JAKing up AML1-ETO

John D. Crispino

doi:10.1182/blood-2012-05-413104

JAKing up AML1-ETO

John D. Crispino^*

^*Corresponding author for this work

Medicine, Hematology Oncology Division

Research output: Contribution to journal › Comment/debate › peer-review

3 Scopus citations

Abstract

In this issue of Blood, Chou et al¹ and Pulikkan et al ² reveal that the (8;21)(q22;q22) translocation product AML1-ETO (RUNX1-RUNX1T1) leads to enhanced JAK/STAT signaling downstream of myeloproliferative leukemia (MPL) virus, which in turn contributes to increased survival of tumor cells. Hijacking of the JAK/STAT pathway through up-regulation of wild-type MPL is a new paradigm for hematologic malignancies.

Original language	English (US)
Pages (from-to)	703-704
Number of pages	2
Journal	Blood
Volume	120
Issue number	4
DOIs	https://doi.org/10.1182/blood-2012-05-413104
State	Published - Jul 26 2012

ASJC Scopus subject areas

Hematology
Biochemistry
Cell Biology
Immunology

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10.1182/blood-2012-05-413104

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title = "JAKing up AML1-ETO",

abstract = "In this issue of Blood, Chou et al1 and Pulikkan et al 2 reveal that the (8;21)(q22;q22) translocation product AML1-ETO (RUNX1-RUNX1T1) leads to enhanced JAK/STAT signaling downstream of myeloproliferative leukemia (MPL) virus, which in turn contributes to increased survival of tumor cells. Hijacking of the JAK/STAT pathway through up-regulation of wild-type MPL is a new paradigm for hematologic malignancies.",

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AU - Crispino, John D.

PY - 2012/7/26

Y1 - 2012/7/26

N2 - In this issue of Blood, Chou et al1 and Pulikkan et al 2 reveal that the (8;21)(q22;q22) translocation product AML1-ETO (RUNX1-RUNX1T1) leads to enhanced JAK/STAT signaling downstream of myeloproliferative leukemia (MPL) virus, which in turn contributes to increased survival of tumor cells. Hijacking of the JAK/STAT pathway through up-regulation of wild-type MPL is a new paradigm for hematologic malignancies.

AB - In this issue of Blood, Chou et al1 and Pulikkan et al 2 reveal that the (8;21)(q22;q22) translocation product AML1-ETO (RUNX1-RUNX1T1) leads to enhanced JAK/STAT signaling downstream of myeloproliferative leukemia (MPL) virus, which in turn contributes to increased survival of tumor cells. Hijacking of the JAK/STAT pathway through up-regulation of wild-type MPL is a new paradigm for hematologic malignancies.

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DO - 10.1182/blood-2012-05-413104

M3 - Comment/debate

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SP - 703

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JO - Blood

JF - Blood

IS - 4

ER -

JAKing up AML1-ETO

Abstract

ASJC Scopus subject areas

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