Eva Grundschober

Vienna, Austria

Last Updated: 09/26/2026

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Found 9 publications

A kinase-independent role for CDK8 in BCR-ABL1+ leukemia.

A kinase-independent role for CDK8 in BCR-ABL1+ leukemia.

Journal: Nature communications
Published: January 12, 2019

Twins with different personalities: STAT5B-but not STAT5A-has a key role in BCR/ABL-induced leukemia.

Twins with different personalities: STAT5B-but not STAT5A-has a key role in BCR/ABL-induced leukemia.

Journal: Leukemia
Published: June 05, 2018

STAT5BN642H is a driver mutation for T cell neoplasia.

STAT5BN642H is a driver mutation for T cell neoplasia.

Journal: The Journal of clinical investigation
Published: April 12, 2017

Expansion of BCR/ABL1+ cells requires PAK2 but not PAK1.

Expansion of BCR/ABL1+ cells requires PAK2 but not PAK1.

Journal: British journal of haematology
Published: February 23, 2017

STAT5 Is a Key Regulator in NK Cells and Acts as a Molecular Switch from Tumor Surveillance to Tumor Promotion.

STAT5 Is a Key Regulator in NK Cells and Acts as a Molecular Switch from Tumor Surveillance to Tumor Promotion.

Journal: Cancer discovery
Published: June 17, 2015

Acceleration of Bcr-Abl+ leukemia induced by deletion of JAK2.

Acceleration of Bcr-Abl+ leukemia induced by deletion of JAK2.

Journal: Leukemia
Published: May 06, 2014

PAK-dependent STAT5 serine phosphorylation is required for BCR-ABL-induced leukemogenesis.

PAK-dependent STAT5 serine phosphorylation is required for BCR-ABL-induced leukemogenesis.

Journal: Leukemia
Published: August 27, 2013

Adding a new facet to STAT5 in CML: multitasking for leukemic cells.

Adding a new facet to STAT5 in CML: multitasking for leukemic cells.

Journal: Cell cycle (Georgetown, Tex.)
Published: May 28, 2013

STAT5 triggers BCR-ABL1 mutation by mediating ROS production in chronic myeloid leukaemia.

STAT5 triggers BCR-ABL1 mutation by mediating ROS production in chronic myeloid leukaemia.

Journal: Oncotarget
Published: March 06, 2013
Showing 1-9 of 9

Last Updated: 09/26/2026