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Your search keyword '"Reddy, E. Premkumar"' showing total 20 results
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20 results on '"Reddy, E. Premkumar"'

5. The Sequenced Combination of Rigosertib and Azacitidine Has Modulatory Effects on CXCL8, RIG-I like Receptor (RLR) and Wnt/β-Catenin Signaling and Downstream Hematopoiesis Pathways in an in Vitro Model of the Myelodysplastic Syndrome

Author

Rai, Richa, primary, Melana, Stella, additional, Navada, Shyamala C., additional, Odchimar-Reissig, Rosalie, additional, Demakos, Erin P., additional, Reddy, E. Premkumar, additional, and Silverman, Lewis R., additional

Published
2019
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8. Weighted Gene Co-Expression Network Analysis (WGCNA) Identifies Highly Proliferative Myeloma Subgroup Responsive to CDK4/ARK5 Inhibition

Author

Perumal, Deepak, primary, Leshchenko, Violetta V., additional, Kuo, Pei-Yu, additional, Jiang, Zewei, additional, Readhead, Ben, additional, Eden, Caroline, additional, Athaluri Divakar, Sai Krishna, additional, Zhang, Weijia, additional, Cho, Hearn Jay, additional, Chari, Ajai, additional, Reddy, M.V.Ramana, additional, Reddy, E. Premkumar, additional, Dudley, Joel, additional, Jagannath, Sundar, additional, and Parekh, Samir, additional

Published
2014
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18. Mechanisms associated with IL-6–induced up-regulation of Jak3and its role in monocytic differentiation

Author

Mangan, James K., Rane, Sushil G., Kang, Anthony D., Amanullah, Arshad, Wong, Brian C., and Reddy, E. Premkumar

Abstract

We report here that Janus kinase 3 (Jak3)is a primary response gene for interleukin-6 (IL-6) in macrophage differentiation, and ectopic overexpression of Jak3 accelerates monocytic differentiation of normal mouse bone marrow cells stimulated with cytokines. Furthermore, we show that incubation of normal mouse bone marrow cells with a JAK3-specific inhibitor results in profound inhibition of myeloid colony formation in response to granulocyte-macrophage colony-stimulating factor or the combination of stem cell factor, IL-3, and IL-6. In addition, mutagenesis of the Jak3promoter has revealed that Sp1 binding sites within a -67 to -85 element and a signal transducer and activator of transcription (Stat) binding site at position -44 to -53 are critical for activation of Jak3transcription in murine M1 myeloid leukemia cells stimulated with IL-6. Electrophoretic mobility shift assay (EMSA) analysis has demonstrated that Sp1 can bind to the -67 to -85 element and Stat3 can bind to the -44 to -53 STAT site in IL-6-stimulated M1 cells. Additionally, ectopic overexpression of Stat3 enhanced Jak3promoter activity in M1 cells. This mechanism of activation of the murine Jak3promoter in myeloid cells is distinct from a recently reported mechanism of activation of the human JAK3promoter in activated T cells.

Published
2004
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19. Effects of Rigosertib (RIGO) Alone or in Combination with Azacitidine or Vorinostat on Epigenetic Reprogramming of CD34+ Cells in the Myelodysplastic Syndrome

Author

Silverman, Lewis R, Chaurasia, Pratima, Melana, Stella, Odchimar-Reissig, Rosalie, Demakos, Erin P., Navada, Shyamala C., and Reddy, E. Premkumar

Abstract

Rigosertib (RIG) which functions as a RAS-mimetic, binds to the RAS-binding domain (RBD) impacting many pathways that involve RBD-mediated interactions, including the RAS-Raf and AKT/PI3-kinase pathways (Divakar et al., Cell 2016). Recently, we demonstrated that RIG also functions as an epigenetic modifier in MDS. RIG alone or in combination with Azacitidine (AZA) exerted epigenetic effects on the global histone post-translational modifications (PTMs), chromatin remodelers, HDACs, and DNMTs and caused enhanced apoptosis in MDS (MDS-L) and AML (BW-90) cell lines as well as in bone marrow cells (BM) derived from pts with MDS (Chaurasia et al ASCO 2016). In clinical trials, the combination of RIG and AZA demonstrated an overall response rate of 76% in all MDS patients; 62% response in pts who had failed prior hypomethyating agent (HMA) (Navada et al ASH 2016) and 85% in HMA naive pts. The growing evidence suggests that combined therapy may be more effective than either agent alone. To further study these effects, we explored activity of RIG in combination with Vorinostat (VOR), a histone deacetylase inhibitor, on the cell lines. Combined treatment in sequential order VOR/RIG and RIG/VOR potentiates far greater effects on the global PTMs, HDACs, DNMTs, chromatin remodelers, cell cycle checkpoint proteins and PI3/AKT pathway than RIG/AZA or AZA/RIG.

Published
2017
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