S
Shmuel Yaccoby
High Impact
Professor
faculty
Internal Med, College of Medicine
46 h-index
199 pubs
8,109 cited
Research Areas
Links
Biography and Research Information
OverviewAI-generated summary
Shmuel Yaccoby's research focuses on understanding the molecular mechanisms underlying multiple myeloma and identifying potential therapeutic targets. His work investigates the complex interactions within the bone marrow microenvironment, particularly the roles of mesenchymal stem cells and their secreted factors in controlling myeloma cell growth, dormancy, and bone disease.
Recent publications from Yaccoby's laboratory have explored epigenomic alterations in oncogenes, the potential of PHF19 inhibition as a therapeutic strategy, and the expansion of EDNRA-expressing mesenchymal cells in myeloma progression. His group has also studied the impact of mesenchymal stem cell cytotherapy on osteoclastogenesis and myeloma-induced bone disease. Furthermore, his research has examined the effects of cyclin-dependent kinase inhibitors, such as dinaciclib, on homologous recombination and their synergistic potential with PARP inhibitors in multiple myeloma treatment. Yaccoby's work has been recognized through a high-impact researcher designation, supported by a publication record of 199 papers and over 8,000 citations, with an h-index of 46.
Metrics
- h-index: 46
- Publications: 199
- Citations: 8,109
Selected Publications
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Induction of HMOX1 by mesenchymal stem cell cytotherapy inhibits osteoclastogenesis and myeloma‐induced bone disease (2025)
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EDNRA-Expressing Mesenchymal Cells Are Expanded in Myeloma Interstitial Bone Marrow and Associated with Disease Progression (2023)
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Growth and dormancy control of myeloma cells by mesenchymal stem cells (2023)
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Epigenomic translocation of H3K4me3 broad domains over oncogenes following hijacking of super-enhancers (2021)
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PHF19 inhibition as a therapeutic target in multiple myeloma (2021)
Grants & Funding
- Effect of TACI-lg and BAFFR-lg on primary myeloma growth in SCID-hu mice ZymoGenetics, Inc Principal Investigator
- Effect of VELCADE on Myeloma Bone Disease and Tumor Progression in a SCID-rab model for Primary Lymphoma Millennium Pharmaceuticals, Inc. Principal Investigator
- Inhibition of primary myeloma by Thrombospondin-1 Peptide Mimetic in vivo Abbott, Inc. Principal Investigator
- DEAP Awards - S Yaccoby - UAMS VCRI - FY26 UAMS Division of Research and Innovation Principal Investigator
- Anti-myeloma efficacy of PDACs/HPP Celgene Principal Investigator
- Effect of BI-505 ICAM-1 antibody on growth of myeloma cells in vitro and in vivo BioInvent Principal Investigator
- Inhibition of primary myeloma by Thrombospondin-1 Peptide Mimetic in vivo Abbott, Inc. Principal Investigator
- Role of SPRPs in the anti-myeloma response of osteoblasts Multiple Myeloma Research Foundation Principal Investigator
Collaboration Network
Top Collaborators
Frits van Rhee
Winthrop Rockefeller Foundation
19 shared publications
In database
- Epigenomic translocation of H3K4me3 broad domains over oncogenes following hijacking of super-enhancers
- PHF19 inhibition as a therapeutic target in multiple myeloma
- EDNRA-Expressing Mesenchymal Cells Are Expanded in Myeloma Interstitial Bone Marrow and Associated with Disease Progression
- Growth and dormancy control of myeloma cells by mesenchymal stem cells
- Supplementary Data from Combinatorial efficacy of anti-CS1 monoclonal antibody elotuzumab (HuLuc63) and bortezomib against multiple myeloma
Showing 5 of 19 shared publications
Bart Barlogie
University of Arkansas for Medical Sciences
16 shared publications
In database
- PHF19 inhibition as a therapeutic target in multiple myeloma
- Supplementary Data from Combinatorial efficacy of anti-CS1 monoclonal antibody elotuzumab (HuLuc63) and bortezomib against multiple myeloma
- Supplementary Data from Combinatorial efficacy of anti-CS1 monoclonal antibody elotuzumab (HuLuc63) and bortezomib against multiple myeloma
- Data from Combinatorial efficacy of anti-CS1 monoclonal antibody elotuzumab (HuLuc63) and bortezomib against multiple myeloma
- Data from Combinatorial efficacy of anti-CS1 monoclonal antibody elotuzumab (HuLuc63) and bortezomib against multiple myeloma
Showing 5 of 16 shared publications
Maurizio Zangari
Winthrop Rockefeller Foundation
15 shared publications
In database
- Epigenomic translocation of H3K4me3 broad domains over oncogenes following hijacking of super-enhancers
- PHF19 inhibition as a therapeutic target in multiple myeloma
- EDNRA-Expressing Mesenchymal Cells Are Expanded in Myeloma Interstitial Bone Marrow and Associated with Disease Progression
- Growth and dormancy control of myeloma cells by mesenchymal stem cells
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
Showing 5 of 15 shared publications
Gareth J. Morgan
11 shared publications
- Epigenomic translocation of H3K4me3 broad domains over oncogenes following hijacking of super-enhancers
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
- Supplementary Tables from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Supplementary Figures from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
Showing 5 of 11 shared publications
Joshua Epstein
University of Arkansas for Medical Sciences (US)
11 shared publications
- Growth and dormancy control of myeloma cells by mesenchymal stem cells
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
- Supplementary Tables from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Supplementary Figures from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
