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Polycythemia vera erythroid precursors exhibit increased proliferation and apoptosis resistance associated with abnormal RAS and PI3K pathway activation
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“aberrant activations of RAC2, PAK1 and PI3K-AKT have been separately described17,22,41,42.”
From Gadd45g insufficiency drives the pathogenesis of myeloproliferative neoplasms (2024) · cites this paper as [42]
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Citations
Cites
Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disorders
Jones, A. V. (2005) · Blood · doi:10.1182/blood-2005-03-1320 · Cited by 843 · cited 1×
“The discovery of an acquired, somatic mutation JAK2V617F present within the gene encoding the cytoplasmic tyrosine kinase JAK2 detected in the majority (95%) of PV patients provided insight as to how the molecular and biological characteristics of the disease might relate to its clinical phenotype [6-11].”
Background
Research works printed but not linked: 51
- Prchal, 1974, Letter: Bone-marrow responses in polycythemia vera, N Engl J Med, 290, 1382, 10.1056/NEJM197406132902419 · DOI
- Eaves, 1978, Erythropoietin (Ep) dose-response curves for three classes of erythroid progenitors in normal human marrow and in patients with polycythemia vera, Blood, 52, 1196, 10.1182/blood.V52.6.1196.1196 · DOI
- Casadevall, 1982, Erythroid progenitors in polycythemia vera: demonstration of their hypersensitivity to erythropoietin using serum free cultures, Blood, 59, 447, 10.1182/blood.V59.2.447.447 · DOI
- Means, 1989, Erythropoietin receptors in polycythemia vera, J Clin Invest, 84, 1340, 10.1172/JCI114303 · DOI
- Hess, 1994, Molecular analysis of the erythropoietin receptor system in patients with polycythaemia vera, Br J Haematol, 88, 794, 10.1111/j.1365-2141.1994.tb05119.x · DOI
- James, 2005, A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera, Nature, 434, 1144, 10.1038/nature03546 · DOI
- Levine, 2005, Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis, Cancer Cell, 7, 387, 10.1016/j.ccr.2005.03.023 · DOI · Paper page
- Kralovics, 2005, A gain-of-function mutation of JAK2 in myeloproliferative disorders, N Engl J Med, 352, 1779, 10.1056/NEJMoa051113 · DOI · Paper page
- Baxter, 2005, Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders, Lancet, 365, 1054, 10.1016/S0140-6736(05)74230-6 · DOI · Paper page
- Zhao, 2005, Identification of an acquired JAK2 mutation in polycythemia vera, J Biol Chem, 280, 22788, 10.1074/jbc.C500138200 · DOI
- Wernig, 2006, Expression of Jak2V617F causes a polycythemia vera-like disease with associated myelofibrosis in a murine bone marrow transplant model, Blood, 107, 4274, 10.1182/blood-2005-12-4824 · DOI
- Bumm, 2006, Characterization of murine JAK2V617F-positive myeloproliferative disease, Cancer Res, 66, 11156, 10.1158/0008-5472.CAN-06-2210 · DOI
- Lacout, 2006, JAK2V617F expression in murine hematopoietic cells leads to MPD mimicking human PV with secondary myelofibrosis, Blood, 108, 1652, 10.1182/blood-2006-02-002030 · DOI
- Zaleskas, 2006, Molecular pathogenesis and therapy of polycythemia induced in mice by JAK2 V617F, PLoS ONE, 1, e18, 10.1371/journal.pone.0000018 · DOI
- Tiedt, 2008, Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic mice, Blood, 111, 3931, 10.1182/blood-2007-08-107748 · DOI
- Shide, 2008, Development of ET, primary myelofibrosis and PV in mice expressing JAK2 V617F, Leukemia, 22, 87, 10.1038/sj.leu.2405043 · DOI
- Rumi, 2006, JAK2 (V617F) as an acquired somatic mutation and a secondary genetic event associated with disease progression in familial myeloproliferative disorders, Cancer, 107, 2206, 10.1002/cncr.22240 · DOI
