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Mir-23b Plays a Critical Role As a Tumor Suppressor miRNA In Multiple Myeloma
Deregulated expression of microRNAs (miR) is a hallmark of cancer. Tumor suppressor miRNAs are generally down-regulated in cancer cells compared to their normal counterpart, and their enforcedExpand
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Targeting IL-17A in Multiple Myeloma: A Potential Novel Therapeutic Approach in Myeloma
We have previously demonstrated that interleukin-17A (IL-17) producing T helper 17 cells are significantly elevated in blood and bone marrow (BM) in multiple myeloma (MM) and IL-17A promotes MM cellExpand
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miR-23b/SP1/c-myc forms a feed-forward loop supporting multiple myeloma cell growth
Deregulated microRNA (miR)/transcription factor (TF)-based networks represent a hallmark of cancer. We report here a novel c-Myc/miR-23b/Sp1 feed-forward loop with a critical role in multiple myelomaExpand
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Cytoskeleton Regulator PAK4 Plays a Role in Growth and Survival of Myeloma with a Potential Therapeutic Intervention Using PAK4 Allosteric Modulators (PAMs)
P21-activated serine/threonine kinase 4 (PAK4) is a major effector of Cdc42 and is essential for cytoskeleton reorganization. PAK4 is activated in cancer cells, promotes cell migration andExpand
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MYD88-independent growth and survival effects of Sp1 transactivation in Waldenstrom macroglobulinemia.
Sp1 transcription factor controls a pleiotropic group of genes and its aberrant activation has been reported in a number of malignancies, including multiple myeloma. In this study, we investigate andExpand
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LYMPHOID NEOPLASIA MYD 88-independent growth and survival effects of Sp 1 transactivation in Waldenström macroglobulinemia
Gene expression and proteomic studies have advanced our understanding of Waldenström macroglobulinemia (WM) and identified potential therapeutic targets.Whole-genome sequencing identified somaticExpand
Functional and Molecular Impact Of Dp1-Dependent Alternate Splicing In Multiple Myeloma
Transcription factors (TFs) are important oncogenic regulator and are altered during tumor initiation and progression. Our oncogenomic analysis of gene expression data from large clinically-annotatedExpand