Affiliation: University of California
- E-cadherin gene re-expression in chronic lymphocytic leukemia cells by HDAC inhibitorsGwen Jordaan
Division of Hematology Oncology, Greater Los Angeles VA Healthcare Center, UCLA School of Medicine, 11301 Wilshire Blvd, LA, CA 90073, USA
BMC Cancer 13:88. 2013..The tumor suppressor gene E-cadherin gene is frequently silenced in chronic lymphocytic leukemia (CLL) cells and results in wnt-pathway activation. We analyzed the role of histone epigenetic modifications in E-cadherin gene silencing...
- Dexamethasone-induced apoptotic mechanisms in myeloma cells investigated by analysis of mutant glucocorticoid receptorsSanjai Sharma
Department of Hematology Oncology, Division of Hematology Oncology, UCLA West Los Angeles, VA Medical Center, Los Angeles, CA 90073, USA
Blood 112:1338-45. 2008..MM1R cells expressing mutant GRs will be helpful in defining the molecular mechanisms of dexamethasone-induced apoptosis of myeloma cells...
- Involvement of hepcidin in the anemia of multiple myelomaSanjai Sharma
West Los Angeles VA University of California Los Angeles Medical Center, Los Angeles, CA 90073, USA
Clin Cancer Res 14:3262-7. 2008..Because interleukin (IL)-6 is a potent inducer of hepcidin expression and its levels are elevated in multiple myeloma, we studied the role of hepcidin in the anemia of multiple myeloma...
- Aberrant splicing of the E-cadherin transcript is a novel mechanism of gene silencing in chronic lymphocytic leukemia cellsSanjai Sharma
Division of Hematology Oncology, University of California West Los Angeles Veterans Administration Medical Center, Los Angeles, CA 90073, USA
Blood 114:4179-85. 2009..Our data point to a novel mechanism of E-cadherin gene inactivation, with CLL cells displaying a higher proportion of aberrant nonfunctional transcripts and resulting up-regulation of the wnt-beta-catenin pathway...
- Exon 11 skipping of E-cadherin RNA downregulates its expression in head and neck cancer cellsSanjai Sharma
Division of Hematology Oncology, UCLA West Los Angeles VA Medical Center, 11301 Wilshire Blvd, Bldg 304, Rm E1 115, Los Angeles, CA 90073, USA
Mol Cancer Ther 10:1751-9. 2011..Our findings reveal that promoter methylation and an upregulated splicing factor (SFRS2) are involved in the E-cadherin missplicing in tumors...
- Mechanism by which mammalian target of rapamycin inhibitors sensitize multiple myeloma cells to dexamethasone-induced apoptosisHuajun Yan
Department of Medicine, Greater Los Angeles VA Healthcare Center, University of California at Los Angeles School of Medicine, Los Angeles, California, USA
Cancer Res 66:2305-13. 2006..This study supports the strategy of combining dexamethasone with mTOR inhibitors in multiple myeloma and identifies a mechanism by which the synergistic effect is achieved...
- Oncogenic RAS mutations in myeloma cells selectively induce cox-2 expression, which participates in enhanced adhesion to fibronectin and chemoresistanceBao Hoang
David Geffen School of Medicine, University of California, Los Angeles, USA
Blood 107:4484-90. 2006..These results indicate a selective induction of cox-2 in MM cells containing RAS mutations, which results in heightened binding to extracellular matrix protein and chemotherapeutic drug resistance...
- Metabolomics identifies pyrimidine starvation as the mechanism of 5-aminoimidazole-4-carboxamide-1-β-riboside-induced apoptosis in multiple myeloma cellsCarolyne Bardeleben
Division of Hematology Oncology, Greater Los Angeles VA Healthcare Center, 111H, VA West LA Med Ctr, 11301 Wilshire Blvd, Los Angeles, CA 90073, USA
Mol Cancer Ther 12:1310-21. 2013..These data identify pyrimidine biosynthesis as a potential molecular target for future therapeutics in multiple myeloma cells...
- Interleukin-6 activates phosphoinositol-3' kinase in multiple myeloma tumor cells by signaling through RAS-dependent and, separately, through p85-dependent pathwaysJung hsin Hsu
Department of Medicine, West LA VA UCLA Medical Center and Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA 90073, USA
Oncogene 23:3368-75. 2004..These data indicate two potential independent pathways of PI3-K/AKT activation in MM cells: one mediated via signaling through RAS which is independent of p85 and a second mediated via p85 and due to a STAT-3-containing complex...
- IL-6-induced stimulation of c-myc translation in multiple myeloma cells is mediated by myc internal ribosome entry site function and the RNA-binding protein, hnRNP A1Yijiang Shi
Department of Medicine, Greater Los Angeles VA Healthcare System and University of California at Los Angeles Medical School, Los Angeles, California, USA
Cancer Res 68:10215-22. 2008..These data point to hnRNP A1 as a critical regulator of c-myc translation and a potential therapeutic target in multiple myeloma...