- Bellanne-Chantelot, 2006, Genetic and clinical implications of the Val617Phe JAK2 mutation in 72 families with myeloproliferative disorders, Blood, 108, 346, 10.1182/blood-2005-12-4852 · DOI
- Nussenzveig, 2007, Polycythemia vera is not initiated by JAK2V617F mutation, Exp Hematol, 35, 32, 10.1016/j.exphem.2006.11.012 · DOI
- Kralovics, 2006, Acquisition of the V617F mutation of JAK2 is a late genetic event in a subset of patients with myeloproliferative disorders, Blood, 108, 1377, 10.1182/blood-2005-11-009605 · DOI
- Parganas, 1998, Jak2 is essential for signaling through a variety of cytokine receptors, Cell, 93, 385, 10.1016/S0092-8674(00)81167-8 · DOI
- Witthuhn, 1993, JAK2 associates with the erythropoietin receptor and is tyrosine phosphorylated and activated following stimulation with erythropoietin, Cell, 74, 227, 10.1016/0092-8674(93)90414-L · DOI
- Feng, 1997, Activation of Jak2 catalytic activity requires phosphorylation of Y1007 in the kinase activation loop, Mol Cell Biol, 17, 2497, 10.1128/MCB.17.5.2497 · DOI
- Richmond, 2005, Turning cells red: signal transduction mediated by erythropoietin, Trends Cell Biol, 15, 146, 10.1016/j.tcb.2005.01.007 · DOI
- Klingmuller, 1995, Specific recruitment of SH-PTP1 to the erythropoietin receptor causes inactivation of JAK2 and termination of proliferative signals, Cell, 80, 729, 10.1016/0092-8674(95)90351-8 · DOI
- Sokol, 1995, Primary familial polycythemia: a frameshift mutation in the erythropoietin receptor gene and increased sensitivity of erythroid progenitors to erythropoietin, Blood, 86, 15, 10.1182/blood.V86.1.15.bloodjournal86115 · DOI
- Arcasoy, 1999, A human erythropoietin receptor gene mutant causing familial erythrocytosis is associated with deregulation of the rates of Jak2 and Stat5 inactivation, Exp Hematol, 27, 63, 10.1016/S0301-472X(98)00003-4 · DOI
- Watowich, 1999, Erythropoietin receptor mutations associated with familial erythrocytosis cause hypersensitivity to erythropoietin in the heterozygous state, Blood, 94, 2530, 10.1182/blood.V94.7.2530.419k35_2530_2532 · DOI
- Socolovsky, 1999, Fetal anemia and apoptosis of red cell progenitors in Stat5a-/-5b-/- mice: a direct role for Stat5 in Bcl-X(L) induction, Cell, 98, 181, 10.1016/S0092-8674(00)81013-2 · DOI
- Socolovsky, 2001, Ineffective erythropoiesis in Stat5a(-/-)5b(-/-) mice due to decreased survival of early erythroblasts, Blood, 98, 3261, 10.1182/blood.V98.12.3261 · DOI
- Garcon, 2006, Constitutive activation of STAT5 and Bcl-xL overexpression can induce endogenous erythroid colony formation in human primary cells, Blood, 108, 1551, 10.1182/blood-2005-10-009514 · DOI
- Grebien, 2008, Stat5 activation enables erythropoiesis in the absence of EPOR and Jak2, Blood, 111, 4511, 10.1182/blood-2007-07-102848 · DOI
- Zhang, 2004, Constitutive activation of the MEK/ERK pathway mediates all effects of oncogenic H-ras expression in primary erythroid progenitors, Blood, 104, 1679, 10.1182/blood-2004-04-1362 · DOI
- Menon, 2006, Core erythropoietin receptor signals for late erythroblast development, Blood, 107, 2662, 10.1182/blood-2005-02-0684 · DOI
- Klingmuller, 1997, Identification of a novel pathway important for proliferation and differentiation of primary erythroid progenitors, Proc Natl Acad Sci U S A, 94, 3016, 10.1073/pnas.94.7.3016 · DOI
- Ghaffari, 2006, AKT induces erythroid-cell maturation of JAK2-deficient fetal liver progenitor cells and is required for Epo regulation of erythroid-cell differentiation, Blood, 107, 1888, 10.1182/blood-2005-06-2304 · DOI
- Arcasoy, 2005, Co-operative signalling mechanisms required for erythroid precursor expansion in response to erythropoietin and stem cell factor, Br J Haematol, 130, 121, 10.1111/j.1365-2141.2005.05580.x · DOI
