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Nitin Jain et al.
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J. Deng et al.
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Microenvironmental agonists generate de novo phenotypic resistance to combined ibrutinib plus venetoclax in CLL and MCL
Kallesh D. Jayappa et al.
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Vikas A. Gupta et al.
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Andrew W. Roberts et al.
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Marina Konopleva et al.
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Big data analysis of treatment patterns and outcomes among elderly acute myeloid leukemia patients in the United States
Bruno C. Medeiros et al.
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FLT3-ITD and TLR9 use Bruton tyrosine kinase to activate distinct transcriptional programs mediating AML cell survival and proliferation
Thomas Oellerich et al.
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Acute Myeloid Leukemia
Hartmut Doehner et al.
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A. Berglof et al.
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David Chiron et al.
ONCOTARGET (2015)
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Bhagwan Yadav et al.
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Xiaoxian Zhao et al.
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Adam A. Friedman et al.
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Ellen Scheers et al.
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Identification of Bruton's tyrosine kinase as a therapeutic target in acute myeloid leukemia
Stuart A. Rushworth et al.
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Combinatorial drug screening identifies synergistic co-targeting of Bruton's tyrosine kinase and the proteasome in mantle cell lymphoma
M. Axelrod et al.
LEUKEMIA (2014)
The Reactome pathway knowledgebase
David Croft et al.
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Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2
Michael I. Love et al.
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Jeffrey W. Tyner et al.
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F. Lo-Coco et al.
NEW ENGLAND JOURNAL OF MEDICINE (2013)
Removing technical variability in RNA-seq data using conditional quantile normalization
Kasper D. Hansen et al.
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graphite - a Bioconductor package to convert pathway topology to gene network
Gabriele Sales et al.
BMC BIOINFORMATICS (2012)
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M. Vogler
CELL DEATH AND DIFFERENTIATION (2012)
A Topology-Based Score for Pathway Enrichment
Maysson Al-Haj Ibrahim et al.
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Derek Yecies et al.
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Lee A. Honigberg et al.
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Meike Vogler et al.
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Reactome knowledgebase of human biological pathways and processes
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Jeffrey T. Leek et al.
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Zhengying Pan et al.
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Skewed Th 1 Responses Caused by Excessive Expression of Txk, a Member of the Tec Family of Tyrosine Kinases, in Patients with Behcet's Disease
Noboru Suzuki et al.
CLINICAL MEDICINE & RESEARCH (2006)
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