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Paul G. Richardson

Researcher at Harvard University

Publications -  1631
Citations -  174221

Paul G. Richardson is an academic researcher from Harvard University. The author has contributed to research in topics: Multiple myeloma & Bortezomib. The author has an hindex of 183, co-authored 1533 publications receiving 155912 citations. Previous affiliations of Paul G. Richardson include Broomfield Hospital & Dartmouth College.

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The Interaction of Bortezomib with P-Gp, MRP-1 and BCRP Drug Transporters: Implications for Therapeutic Applications of Bortezomib in Advanced Multiple Myeloma and Other Neoplasias.

TL;DR: The studies show that bortezomib is a substrate for Pgp but not the other drug efflux pumps, and suggests that in the subset of patients with advanced multiple myeloma or solid tumors which express high levels of Pgp, the efficacy of bortzomIB is synergistically enhanced by combinations with a Pgp inhibitor, while bortazomib treatment itself can reduce the expression of P gp.
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Bone Turnover Biomarkers Are Useful In Monitoring Myeloma Bone Disease and As Early Predictor Biomarkers For Relapse Disease In Multiple Myeloma

TL;DR: Osteoclast biomarker serum CTX-1 correlates accurately with the disease burden in newly diagnosed multiple myeloma patients as compared to the rest of the groups and is a more sensitive early predictor of relapse/progressive disease than established biomarkers.
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The role of E3 ubiquitin ligase in multiple myeloma: potential for cereblon E3 ligase modulators in the treatment of relapsed/refractory disease

TL;DR: A review of the ubiquitin-proteasome system (UPS) and strategies for co-opting the UPS to reduce or eliminate proteins or survival factors key to malignant pathobiology, including multiple myeloma (MM) in particular, is provided in this article .
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Landscape of Recurrent Mutations in Non-Coding Genome with Functional Implications in Newly-Diagnosed Multiple Myeloma

TL;DR: A deep whole genome sequencing on 260 MM samples was performed to comprehensively analyze recurrent somatic alterations in non-coding regions and showed that these frequent mutations have higher cancer cell fraction (CCF) [median CCF > 0.75] suggesting their occurrence earlier in the disease development.