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Richard J. Jones

Researcher at University of Texas MD Anderson Cancer Center

Publications -  105
Citations -  3817

Richard J. Jones is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Bortezomib & Transplantation. The author has an hindex of 34, co-authored 105 publications receiving 3415 citations. Previous affiliations of Richard J. Jones include University of Birmingham.

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Transplantation of ex vivo expanded cord blood cells using the copper chelator tetraethylenepentamine: a phase I/II clinical trial.

TL;DR: The copper chelator tetraethylenepentamine (TEPA; StemEx) was shown to attenuate the differentiation of ex vivo cultured hematopoietic cells resulting in preferential expansion of early progenitors resulting in 100-day survival and this strategy is feasible.
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Role of NADPH oxidase in arsenic-induced reactive oxygen species formation and cytotoxicity in myeloid leukemia cells.

TL;DR: It is reported here that NADPH oxidase, an enzyme complex required for the normal antibacterial function of white blood cells, is the main target of arsenic-induced ROS production, and a synergism between arsenic and the clinically used phorbol myristate acetate analog, bryostatin 1, can be expected.
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Novel Oligoamine Analogues Inhibit Lysine-Specific Demethylase 1 and Induce Reexpression of Epigenetically Silenced Genes

TL;DR: Cotreatment with low doses of oligoamines and a DNA methyltransferase inhibitor highly induces the reexpression of the aberrantly silenced SFRP2 gene and results in significant inhibition of the growth of established tumors in a human colon tumor model in vivo.
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Targeting the insulin-like growth factor-1 receptor to overcome bortezomib resistance in preclinical models of multiple myeloma

TL;DR: Data support the hypothesis that signaling through the IGF-1/IGF-1R axis contributes to acquired bortezomib resistance, and provide a rationale for combining bortazomib with IGF- 1R inhibitors like OSI-906 to overcome or possibly prevent the emergence of bortzomib-refractory disease in the clinic.
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Regulation of human hematopoietic stem cell self-renewal by the microenvironment’s control of retinoic acid signaling

TL;DR: Primitive hematopoietic cells appear to be intrinsically programmed to undergo RA-mediated differentiation unless prevented from doing so by bone marrow niche CYP26, andModulation of RA signaling also holds promise for clinical HSC expansion, a prerequisite for the wide-scale use of these cells in regenerative medicine and gene therapy.