Author
Philip L. McCarthy
Other affiliations: Howard Hughes Medical Institute, Medical College of Wisconsin, Brigham and Women's Hospital ...read more
Bio: Philip L. McCarthy is an academic researcher from Roswell Park Cancer Institute. The author has contributed to research in topics: Transplantation & Multiple myeloma. The author has an hindex of 28, co-authored 54 publications receiving 7802 citations. Previous affiliations of Philip L. McCarthy include Howard Hughes Medical Institute & Medical College of Wisconsin.
Papers published on a yearly basis
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Mayo Clinic1, University of Navarra2, Harvard University3, Cedars-Sinai Medical Center4, Memorial Sloan Kettering Cancer Center5, Emory University6, National and Kapodistrian University of Athens7, Mount Sinai Hospital8, University of Turin9, University of Texas MD Anderson Cancer Center10, Heidelberg University11, Alfred Hospital12, University Health System13, Carolinas Healthcare System14, University of Bologna15, Aalborg University16, Dalhousie University17, Erasmus University Rotterdam18, Roswell Park Cancer Institute19, Columbia University20, University of Toulouse21
TL;DR: Several aspects of disease response assessment are clarified, along with endpoints for clinical trials, and future directions for disease response assessments are highlighted, to allow uniform reporting within and outside clinical trials.
Abstract: Treatment of multiple myeloma has substantially changed over the past decade with the introduction of several classes of new effective drugs that have greatly improved the rates and depth of response. Response criteria in multiple myeloma were developed to use serum and urine assessment of monoclonal proteins and bone marrow assessment (which is relatively insensitive). Given the high rates of complete response seen in patients with multiple myeloma with new treatment approaches, new response categories need to be defined that can identify responses that are deeper than those conventionally defined as complete response. Recent attempts have focused on the identification of residual tumour cells in the bone marrow using flow cytometry or gene sequencing. Furthermore, sensitive imaging techniques can be used to detect the presence of residual disease outside of the bone marrow. Combining these new methods, the International Myeloma Working Group has defined new response categories of minimal residual disease negativity, with or without imaging-based absence of extramedullary disease, to allow uniform reporting within and outside clinical trials. In this Review, we clarify several aspects of disease response assessment, along with endpoints for clinical trials, and highlight future directions for disease response assessments.
1,681 citations
Roswell Park Cancer Institute1, Duke University2, Ohio State University3, Wake Forest University4, Memorial Sloan Kettering Cancer Center5, Harvard University6, University of Pennsylvania7, University of Minnesota8, Washington University in St. Louis9, University of Florida10, University of Wisconsin-Madison11, University of Chicago12, State University of New York Upstate Medical University13, Icahn School of Medicine at Mount Sinai14, Oregon Health & Science University15, University of North Carolina at Chapel Hill16, University of California, San Francisco17, University of Texas MD Anderson Cancer Center18, Medical College of Wisconsin19
TL;DR: Lenalidomide maintenance therapy, initiated at day 100 after hematopoietic stem-cell transplantation, was associated with more toxicity and second cancers but a significantly longer time to disease progression and significantly improved overall survival among patients with myeloma.
Abstract: Background Data are lacking on whether lenalidomide maintenance therapy prolongs the time to disease progression after autologous hematopoietic stem-cell transplantation in patients with multiple myeloma. Methods Between April 2005 and July 2009, we randomly assigned 460 patients who were younger than 71 years of age and had stable disease or a marginal, partial, or complete response 100 days after undergoing stem-cell transplantation to lenalidomide or placebo, which was administered until disease progression. The starting dose of lenalidomide was 10 mg per day (range, 5 to 15). Results The study-drug assignments were unblinded in 2009, when a planned interim analysis showed a significantly longer time to disease progression in the lenalidomide group. At unblinding, 20% of patients who received lenalidomide and 44% of patients who received placebo had progressive disease or had died (P<0.001); of the remaining 128 patients who received placebo and who did not have progressive disease, 86 crossed over to ...
996 citations
TL;DR: Cotransplantation of HLA-identical sibling culture-expanded MSCs with an HLA and hematopoietic HSC transplant is feasible and seems to be safe, without immediate infusional or late MSC-associated toxicities.
832 citations
University of Turin1, University of Salamanca2, Mayo Clinic3, Roswell Park Cancer Institute4, Emory University5, VU University Medical Center6, National and Kapodistrian University of Athens7, Cross Cancer Institute8, University of Ostrava9, Harvard University10, Cedars-Sinai Medical Center11, University of Navarra12, Erasmus University Rotterdam13
TL;DR: The frailty score predicts mortality and the risk of toxicity in elderly myeloma patients and is proposed for the measurement of frailty in designing future clinical trials.