- Panzenbock, 1998, Growth and differentiation of human stem cell factor/erythropoietin-dependent erythroid progenitor cells in vitro, Blood, 92, 3658, 10.1182/blood.V92.10.3658 · DOI
- Bild, 2006, Oncogenic pathway signatures in human cancers as a guide to targeted therapies, Nature, 439, 353, 10.1038/nature04296 · DOI
- Potti, 2006, Genomic signatures to guide the use of chemotherapeutics, Nat Med, 12, 1294, 10.1038/nm1491 · DOI
- Anders, 2008, Age-specific differences in oncogenic pathway deregulation seen in human breast tumors, PLoS ONE, 3, e1373, 10.1371/journal.pone.0001373 · DOI
- Montagna, 1994, In vitro sensitivity of human erythroid progenitors to hemopoietic growth factors: studies on primary and secondary polycythemia, Haematologica, 79, 311
- Dupont, 2007, The JAK2 617V > F mutation triggers erythropoietin hypersensitivity and terminal erythroid amplification in primary cells from patients with polycythemia vera, Blood, 110, 1013, 10.1182/blood-2006-10-054940 · DOI
- Somervaille, 2001, Growth factor withdrawal from primary human erythroid progenitors induces apoptosis through a pathway involving glycogen synthase kinase-3 and Bax, Blood, 98, 1374, 10.1182/blood.V98.5.1374 · DOI
- Gaikwad, 2007, In vitro expansion of erythroid progenitors from polycythemia vera patients leads to decrease in JAK2 V617F allele, Exp Hematol, 35, 587, 10.1016/j.exphem.2006.12.007 · DOI
- Zeuner, 2006, Increased death receptor resistance and FLIPshort expression in polycythemia vera erythroid precursor cells, Blood, 107, 3495, 10.1182/blood-2005-07-3037 · DOI
- Schmidt, 2004, PI3 kinase is important for Ras, MEK and Erk activation of Epo-stimulated human erythroid progenitors, BMC Biol, 2, 7, 10.1186/1741-7007-2-7 · DOI
- Halupa, 2005, Erythropoietin receptor Y479 couples to ERK1/2 activation via recruitment of phospholipase Cgamma, Exp Cell Res, 309, 1, 10.1016/j.yexcr.2005.04.030 · DOI
- Verstovsek, 2008, WP1066, a novel JAK2 inhibitor, suppresses proliferation and induces apoptosis in erythroid human cells carrying the JAK2 V617F mutation, Clin Cancer Res, 14, 788, 10.1158/1078-0432.CCR-07-0524 · DOI
- Dai, 2005, Increased erythropoiesis in polycythemia vera is associated with increased erythroid progenitor proliferation and increased phosphorylation of Akt/PKB, Exp Hematol, 33, 152, 10.1016/j.exphem.2004.10.017 · DOI
- Silva, 1998, Expression of Bcl-x in erythroid precursors from patients with polycythemia vera, N Engl J Med, 338, 564, 10.1056/NEJM199802263380902 · DOI
Cited by
Gadd45g insufficiency drives the pathogenesis of myeloproliferative neoplasms
Zhang, P., You, N., Ding, Y., Zhu, W., Wang, N., Xie, Y., Huang, W., Ren, Q., Qin, T., Fu, R., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-47297-2 · Cited by 11
Metadata
- Authors
- Laubach, J. P., Fu, P., Jiang, X., Salter, K. H., Potti, A., & Arcasoy, M. O.
- Venue
- Experimental Hematology
- Publisher
- Elsevier BV
- Published
- 2009-12
- Volume
- 37
- Issue
- 12
- Pages
- 1411-1422
- ISSN
- 0301-472X
- PMC
- PMC2783925
- Cited by
- 41
- References
- 1
- Language
- en
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- CoChat. (2026). Citation check: Polycythemia vera erythroid precursors exhibit increased proliferation and apoptosis resistance associated with abnormal RAS and PI3K pathway activation. https://app.cochat.ai/papers/10.1016/j.exphem.2009.09.009
- The paper
- Laubach, J. P., Fu, P., Jiang, X., Salter, K. H., Potti, A., & Arcasoy, M. O. (2009). Polycythemia vera erythroid precursors exhibit increased proliferation and apoptosis resistance associated with abnormal RAS and PI3K pathway activation. Experimental Hematology. https://doi.org/10.1016/j.exphem.2009.09.009