JAK2V617F but not CALR mutations confer increased molecular responses to interferon-α via JAK1/STAT1 activation
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T. Brümmendorf | G. Müller-Newen | I. Costa | S. Koschmieder | H. Hasselbalch | B. Denecke | Lijuan Han | N. Chatain | C. Schubert | J. Mayer | Z. Ráčil | L. Kjær | S. Cordua | M. Holmström | T. Larsen | V. Skov | J. Czech | T. Knudsen | Tiago Maié | A. Sørensen | Deniz Gezer | B. Kubesova | Julian Baumeister | B. Weinbergerová | A. Maurer | Kristina Feldberg | T. Maié | Assja Crepcia | Blanka Kubesova | Nicolas Chatain
[1] H. Hasselbalch,et al. Safety and efficacy of combination therapy of interferon‐α2 and ruxolitinib in polycythemia vera and myelofibrosis , 2018, Cancer medicine.
[2] I. Svane,et al. Sorted peripheral blood cells identify CALR mutations in B- and T-lymphocytes , 2018, Leukemia & lymphoma.
[3] P. Cony-Makhoul,et al. Benefits and pitfalls of pegylated interferon-α2a therapy in patients with myeloproliferative neoplasm-associated myelofibrosis: a French Intergroup of Myeloproliferative neoplasms (FIM) study , 2017, Haematologica.
[4] S. Swerdlow. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues , 2017 .
[5] G. Schett,et al. JAK1-dependent transphosphorylation of JAK2 limits the antifibrotic effects of selective JAK2 inhibitors on long-term treatment , 2017, Annals of the rheumatic diseases.
[6] W. Vainchenker,et al. Genetic basis and molecular pathophysiology of classical myeloproliferative neoplasms. , 2017, Blood.
[7] T. Decker,et al. Canonical and Non-Canonical Aspects of JAK–STAT Signaling: Lessons from Interferons for Cytokine Responses , 2017, Front. Immunol..
[8] H. Hasselbalch,et al. Differential Dynamics of CALR Mutant Allele Burden in Myeloproliferative Neoplasms during Interferon Alfa Treatment , 2016, PloS one.
[9] U. Vinkemeier,et al. STAT2 Is a Pervasive Cytokine Regulator due to Its Inhibition of STAT1 in Multiple Signaling Pathways , 2016, PLoS biology.
[10] S. Pai,et al. Long-acting interferon for myeloproliferative neoplasms - an update , 2016, Expert review of hematology.
[11] Mario Cazzola,et al. The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. , 2016, Blood.
[12] T. Brümmendorf,et al. Calreticulin-mutant proteins induce megakaryocytic signaling to transform hematopoietic cells and undergo accelerated degradation and Golgi-mediated secretion , 2016, Journal of Hematology & Oncology.
[13] S. Giraudier,et al. Interferon-alpha for the therapy of myeloproliferative neoplasms: targeting the malignant clone , 2016, Leukemia.
[14] F. Al-Shahrour,et al. Mutant Calreticulin Requires Both Its Mutant C-terminus and the Thrombopoietin Receptor for Oncogenic Transformation. , 2016, Cancer discovery.
[15] C. Pecquet,et al. Thrombopoietin receptor activation by myeloproliferative neoplasm associated calreticulin mutants. , 2016, Blood.
[16] C. Pecquet,et al. Calreticulin mutants in mice induce an MPL-dependent thrombocytosis with frequent progression to myelofibrosis. , 2016, Blood.
[17] N. Komatsu,et al. Activation of the thrombopoietin receptor by mutant calreticulin in CALR-mutant myeloproliferative neoplasms. , 2016, Blood.
[18] C. Pecquet,et al. Thrombopoietin receptor is required for the oncogenic function of CALR mutants , 2016, Leukemia.
[19] G. Stark,et al. Response to interferons and antibacterial innate immunity in the absence of tyrosine‐phosphorylated STAT1 , 2016, EMBO reports.
