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Paper Details

Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemia.
Leukemia
100
2015
-, ABL1, BCR, BP-5-, BP-5-087, CML, CML progenitor cells, Philadelphia chromosome-positive leukemia, SH2 domain, STAT3, chronic myeloid leukemia, deuterium, hydrogen, leukemic, leukemic stem cells, malignancies, patients, primary cells, signal transducer and activator of transcription 3, therapy, tyrosine, tyrosine kinase
Author NameAffiliation
Anna M EiringHuntsman Cancer Institute, The University of Utah
Diana ResetcaYork University Chemistry Department
Matthew S ZabriskieHuntsman Cancer Institute, The University of Utah
Jamshid S KhorashadHuntsman Cancer Institute, The University of Utah
Anna SeninaHuntsman Cancer Institute, The University of Utah
Anthony D PomicterHuntsman Cancer Institute, The University of Utah
Srinivas K TantravahiHuntsman Cancer Institute, The University of Utah
Richard MorigglLudwig Boltzmann Institute for Cancer Research
Riccardo BaronThe University of Utah
Thomas O'HareHuntsman Cancer Institute, The University of Utah
Thomas O'HareThe University of Utah
Michael W DeiningerHuntsman Cancer Institute, The University of Utah
Michael W DeiningerThe University of Utah
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Release 1.2