Adriane R. Mosley
Stanford University
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Publication
Featured researches published by Adriane R. Mosley.
Nature Biotechnology | 2011
Chad Tang; Andrew S. Lee; Jens Peter Volkmer; Debashis Sahoo; Divya Nag; Adriane R. Mosley; Matthew A. Inlay; Reza Ardehali; Shawn L. Chavez; Renee A. Reijo Pera; B. Behr; Joseph C. Wu; Irving L. Weissman; Micha Drukker
An important risk in the clinical application of human pluripotent stem cells (hPSCs), including human embryonic and induced pluripotent stem cells (hESCs and hiPSCs), is teratoma formation by residual undifferentiated cells. We raised a monoclonal antibody against hESCs, designated anti–stage-specific embryonic antigen (SSEA)-5, which binds a previously unidentified antigen highly and specifically expressed on hPSCs—the H type-1 glycan. Separation based on SSEA-5 expression through fluorescence-activated cell sorting (FACS) greatly reduced teratoma-formation potential of heterogeneously differentiated cultures. To ensure complete removal of teratoma-forming cells, we identified additional pluripotency surface markers (PSMs) exhibiting a large dynamic expression range during differentiation: CD9, CD30, CD50, CD90 and CD200. Immunohistochemistry studies of human fetal tissues and bioinformatics analysis of a microarray database revealed that concurrent expression of these markers is both common and specific to hPSCs. Immunodepletion with antibodies against SSEA-5 and two additional PSMs completely removed teratoma-formation potential from incompletely differentiated hESC cultures.
Nature Biotechnology | 2012
Micha Drukker; Chad Tang; Reza Ardehali; Yuval Rinkevich; Jun Seita; Andrew S. Lee; Adriane R. Mosley; Irving L. Weissman; Yoav Soen
To identify early populations of committed progenitors derived from human embryonic stem cells (hESCs), we screened self-renewing, BMP4-treated and retinoic acid–treated cultures with >400 antibodies recognizing cell-surface antigens. Sorting of >30 subpopulations followed by transcriptional analysis of developmental genes identified four distinct candidate progenitor groups. Subsets detected in self-renewing cultures, including CXCR4+ cells, expressed primitive endoderm genes. Expression of Cxcr4 in primitive endoderm was confirmed in visceral endoderm of mouse embryos. BMP4-induced progenitors exhibited gene signatures of mesoderm, trophoblast and vascular endothelium, suggesting correspondence to gastrulation-stage primitive streak, chorion and allantois precursors, respectively. Functional studies in vitro and in vivo confirmed that ROR2+ cells produce mesoderm progeny, APA+ cells generate syncytiotrophoblasts and CD87+ cells give rise to vasculature. The same progenitor classes emerged during the differentiation of human induced pluripotent stem cells (hiPSCs). These markers and progenitors provide tools for purifying human tissue-regenerating progenitors and for studying the commitment of pluripotent stem cells to lineage progenitors.
Stem cell reports | 2014
Matthew A. Inlay; Thomas Serwold; Adriane R. Mosley; John W. Fathman; Ivan K. Dimov; Jun Seita; Irving L. Weissman
Summary Hematopoiesis in the embryo proceeds in a series of waves, with primitive erythroid-biased waves succeeded by definitive waves, within which the properties of hematopoietic stem cells (multilineage potential, self-renewal, and engraftability) gradually arise. Whereas self-renewal and engraftability have previously been examined in the embryo, multipotency has not been thoroughly addressed, especially at the single-cell level or within well-defined populations. To identify when and where clonal multilineage potential arises during embryogenesis, we developed a single-cell multipotency assay. We find that, during the initiation of definitive hematopoiesis in the embryo, a defined population of multipotent, engraftable progenitors emerges that is much more abundant within the yolk sac (YS) than the aorta-gonad-mesonephros (AGM) or fetal liver. These experiments indicate that multipotent cells appear in concert within both the YS and AGM and strongly implicate YS-derived progenitors as contributors to definitive hematopoiesis.