[20] T. Barbui,et al. Myeloproliferative neoplasms and inflammation: whether to target the malignant clone or the inflammatory process or both , 2016, Leukemia.
[21] S. Carillo,et al. Clinical and molecular response to interferon-α therapy in essential thrombocythemia patients with CALR mutations. , 2015, Blood.
[22] H. Hasselbalch,et al. MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives , 2015, Mediators of inflammation.
[23] J. Tokarski,et al. Discovery of a Highly Selective JAK2 Inhibitor, BMS-911543, for the Treatment of Myeloproliferative Neoplasms. , 2015, ACS medicinal chemistry letters.
[24] R. Greil,et al. Molecular responses and chromosomal aberrations in patients with polycythemia vera treated with peg-proline-interferon alpha-2b , 2015, American journal of hematology.
[25] Matthew E. Ritchie,et al. limma powers differential expression analyses for RNA-sequencing and microarray studies , 2015, Nucleic acids research.
[26] S. Carillo,et al. Presence of calreticulin mutations in JAK2-negative polycythemia vera. , 2014, Blood.
[27] H. Hasselbalch,et al. Combination therapy with interferon and JAK1-2 inhibitor is feasible: Proof of concept with rapid reduction in JAK2V617F-allele burden in polycythemia vera , 2014, Leukemia research reports.
[28] J. Kiladjian,et al. Interferon alfa therapy in CALR-mutated essential thrombocythemia. , 2014, The New England journal of medicine.
[29] J. D. Fitzpatrick,et al. Somatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2. , 2013, The New England journal of medicine.
[30] G. Superti-Furga,et al. Somatic mutations of calreticulin in myeloproliferative neoplasms. , 2013, The New England journal of medicine.
[31] Francisco Cervantes,et al. Revised response criteria for myelofibrosis: International Working Group-Myeloproliferative Neoplasms Research and Treatment (IWG-MRT) and European LeukemiaNet (ELN) consensus report. , 2013, Blood.
[32] O. Abdel-Wahab,et al. Molecular analysis of patients with polycythemia vera or essential thrombocythemia receiving pegylated interferon α-2a. , 2013, Blood.
[33] J. Galipeau,et al. A Fusion Cytokine Coupling GMCSF to IL9 Induces Heterologous Receptor Clustering and STAT1 Hyperactivation through JAK2 Promiscuity , 2013, PloS one.
[34] 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.
[35] W. Sellers,et al. Modulation of activation-loop phosphorylation by JAK inhibitors is binding mode dependent. , 2012, Cancer discovery.
[36] P. Ross-Macdonald,et al. Characterization of BMS-911543, a functionally selective small-molecule inhibitor of JAK2 , 2012, Leukemia.
[37] B. Bernstein,et al. Heterodimeric JAK-STAT Activation as a Mechanism of Persistence to JAK2 Inhibitor Therapy , 2011, Nature.
[38] M. Carroll,et al. Bcr-abl signals to desensitize chronic myeloid leukemia cells to IFNα via accelerating the degradation of its receptor. , 2011, Blood.
[39] D. Levy,et al. STAT3 Negatively Regulates Type I IFN-Mediated Antiviral Response , 2011, The Journal of Immunology.
[40] C. Schindler,et al. Suppressor of Cytokine Signaling (SOCS) 1 Inhibits Type I Interferon (IFN) Signaling via the Interferon α Receptor (IFNAR1)-associated Tyrosine Kinase Tyk2* , 2011, The Journal of Biological Chemistry.
[41] Philipp Erben,et al. Novel imatinib-sensitive PDGFRA-activating point mutations in hypereosinophilic syndrome induce growth factor independence and leukemia-like disease. , 2011, Blood.
[42] E. Dermitzakis,et al. Distinct clinical phenotypes associated with JAK2V617F reflect differential STAT1 signaling. , 2010, Cancer cell.
