Abcg2 overexpression represents a novel mechanism for acquired resistance to the multi-kinase inhibitor Danusertib in BCR-ABL-positive cells in vitro (Q28477903)

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English	Abcg2 overexpression represents a novel mechanism for acquired resistance to the multi-kinase inhibitor Danusertib in BCR-ABL-positive cells in vitro	scientific article

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Abcg2 overexpression represents a novel mechanism for acquired resistance to the multi-kinase inhibitor Danusertib in BCR-ABL-positive cells in vitro (English)

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Tessa L Holyoake

12

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Carsten Bokemeyer

11

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Carsten Bokemeyer

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author name string

Stefan Balabanov

1

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Artur Gontarewicz

2

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Gunhild Keller

3

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Laura Raddrizzani

4

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Melanie Braig

5

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Roberta Bosotti

6

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Jürgen Moll

7

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Edgar Jost

8

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Christine Barett

9

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Imke Rohe

10

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Tim H Brümmendorf

13

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publication date

26 April 2011

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6

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4

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e19164

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copyright license

Creative Commons Attribution 4.0 International

26 April 2011

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April 2022 Public Data File from Crossref

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LIMMA

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Europe PubMed Central

22 June 2022

https://europepmc.org/article/PMC/3082549

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CZ Software Mentions: A large dataset of software mentions in the biomedical literature

Crystal structure of the T315I Abl mutant in complex with the aurora kinases inhibitor PHA-739358

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Danusertib (formerly PHA-739358)--a novel combined pan-Aurora kinases and third generation Bcr-Abl tyrosine kinase inhibitor

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Simultaneous targeting of Aurora kinases and Bcr-Abl kinase by the small molecule inhibitor PHA-739358 is effective against imatinib-resistant BCR-ABL mutations including T315I.

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BCR/ABL kinase inhibition by imatinib mesylate enhances MAP kinase activity in chronic myelogenous leukemia CD34+ cells

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Hypusination of eukaryotic initiation factor 5A (eIF5A): a novel therapeutic target in BCR-ABL-positive leukemias identified by a proteomics approach

1 reference

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Nilotinib exerts equipotent antiproliferative effects to imatinib and does not induce apoptosis in CD34+ CML cells

1 reference

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based on heuristic

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10.1371/JOURNAL.PONE.0019164

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2011PLoSO...619164B

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