Gli1+ Mesenchymal Stromal Cells Are a Key Driver of Bone Marrow Fibrosis and an Important Cellular Therapeutic Target.

[1]  T. Barbui,et al.  Long-term findings from COMFORT-II, a phase 3 study of ruxolitinib vs best available therapy for myelofibrosis , 2016, Leukemia.

[2]  Steven L. Chang,et al.  Pharmacological GLI2 inhibition prevents myofibroblast cell-cycle progression and reduces kidney fibrosis. , 2015, The Journal of clinical investigation.

[3]  E. Passegué,et al.  Normal and leukemic stem cell niches: insights and therapeutic opportunities. , 2015, Cell stem cell.

[4]  J. Kutok,et al.  Phase II evaluation of IPI-926, an oral Hedgehog inhibitor, in patients with myelofibrosis , 2015, Leukemia & lymphoma.

[5]  B. Ebert,et al.  Perivascular Gli1+ progenitors are key contributors to injury-induced organ fibrosis. , 2015, Cell stem cell.

[6]  T. Brümmendorf,et al.  Activated fibronectin-secretory phenotype of mesenchymal stromal cells in pre-fibrotic myeloproliferative neoplasms , 2014, Journal of Hematology & Oncology.

[7]  A. Tefferi,et al.  The prognostic advantage of calreticulin mutations in myelofibrosis might be confined to type 1 or type 1-like CALR variants. , 2014, Blood.

[8]  A. Ruiz i Altaba,et al.  Context-dependent signal integration by the GLI code: The oncogenic load, pathways, modifiers and implications for cancer therapy , 2014, Seminars in cell & developmental biology.

[9]  A. Mailleux,et al.  Targeting the hedgehog-glioma-associated oncogene homolog pathway inhibits bleomycin-induced lung fibrosis in mice. , 2014, American journal of respiratory cell and molecular biology.

[10]  D. Lai,et al.  Neuropathy of haematopoietic stem cell niche is essential for myeloproliferative neoplasms , 2014, Nature.

[11]  Hongwei Wang,et al.  Epidemiology of myeloproliferative neoplasms in the United States , 2014, Leukemia & lymphoma.

[12]  L. Joosten,et al.  Proteome-wide analysis and CXCL4 as a biomarker in systemic sclerosis. , 2014, The New England journal of medicine.

[13]  G. Superti-Furga,et al.  Somatic mutations of calreticulin in myeloproliferative neoplasms. , 2013, The New England journal of medicine.

[14]  J. D. Fitzpatrick,et al.  Somatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2. , 2013, The New England journal of medicine.

[15]  E. Stanchina,et al.  Improved Efficacy Of Combination Of JAK2 and Hedgehog Inhibitors In Myelofibrosis , 2013 .

[16]  R. Kramann,et al.  Understanding the origin, activation and regulation of matrix‐producing myofibroblasts for treatment of fibrotic disease , 2013, The Journal of pathology.

[17]  A. Bergman,et al.  Arteriolar niches maintain haematopoietic stem cell quiescence , 2013, Nature.

[18]  E. Hsiao,et al.  Myeloproliferative neoplasia remodels the endosteal bone marrow niche into a self-reinforcing leukemic niche. , 2013, Cell stem cell.

[19]  I. Nookaew,et al.  Enriching the gene set analysis of genome-wide data by incorporating directionality of gene expression and combining statistical hypotheses and methods , 2013, Nucleic acids research.

[20]  Jason Gotlib,et al.  A double-blind, placebo-controlled trial of ruxolitinib for myelofibrosis. , 2012, The New England journal of medicine.

[21]  Francisco Cervantes,et al.  JAK inhibition with ruxolitinib versus best available therapy for myelofibrosis. , 2012, The New England journal of medicine.

[22]  A. Tefferi Primary myelofibrosis: 2012 update on diagnosis, risk stratification, and management , 2011, American journal of hematology.

[23]  D. Lai,et al.  Loss of Cxcl12/Sdf-1 in adult mice decreases the quiescent state of hematopoietic stem/progenitor cells and alters the pattern of hematopoietic regeneration after myelosuppression. , 2011, Blood.

[24]  Ben D. MacArthur,et al.  Mesenchymal and haematopoietic stem cells form a unique bone marrow niche , 2010, Nature.

[25]  C. Trautwein,et al.  CXC chemokine ligand 4 (Cxcl4) is a platelet‐derived mediator of experimental liver fibrosis , 2010, Hepatology.

[26]  Sandra A. Moore,et al.  Efficacy of TG101348, a selective JAK2 inhibitor, in treatment of a murine model of JAK2V617F-induced polycythemia vera. , 2008, Cancer cell.

[27]  B. Bain,et al.  Bone marrow fibrosis: pathophysiology and clinical significance of increased bone marrow stromal fibres , 2007, British journal of haematology.

[28]  C. Bloomfield,et al.  Proposals and rationale for revision of the World Health Organization diagnostic criteria for polycythemia vera, essential thrombocythemia, and primary myelofibrosis: recommendations from an ad hoc international expert panel. , 2007, Blood.

[29]  T. Shimokawa,et al.  Inhibition of GLI-mediated transcription and tumor cell growth by small-molecule antagonists , 2007, Proceedings of the National Academy of Sciences.

[30]  F. Wendling,et al.  Pathogenesis of myelofibrosis with myeloid metaplasia: lessons from mouse models of the disease. , 2005, Seminars in oncology.

[31]  R. Hoffman,et al.  Allogeneic hematopoietic stem-cell transplantation with reduced-intensity conditioning in intermediate- or high-risk patients with myelofibrosis with myeloid metaplasia. , 2005, Blood.

[32]  W. Vainchenker,et al.  High thrombopoietin production by hematopoietic cells induces a fatal myeloproliferative syndrome in mice. , 1997, Blood.

[33]  D. Lacey,et al.  A model of myelofibrosis and osteosclerosis in mice induced by overexpressing thrombopoietin (mpl ligand): reversal of disease by bone marrow transplantation. , 1996, Blood.

[34]  J. Adamson,et al.  Platelet factor‐4 excretion in myeloproliferative disease: implications for the aetiology of myelofibrosis , 1984, British journal of haematology.

[35]  S. Schwartz Myeloproliferative Disorders , 1975, Annals of surgery.

[36]  W. Seeger,et al.  Two-Way Conversion between Lipogenic and Myogenic Fibroblastic Phenotypes Marks the Progression and Resolution of Lung Fibrosis. , 2017, Cell stem cell.

[37]  Xijin Ge,et al.  Gene Set Data for Pathway Analysis in Mouse , 2015 .

[38]  R. Levine JAK-mutant myeloproliferative neoplasms. , 2012, Current topics in microbiology and immunology.

[39]  J. Thiele,et al.  Ultrastructure of bone marrow tissue in so-called primary (idiopathic) myelofibrosis-osteomyelosclerosis (agnogenic myeloid metaplasia). I. Abnormalities of megakaryopoiesis and thrombocytes. , 1991, Journal of submicroscopic cytology and pathology.

[40]  N. Abraham,et al.  Modulation of erythropoiesis by novel human bone marrow cytochrome P450-dependent metabolites of arachidonic acid. , 1991, Blood.

[41]  S. Pileri,et al.  Stromal cells in primary myelofibrosis: ultrastructural observations , 1985, Virchows Archiv. B, Cell pathology including molecular pathology.