[43] G. Reuther,et al. Activation of JAK2-V617F by Components of Heterodimeric Cytokine Receptors* , 2010, The Journal of Biological Chemistry.
[44] M. Griesshammer,et al. Response criteria for essential thrombocythemia and polycythemia vera: result of a European LeukemiaNet consensus conference. , 2009, Blood.
[45] N. Shinton. WHO Classification of Tumors of Hematopoietic and Lymphoid Tissues , 2007 .
[46] G. Reuther,et al. Transformation of hematopoietic cells and activation of JAK2-V617F by IL-27R, a component of a heterodimeric type I cytokine receptor , 2007, Proceedings of the National Academy of Sciences.
[47] H. Hasselbalch,et al. The JAK2 V617F mutation involves B‐ and T‐lymphocyte lineages in a subgroup of patients with Philadelphia‐chromosome negative chronic myeloproliferative disorders , 2007, British journal of haematology.
[48] K. Shuai,et al. UBP43 is a novel regulator of interferon signaling independent of its ISG15 isopeptidase activity , 2006, The EMBO journal.
[49] L. Ivashkiv,et al. Role of STAT3 in Type I Interferon Responses , 2006, Journal of Biological Chemistry.
[50] H. Lodish,et al. Expression of a homodimeric type I cytokine receptor is required for JAK2V617F-mediated transformation. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[51] M. David,et al. Cutting Edge: Role of STAT1, STAT3, and STAT5 in IFN-αβ Responses in T Lymphocytes , 2005, The Journal of Immunology.
[52] K. Schroder,et al. Interferon- : an overview of signals, mechanisms and functions , 2004 .
[53] K. Shuai,et al. Regulation of JAK–STAT signalling in the immune system , 2003, Nature Reviews Immunology.
[54] S. Fujita,et al. Constitutive expression of SOCS3 confers resistance to IFN-alpha in chronic myelogenous leukemia cells. , 2002, Blood.
[55] K. Shuai,et al. The Suppressor of Cytokine Signaling (SOCS) 1 and SOCS3 but Not SOCS2 Proteins Inhibit Interferon-mediated Antiviral and Antiproliferative Activities* , 1998, The Journal of Biological Chemistry.
[56] J. Darnell,et al. Transcriptionally active Stat1 is required for the antiproliferative effects of both interferon alpha and interferon gamma. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[57] G. Stark,et al. Kinase‐negative mutants of JAK1 can sustain interferon‐gamma‐inducible gene expression but not an antiviral state. , 1996, The EMBO journal.
[58] S. Ziegler,et al. Proliferative responses and binding properties of hematopoietic cells transfected with low-affinity receptors for leukemia inhibitory factor, oncostatin M, and ciliary neurotrophic factor. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[59] J. Darnell,et al. A single phosphotyrosine residue of Stat91 required for gene activation by interferon-gamma. , 1993, Science.
[60] H. L. Wright,et al. Interferon gene expression signature in rheumatoid arthritis neutrophils correlates with a good response to TNFi therapy. , 2015, Rheumatology.
[61] H. Hasselbalch,et al. Corrigendum to "Combination therapy with interferon and JAK1-2 inhibitor is feasible. Proof of concept with rapid reduction in JAK2V617F-allele burden in Polycythemia Vera" [Leuk. Res. Rep. 3 (2) (2014) 73-75]. , 2015, Leukemia research reports.
[62] M. David,et al. Cutting edge: role of STAT1, STAT3, and STAT5 in IFN-alpha beta responses in T lymphocytes. , 2005, Journal of immunology.
[63] K. Schroder,et al. Interferon-gamma: an overview of signals, mechanisms and functions. , 2004, Journal of leukocyte biology.
[64] R. Foà,et al. Chronic myeloid leukemia cells resistant to interferon-alpha lack STAT1 expression. , 2000, The hematology journal : the official journal of the European Haematology Association.