Institution
Hudson Institute
Nonprofit•Washington D.C., District of Columbia, United States•
About: Hudson Institute is a nonprofit organization based out in Washington D.C., District of Columbia, United States. It is known for research contribution in the topics: Follistatin & Stem cell. The organization has 607 authors who have published 830 publications receiving 35790 citations.
Topics: Follistatin, Stem cell, Cellular differentiation, Cancer, Population
Papers published on a yearly basis
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National Institute for Biological Standards and Control1, University of Sheffield2, Karolinska Institutet3, Technion – Israel Institute of Technology4, Leeds Teaching Hospitals NHS Trust5, Monash University6, Hebrew University of Jerusalem7, Thermo Fisher Scientific8, National Institutes of Health9, University of Cambridge10, University of Kansas11, University of Toronto12, Masaryk University13, Academy of Sciences of the Czech Republic14, Uppsala University15, Stanford University16, Newcastle University17, Pierre-and-Marie-Curie University18, WiCell19, University of Helsinki20, King's College London21, Kyoto University22, Hudson Institute23
TL;DR: The International Stem Cell Initiative characterized 59 human embryonic stem cell lines from 17 laboratories worldwide and found that despite diverse genotypes and different techniques used for derivation and maintenance, all lines exhibited similar expression patterns for several markers ofhuman embryonic stem cells.
Abstract: The International Stem Cell Initiative characterized 59 human embryonic stem cell lines from 17 laboratories worldwide. Despite diverse genotypes and different techniques used for derivation and maintenance, all lines exhibited similar expression patterns for several markers of human embryonic stem cells. They expressed the glycolipid antigens SSEA3 and SSEA4, the keratan sulfate antigens TRA-1-60, TRA-1-81, GCTM2 and GCT343, and the protein antigens CD9, Thy1 (also known as CD90), tissue- nonspecific alkaline phosphatase and class 1 HLA, as well as the strongly developmentally regulated genes NANOG, POU5F1 (formerly known as OCT4), TDGF1, DNMT3B, GABRB3 and GDF3. Nevertheless, the lines were not identical: differences in expression of several lineage markers were evident, and several imprinted genes showed generally similar allele-specific expression patterns, but some gene-dependent variation was observed. Also, some female lines expressed readily detectable levels of XIST whereas others did not. No significant contamination of the lines with mycoplasma, bacteria or cytopathic viruses was detected.
1,064 citations
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TL;DR: Clinical investigations using stem cell products in regenerative medicine are addressing a wide spectrum of conditions using a variety of stem cell types and applications are progressing in trials, some with early benefits to patients.
1,040 citations
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TL;DR: NVP-BEZ235 inhibits the PI3K/mTOR axis and results in antiproliferative and antitumoral activity in cancer cells with both wild-type and mutated p110-alpha, suggesting that skin may serve as surrogate tissue for pharmacodynamic studies.
Abstract: Phosphatidylinositol-3-kinase (PI3K) pathway deregulation is a common event in human cancer, either through inactivation of the tumor suppressor phosphatase and tensin homologue deleted from chromosome 10 or activating mutations of p110-alpha These hotspot mutations result in oncogenic activity of the enzyme and contribute to therapeutic resistance to the anti-HER2 antibody trastuzumab The PI3K pathway is, therefore, an attractive target for cancer therapy We have studied NVP-BEZ235, a dual inhibitor of the PI3K and the downstream mammalian target of rapamycin (mTOR) NVP-BEZ235 inhibited the activation of the downstream effectors Akt, S6 ribosomal protein, and 4EBP1 in breast cancer cells The antiproliferative activity of NVP-BEZ235 was superior to the allosteric selective mTOR complex inhibitor everolimus in a panel of 21 cancer cell lines of different origin and mutation status The described Akt activation due to mTOR inhibition was prevented by higher doses of NVP-BEZ235 NVP-BEZ235 reversed the hyperactivation of the PI3K/mTOR pathway caused by the oncogenic mutations of p110-alpha, E545K, and H1047R, and inhibited the proliferation of HER2-amplified BT474 cells exogenously expressing these mutations that render them resistant to trastuzumab In trastuzumab-resistant BT474 H1047R breast cancer xenografts, NVP-BEZ235 inhibited PI3K signaling and had potent antitumor activity In treated animals, there was complete inhibition of PI3K signaling in the skin at pharmacologically active doses, suggesting that skin may serve as surrogate tissue for pharmacodynamic studies In summary, NVP-BEZ235 inhibits the PI3K/mTOR axis and results in antiproliferative and antitumoral activity in cancer cells with both wild-type and mutated p110-alpha
706 citations
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TL;DR: DC activation by type I IFNs represents a novel mechanism of immunomodulation by these cytokines, which could be important during antiviral responses and autoimmune reactions.
