Limited miR-17-92 overexpression drives hematologic malignancies

Laura S. Danielson; Linsey Reavie; Marc Coussens; Veronica Davalos; Mireia Castillo-Martin; Maria V. Guijarro; Maryaline Coffre; Carlos Cordon-Cardo; Iannis Aifantis; Sherif Ibrahim; Cynthia Liu; Sergei B. Koralov; Eva Hernando

doi:10.1016/j.leukres.2014.12.002

Limited miR-17-92 overexpression drives hematologic malignancies

Laura S. Danielson, Linsey Reavie, Marc Coussens, Veronica Davalos, Mireia Castillo-Martin, Maria V. Guijarro, Maryaline Coffre, Carlos Cordon-Cardo, Iannis Aifantis, Sherif Ibrahim, Cynthia Liu, Sergei B. Koralov, Eva Hernando

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17 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	335-341
Number of pages	7
Journal	Leukemia Research
Volume	39
Issue number	3
DOIs	https://doi.org/10.1016/j.leukres.2014.12.002
State	Published - 1 Mar 2015

Keywords

Lymphoma
MiR-17-92
Mouse model

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10.1016/j.leukres.2014.12.002

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title = "Limited miR-17-92 overexpression drives hematologic malignancies",

abstract = "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.",

keywords = "Lymphoma, MiR-17-92, Mouse model",

author = "Danielson, \{Laura S.\} and Linsey Reavie and Marc Coussens and Veronica Davalos and Mireia Castillo-Martin and Guijarro, \{Maria V.\} and Maryaline Coffre and Carlos Cordon-Cardo and Iannis Aifantis and Sherif Ibrahim and Cynthia Liu and Koralov, \{Sergei B.\} and Eva Hernando",

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year = "2015",

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day = "1",

doi = "10.1016/j.leukres.2014.12.002",

language = "English",

volume = "39",

pages = "335--341",

journal = "Leukemia Research",

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TY - JOUR

T1 - Limited miR-17-92 overexpression drives hematologic malignancies

AU - Danielson, Laura S.

AU - Reavie, Linsey

AU - Coussens, Marc

AU - Davalos, Veronica

AU - Castillo-Martin, Mireia

AU - Guijarro, Maria V.

AU - Coffre, Maryaline

AU - Cordon-Cardo, Carlos

AU - Aifantis, Iannis

AU - Ibrahim, Sherif

AU - Liu, Cynthia

AU - Koralov, Sergei B.

AU - Hernando, Eva

PY - 2015/3/1

Y1 - 2015/3/1

N2 - 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.

AB - 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.

KW - Lymphoma

KW - MiR-17-92

KW - Mouse model

UR - https://www.scopus.com/pages/publications/84924044294

U2 - 10.1016/j.leukres.2014.12.002

DO - 10.1016/j.leukres.2014.12.002

M3 - Article

C2 - 25597017

AN - SCOPUS:84924044294

SN - 0145-2126

VL - 39

SP - 335

EP - 341

JO - Leukemia Research

JF - Leukemia Research

IS - 3

ER -

Limited miR-17-92 overexpression drives hematologic malignancies

Abstract

Keywords

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