Showing 5 of 11 shared publications
Antje Hoering
10 shared publications
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
- Supplementary Tables from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Supplementary Figures from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
- Data from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
Showing 5 of 10 shared publications
Carolina Schinke
University of Arkansas for Medical Sciences
8 shared publications
In database
- Epigenomic translocation of H3K4me3 broad domains over oncogenes following hijacking of super-enhancers
- PHF19 inhibition as a therapeutic target in multiple myeloma
- EDNRA-Expressing Mesenchymal Cells Are Expanded in Myeloma Interstitial Bone Marrow and Associated with Disease Progression
- Growth and dormancy control of myeloma cells by mesenchymal stem cells
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
Showing 5 of 8 shared publications
Sharmilan Thanendrarajan
Winthrop Rockefeller Foundation
8 shared publications
In database
- Epigenomic translocation of H3K4me3 broad domains over oncogenes following hijacking of super-enhancers
- PHF19 inhibition as a therapeutic target in multiple myeloma
- EDNRA-Expressing Mesenchymal Cells Are Expanded in Myeloma Interstitial Bone Marrow and Associated with Disease Progression
- Growth and dormancy control of myeloma cells by mesenchymal stem cells
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
Showing 5 of 8 shared publications
David A. Alagpulinsa
8 shared publications
- Supplementary Figure 3: Dinaciclib reduces the mRNA transcripts of Rad51, its paralogs and Brca1 in vivo from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 1: Dinaciclib potentiates cytotoxic effects of doxorubicin from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 2: Dinaciclib induces S-phase accumulation and reduces G2/M-phase accumulation from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 2: Dinaciclib induces S-phase accumulation and reduces G2/M-phase accumulation from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 1: Dinaciclib potentiates cytotoxic effects of doxorubicin from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
Showing 5 of 8 shared publications
Srinivas Ayyadevara
8 shared publications
In database
- Supplementary Figure 3: Dinaciclib reduces the mRNA transcripts of Rad51, its paralogs and Brca1 in vivo from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 1: Dinaciclib potentiates cytotoxic effects of doxorubicin from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 2: Dinaciclib induces S-phase accumulation and reduces G2/M-phase accumulation from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 2: Dinaciclib induces S-phase accumulation and reduces G2/M-phase accumulation from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 1: Dinaciclib potentiates cytotoxic effects of doxorubicin from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
Showing 5 of 8 shared publications
Robert J. Shmookler Reis
8 shared publications
In database
- Supplementary Figure 3: Dinaciclib reduces the mRNA transcripts of Rad51, its paralogs and Brca1 in vivo from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 1: Dinaciclib potentiates cytotoxic effects of doxorubicin from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 2: Dinaciclib induces S-phase accumulation and reduces G2/M-phase accumulation from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 2: Dinaciclib induces S-phase accumulation and reduces G2/M-phase accumulation from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
- Supplementary Figure 1: Dinaciclib potentiates cytotoxic effects of doxorubicin from A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition
Showing 5 of 8 shared publications
Syed J. Mehdi
University of Arkansas for Medical Sciences (US)
6 shared publications
- EDNRA-Expressing Mesenchymal Cells Are Expanded in Myeloma Interstitial Bone Marrow and Associated with Disease Progression
- Growth and dormancy control of myeloma cells by mesenchymal stem cells
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
- Data from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
Showing 5 of 6 shared publications
Sadie Johnson
University of Arkansas for Medical Sciences (US)
6 shared publications
- EDNRA-Expressing Mesenchymal Cells Are Expanded in Myeloma Interstitial Bone Marrow and Associated with Disease Progression
- Growth and dormancy control of myeloma cells by mesenchymal stem cells
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
- Supplemental Text from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
- Data from The Pattern of Mesenchymal Stem Cell Expression Is an Independent Marker of Outcome in Multiple Myeloma
Showing 5 of 6 shared publications
Yogesh Jethava
6 shared publications
- Supplementary Tables from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Supplementary Figures from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Data from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Data from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Supplementary Figures from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
Showing 5 of 6 shared publications
Alan Mitchell
6 shared publications
- Supplementary Tables from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Supplementary Figures from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Data from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Data from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
- Supplementary Figures from Adverse Metaphase Cytogenetics Can Be Overcome by Adding Bortezomib and Thalidomide to Fractionated Melphalan Transplants
Showing 5 of 6 shared publications
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