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Summary The International Society for Stem Cell Research has updated its Guidelines for Stem Cell Research and Clinical Translation in order to address advances in stem cell science and other relevant fields, together with the associated ethical, social, and policy issues that have arisen since the last update in 2016. While growing to encompass the evolving science, clinical applications of stem cells, and the increasingly complex implications of stem cell research for society, the basic principles underlying the Guidelines remain unchanged, and they will continue to serve as the standard for the field and as a resource for scientists, regulators, funders, physicians, and members of the public, including patients. A summary of the key updates and issues is presented here., The updated Guidelines for Stem Cell Research and Clinical Translation describe the ethical principles and best practices for basic, translational, and clinical research involving stem cells and human embryos. The updated Guidelines include new recommendations to address the recent scientific advances involving embryos, stem cell-based embryo models, chimeras, organoids, and genome editing.

In a comparison of gene expression by A2B5-defined glial tumor progenitor cells (TPCs) to glial progenitor cells derived from normal adult human brain (Cell Reports 3:2127-41, 2013), we found that the F2R gene encoding PAR1 was differentially over-expressed by TPCs isolated from primary gliomas at every stage of glioma progression. In this study, we therefore asked if PAR1 activation was causally associated with glioma progression. Lentiviral shRNAi knock-down of PAR1 inhibited the expansion and proliferation of glioma TPCs in vitro. We further found that the PAR-1 receptor antagonists SCH79797 and SCH530348 (vorapaxar) inhibited A2B5+ TPC expansion and migration in vitro. PAR1 knockdown also suppressed the tumorigenic potential of A2B5+ TPCs after transplantation into the brains of immunodeficient mice. In addition, mice given subcutaneous grafts of A2B5+ human glioma TPCs exhibited delayed tumor growth if treated with Vorapaxar, relative to xenografted control mice treated with only vehicle. Together, these data suggest that PAR1 may contribute to glioma progenitor expansion and tumor growth; as such, the abrogation of PAR1 signaling may contribute to the treatment of malignant glioma.