr Blood Cancer. 2020 Jul;67(7):e28284. doi: 10.1002/pbc.28284. Epub 2020 Apr 25.

DOI:10.1002/pbc.28284
PMID:32333633
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10286575/
Abstract

BACKGROUND

VTP-50469 is a potent inhibitor of the menin-MLL1 interaction and is implicated in signaling downstream of EWSR1-FLI1.

PROCEDURE

VTP-50469 was evaluated against seven Ewing sarcoma (EwS) xenograft models and in vitro against EwS cell lines.

RESULTS

VTP-50469 showed limited antitumor activity, statistically significantly slowing tumor progression in four tumor models but with no evidence of tumor regression. In vitro, the IC concentration was 10 nM for the mixed lineage leukemia (MLL)-rearranged leukemia cell line MV4;11, but > 3 μM for EwS cell lines.

CONCLUSIONS

In contrast to its high level of activity against MLL1-rearranged leukemia xenografts, VTP-50469 shows little activity against EwS models.

摘要

背景

VTP-50469 是一种 Menin-MLL1 相互作用的有效抑制剂，与 EWSR1-FLI1 下游信号传导有关。

过程

评估 VTP-50469 对七种尤文肉瘤（EwS）异种移植模型的疗效，并在体外对 EwS 细胞系进行评估。

结果

VTP-50469 显示出有限的抗肿瘤活性，在四个肿瘤模型中统计学上显著减缓肿瘤进展，但没有肿瘤消退的证据。在体外，混合谱系白血病（MLL）重排白血病细胞系 MV4；11 的 IC浓度为 10 nM，但 EwS 细胞系的浓度>3 μM。

结论

与 VTP-50469 对 MLL1 重排白血病异种移植的高活性相比，其对 EwS 模型的活性很小。