533 citations
Veterans Health Administration1, University of Minnesota2, University of Washington3, Duke University4, Roswell Park Cancer Institute5, Harvard University6, University of Barcelona7, National Institutes of Health8, Center for International Blood and Marrow Transplant Research9, Medical College of Wisconsin10, Cleveland Clinic11, Ottawa Hospital Research Institute12, Joseph Fourier University13, Columbia University14, Princess Margaret Cancer Centre15, Mayo Clinic16
TL;DR: Conditioning intensity, TBI and graft source have a combined effect on risk of AGVHD that must be considered in deciding on a treatment strategy for individual patients.
528 citations
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01 Feb 2015
TL;DR: In this article, the authors describe the integrative analysis of 111 reference human epigenomes generated as part of the NIH Roadmap Epigenomics Consortium, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression.
Abstract: The reference human genome sequence set the stage for studies of genetic variation and its association with human disease, but epigenomic studies lack a similar reference. To address this need, the NIH Roadmap Epigenomics Consortium generated the largest collection so far of human epigenomes for primary cells and tissues. Here we describe the integrative analysis of 111 reference human epigenomes generated as part of the programme, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression. We establish global maps of regulatory elements, define regulatory modules of coordinated activity, and their likely activators and repressors. We show that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease. Our results demonstrate the central role of epigenomic information for understanding gene regulation, cellular differentiation and human disease.
4,409 citations
Vanderbilt University Medical Center1, Medical University of Vienna2, University of Minnesota3, National Institutes of Health4, University of Regensburg5, Mayo Clinic6, Brigham and Women's Hospital7, Fred Hutchinson Cancer Research Center8, BC Cancer Agency9, State University of Campinas10, Stanford University11, University of Michigan12, Harvard University13, Johns Hopkins University School of Medicine14
TL;DR: The 2014 NIH consensus maintains the framework of the prior consensus with further refinement based on new evidence, and focuses attention on the causes of organ-specific abnormalities to chronic GVHD.
4,122 citations
Veterans Health Administration1, Medical University of Vienna2, University of Minnesota3, University of Regensburg4, National Institutes of Health5, Mayo Clinic6, Harvard University7, Fred Hutchinson Cancer Research Center8, University of British Columbia9, Stanford University10, University of Michigan11, Johns Hopkins University12
TL;DR: In this article, the authors proposed a new clinical scoring system (0-3) that describes the extent and severity of chronic graft-versus-host disease for each organ or site at any given time, taking functional impact into account.
2,883 citations
TL;DR: Infusion of mesenchymal stem cells expanded in vitro, irrespective of the donor, might be an effective therapy for patients with steroid-resistant, acute GVHD.
2,510 citations
TL;DR: Harnessing the migratory potential of MSCs by modulating their chemokine‐chemokine receptor interactions may be a powerful way to increase their ability to correct inherited disorders of mesenchymal tissues or facilitate tissue repair in vivo.
Abstract: MSCs are nonhematopoietic stromal cells that are capable of differentiating into, and contribute to the regeneration of, mesenchymal tissues such as bone, cartilage, muscle, ligament, tendon, and adipose. MSCs are rare in bone marrow, representing approximately 1 in 10,000 nucleated cells. Although not immortal, they have the ability to expand manyfold in culture while retaining their growth and multilineage potential. MSCs are identified by the expression of many molecules including CD105 (SH2) and CD73 (SH3/4) and are negative for the hematopoietic markers CD34, CD45, and CD14. The properties of MSCs make these cells potentially ideal candidates for tissue engineering. It has been shown that MSCs, when transplanted systemically, are able to migrate to sites of injury in animals, suggesting that MSCs possess migratory capacity. However, the mechanisms underlying the migration of these cells remain unclear. Chemokine receptors and their ligands and adhesion molecules play an important role in tissue-specific homing of leukocytes and have also been implicated in trafficking of hematopoietic precursors into and through tissue. Several studies have reported the functional expression of various chemokine receptors and adhesion molecules on human MSCs. Harnessing the migratory potential of MSCs by modulating their chemokine-chemokine receptor interactions may be a powerful way to increase their ability to correct inherited disorders of mesenchymal tissues or facilitate tissue repair in vivo. The current review describes what is known about MSCs and their capacity to home to tissues together with the associated molecular mechanisms involving chemokine receptors and adhesion molecules.
2,339 citations