Gene set enrichment analysis unveils the mechanism for the phosphodiesterase 4B control of glucocorticoid response in B-cell lymphoma

Clinical Cancer Research

Volumn 17, Issue 21, 2011, Pages 6723-6732

  Kim, Sang Woo ^a   Rai, Deepak ^a   Aguiar, Ricardo C T ^a  

^a Mays Cancer Center at UT Health San Antonio   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BIOLOGICAL MARKER; DEXAMETHASONE; DNA; GLUCOCORTICOID; MAMMALIAN TARGET OF RAPAMYCIN; PHOSPHODIESTERASE IV; PHOSPHODIESTERASE IVB; PROTEIN KINASE B; ROLIPRAM; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; B CELL LYMPHOMA; CANCER INHIBITION; CHEMOSENSITIVITY; CONTROLLED STUDY; DNA MODIFICATION; ENZYME ACTIVITY; ENZYME INHIBITION; ENZYME REGULATION; GAIN OF FUNCTION MUTATION; GENE OVEREXPRESSION; GENETIC ANALYSIS; GENETIC MODEL; HUMAN; HUMAN CELL; IN VITRO STUDY; IN VIVO STUDY; LARGE CELL LYMPHOMA; LOSS OF FUNCTION MUTATION; LYMPHOCYTE; LYMPHOMA CELL LINE; MOUSE; NONHUMAN; PRIORITY JOURNAL; TUMOR XENOGRAFT;

ANIMALS; APOPTOSIS; CELL LINE, TUMOR; CYCLIC AMP; CYCLIC NUCLEOTIDE PHOSPHODIESTERASES, TYPE 4; DEXAMETHASONE; DRUG RESISTANCE, NEOPLASM; GENE EXPRESSION PROFILING; GLUCOCORTICOIDS; HUMANS; LYMPHOMA, LARGE B-CELL, DIFFUSE; MICE; MICE, INBRED C57BL; PROTO-ONCOGENE PROTEINS C-AKT; SIGNAL TRANSDUCTION; TOR SERINE-THREONINE KINASES;

EID: 80455173445     PISSN: 10780432     EISSN: 15573265     Source Type: Journal    
DOI: 10.1158/1078-0432.CCR-11-0770     Document Type: Article

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