Limited miR-17-92 overexpression drives hematologic malignancies

被引：18

作者：

Danielsona, Laura S. ^{[1
]}

Reavie, Linsey ^{[1
]}

Coussens, Marc ^{[1
]}

Davalos, Veronica ^{[1
]}

Castillo-Martin, Mireia ^{[2
]}

Guijarro, Maria V. ^{[1
]}

Coffre, Maryaline ^{[1
]}

Cordon-Cardo, Carlos ^{[2
]}

Aifantis, Iannis ^{[1
]}

Ibrahim, Sherif ^{[1
]}

Liu, Cynthia ^{[1
]}

Koralov, Sergei B. ^{[1
]}

Hernando, Eva ^{[1
]}

机构：

[1] NYU, Sch Med, Dept Pathol, New York, NY 10003 USA

[2] Mt Sinai Sch Med, Dept Pathol, New York, NY USA

来源：

LEUKEMIA RESEARCH | 2015年 / 39卷 / 03期

关键词：

miR-17-92; Mouse model; Lymphoma; TRANSGENIC MICE; NEURAL CREST; CELLS; EXPRESSION; DIFFERENTIATION; MICRORNAS; DISEASE; CLUSTER; CANCER; SIGNATURE;

D O I：

10.1016/j.leukres.2014.12.002

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The overexpression of microRNA cluster miR-17-92 has been implicated in development of solid tumors and hematological malignancies. The role of miR-17-92 in lymphomagenesis has been extensively investigated; however, because of the developmental defects caused by miR-17-92 dysregulation, its ability to drive tumorigenesis has remained undetermined until recently. Here we demonstrate that overexpression of miR-17-92 in a limited number of hematopoietic cells is sufficient to cause B cell malignancies. In sum, our study provides a novel and physiologically relevant model that exposes the potent ability of miR-17-92 to act as a driver of tumorigenesis. (C) Elsevier Ltd. All rights reserved.

引用

页码：335 / 341

页数：7

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