Abstract: This study identifies type I IFNs as activating cytokines in a serum-free system in which human dendritic cells (DC) were generated from CD34+ progenitor cells. After 14 days of culture in GM-CSF, TNF-alpha, and IL-4, CD34+ progenitors gave rise to a population of large, immature DC expressing CD1a and CD11b but lacking CD14, CD80, CD83, CD86, and CMRF44. During the next 2 wk, this population spontaneously matured into nonadherent, CD1a(low/-), CD11b(low/-), CD14-, CD80+, CD83+, CD86+, CMRF44+ DC with high allostimulatory activity in the MLR. To examine which factors influenced this maturation, 25 different cytokines or factors were added to the immature DC culture. Only type I IFNs (alpha or beta) accelerated this maturation in a dose-dependent manner, so that after only 3 days the majority of large cells acquired the morphology, phenotype, and function characteristics of mature DC. Furthermore, supernatants from cultures containing spontaneously maturing DC revealed low levels of endogenous IFN production. Because of the similarity of the activation of DC in our culture system with the phenotypic and functional changes observed during Langerhans cells activation and migration in vivo, we investigated the effect of IFN-alpha on human Langerhans cell migration. IFN-alpha also activated the migration of human split skin-derived DC, demonstrating that this effect was not limited to DC derived in vitro from hemopoietic progenitor cells. DC activation by type I IFNs represents a novel mechanism of immunomodulation by these cytokines, which could be important during antiviral responses and autoimmune reactions.
662 citations
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TL;DR: It is shown that endogenous signaling by bone morphogenetic protein-2 controls the differentiation of embryonic stem cells into this lineage, and that the conservation of developmental mechanisms at the cellular level can be exploited in this system to provide a facile route for the generation of neural precursors from pluripotent cells.
Abstract: Human embryonic stem cells differentiate spontaneously in vitro into a range of cell types, and they frequently give rise to cells with the properties of extra-embryonic endoderm. We show here that endogenous signaling by bone morphogenetic protein-2 controls the differentiation of embryonic stem cells into this lineage. Treatment of embryonic stem cell cultures with the bone morphogenetic protein antagonist noggin blocks this form of differentiation and induces the appearance of a novel cell type that can give rise to neural precursors. These findings indicate that bone morphogenetic protein-2 controls a key early commitment step in human embryonic stem cell differentiation, and show that the conservation of developmental mechanisms at the cellular level can be exploited in this system--in this case, to provide a facile route for the generation of neural precursors from pluripotent cells.
509 citations
Authors
Showing all 611 results
Name | H-index | Papers | Citations |
---|---|---|---|
David Robertson | 127 | 1106 | 67914 |
Jun Liu | 100 | 1165 | 73692 |
Bryan R.G. Williams | 97 | 381 | 40306 |
Atul Malhotra | 97 | 794 | 40203 |
Alan O Trounson | 92 | 541 | 33785 |
David K. Gardner | 92 | 398 | 25301 |
Di Wu | 87 | 965 | 48697 |
Henry G. Burger | 78 | 345 | 21590 |
Michelle Lane | 77 | 251 | 19032 |
John W. Funder | 74 | 397 | 20195 |
Lois A. Salamonsen | 73 | 298 | 15132 |
D. M. De Kretser | 68 | 275 | 15098 |
Paul J. Hertzog | 67 | 276 | 21157 |
Jock K. Findlay | 67 | 287 | 14455 |
Robert I McLachlan | 66 | 327 | 14371 |