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1.
Rheum Dis Clin North Am ; 48(1): 331-342, 2022 02.
Article in English | MEDLINE | ID: mdl-34798956

ABSTRACT

Implementation science is the study of processes that promote reliable uptake of evidence-based practices into clinical care. The integration of implementation science and health disparities research approaches has been proposed as a method to reduce health inequity through detection, understanding, and implementation of health equity-focused interventions. In this review, we provide an argument for the study of implementation science in pediatric rheumatology in light of previously observed health disparities, present a framework for the study of health equity and implementation science in pediatric rheumatology, and propose next steps to accelerate action.


Subject(s)
Health Equity , Rheumatology , Child , Healthcare Disparities , Humans , Implementation Science , Research Design
2.
Cancer Res ; 67(15): 7124-31, 2007 Aug 01.
Article in English | MEDLINE | ID: mdl-17671179

ABSTRACT

Aggressive fibromatosis (also called desmoid tumor) is a benign, locally invasive, soft tissue tumor composed of cells with mesenchymal characteristics. These tumors are characterized by increased levels of beta-catenin-mediated T-cell factor (TCF)-dependent transcriptional activation. We found that type 1 IFN signaling is activated in human and murine aggressive fibromatosis tumors and that the expression of associated response genes is regulated by beta-catenin. When mice deficient for the type 1 IFN receptor (Ifnar1-/-) were crossed with mice predisposed to developing aggressive fibromatosis tumors (Apc/Apc1638N), a significant decrease in aggressive fibromatosis tumor formation was observed compared with littermate controls, showing a novel role for type 1 IFN signaling in promoting tumor formation. Type 1 IFN activation inhibits cell proliferation but does not alter cell apoptosis or the level of beta-catenin-mediated TCF-dependent transcriptional activation in aggressive fibromatosis cell cultures. Thus, these changes cannot explain our in vivo results. Intriguingly, Ifnar1-/- mice have smaller numbers of mesenchymal progenitor cells compared with littermate controls, and treatment of aggressive fibromatosis cell cultures with IFN increases the proportion of cells that exclude Hoechst dye and sort to the side population, raising the possibility that type 1 IFN signaling regulates the number of precursor cells present that drive aggressive fibromatosis tumor formation and maintenance. This study identified a novel role for IFN type 1 signaling as a positive regulator of neoplasia and suggests that IFN treatment is a less than optimal therapy for this tumor type.


Subject(s)
Fibromatosis, Aggressive/metabolism , Genes, APC/physiology , Interferon-beta/physiology , Receptor, Interferon alpha-beta/metabolism , Receptor, Interferon alpha-beta/physiology , Signal Transduction/physiology , Animals , Blotting, Western , Cell Proliferation , Cell Transformation, Neoplastic , Colony-Forming Units Assay , Female , Fibroblasts/metabolism , Fibromatosis, Aggressive/pathology , Flow Cytometry , Humans , Male , Mesenchymal Stem Cells , Mice , Neoplasm Invasiveness/pathology , Receptor, Interferon alpha-beta/genetics , T Cell Transcription Factor 1/metabolism , Transcription, Genetic , Transgenes/physiology , Tumor Cells, Cultured , beta Catenin/metabolism
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