Stem Cells | 2012
Natesh Parashurama; Neethan Lobo; Ken Ito; Adriane R. Mosley; Frezghi Habte; Maider Zabala; Bryan Smith; Jessica Lam; Irving L. Weissman; Michael F. Clarke; Sanjiv S. Gambhir
Poorly regulated tissue remodeling results in increased breast cancer risk, yet how breast cancer stem cells (CSC) participate in remodeling is unknown. We performed in vivo imaging of changes in fluorescent, endogenous duct architecture as a metric for remodeling. First, we quantitatively imaged physiologic remodeling of primary branches of the developing and regenerating mammary tree. To assess CSC‐specific remodeling events, we isolated CSC from MMTV‐Wnt1 (mouse mammary tumor virus long‐term repeat enhancer driving Wnt1 oncogene) breast tumors, a well studied model in which tissue remodeling affects tumorigenesis. We confirm that CSC drive tumorigenesis, suggesting a link between CSC and remodeling. We find that normal, regenerating, and developing gland maintain a specific branching pattern. In contrast, transplantation of CSC results in changes in the branching patterns of endogenous ducts while non‐CSC do not. Specifically, in the presence of CSC, we identified an increased number of branches, branch points, ducts which have greater than 40 branches (5/33 for CSC and 0/39 for non‐CSC), and histological evidence of increased branching. Moreover, we demonstrate that only CSC implants invade into surrounding stroma with structures similar to developing mammary ducts (nine for CSC and one for non‐CSC). Overall, we demonstrate a novel approach for imaging physiologic and pathological remodeling. Furthermore, we identify unique, CSC‐specific, remodeling events. Our data suggest that CSC interact with the microenvironment differently than non‐CSC, and that this could eventually be a therapeutic approach for targeting CSC. STEM Cells2012;30:2114–2127
Oncotarget | 2017
Renumathy Dhanasekaran; Meital Gabay-Ryan; Virginie Baylot; Ian Lai; Adriane R. Mosley; Xinqiang Huang; Sonya Zabludoff; Jian Li; Vivek Kaimal; Priya Karmali; Dean W. Felsher
Hepatocellular carcinoma (HCC) remains a significant clinical challenge with few therapeutic options. Genomic amplification and/or overexpression of the MYC oncogene is a common molecular event in HCC, thus making it an attractive target for drug therapy. Unfortunately, currently there are no direct drug therapies against MYC. As an alternative strategy, microRNAs regulated by MYC may be downstream targets for therapeutic blockade. MiR-17 family is a microRNA family transcriptionally regulated by MYC and it is commonly overexpressed in human HCCs. In this study, we performed systemic delivery of a novel lipid nanoparticle (LNP) encapsulating an anti-miR-17 oligonucleotide in a conditional transgenic mouse model of MYC driven HCC. Treatment with anti-miR-17 in vivo, but not with a control anti-miRNA, resulted in significant de-repression of direct targets of miR-17, robust apoptosis, decreased proliferation and led to delayed tumorigenesis in MYC-driven HCCs. Global gene expression profiling revealed engagement of miR-17 target genes and inhibition of key transcriptional programs of MYC, including cell cycle progression and proliferation. Hence, anti-miR-17 is an effective therapy for MYC-driven HCC.
Cell Cycle | 2011
Reza Ardehali; Shah R. Ali; Matthew A. Inlay; Adriane R. Mosley; Irving L. Weissman
Comment on: Ardehali R, et al. Proc Natl Acad Sci USA. 2011; 108:3282-7.
Proceedings of the National Academy of Sciences of the United States of America | 2012
Stephen B. Willingham; Jens-Peter Volkmer; Andrew J. Gentles; Debashis Sahoo; Piero Dalerba; Siddhartha Mitra; Jian Wang; Humberto Contreras-Trujillo; Robin Martin; Justin D. Cohen; Patricia Lovelace; Ferenc A. Scheeren; Mark P. Chao; Kipp Weiskopf; Chad Tang; Anne K. Volkmer; Tejaswitha J Naik; Theresa A. Storm; Adriane R. Mosley; Badreddin Edris; Seraina Schmid; Chris K. Sun; Mei-Sze Chua; Oihana Murillo; Pradeep S. Rajendran; Adriel C. Cha; Robert K. Chin; Dongkyoon Kim; Maddalena Adorno; Tal Raveh
Cancer Immunology, Immunotherapy | 2018
Jonathan Hebb; Adriane R. Mosley; Felipe Vences-Catalán; Narendiran Rajasekaran; Anna Rosén; Peter Ellmark; Dean W. Felsher
Cancer Research | 2017
Srividya Swaminathan; Adriane R. Mosley; Crista Horton; Daniel Liefwalker; Anja Deutzmann; Renumathy Dhanasekaran; Arvin M. Gouw; Andrew J. Gentles; Martin Eilers; Holden T. Maecker; Dean W. Felsher
Blood | 2016
Jonathan P. O. Hebb; Adriane R. Mosley; Felipe Vences Catalan; Peter Ellmark; Per Norlén; Dean W. Felsher