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Critical Reviews™ in Eukaryotic Gene Expression

Publication de 6  numéros par an

ISSN Imprimer: 1045-4403

ISSN En ligne: 2162-6502

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 1.6 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.2 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.3 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00058 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.33 SJR: 0.345 SNIP: 0.46 CiteScore™:: 2.5 H-Index: 67

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Mutational Status of Myeloproliferative Neoplasms

Volume 20, Numéro 1, 2010, pp. 61-76
DOI: 10.1615/CritRevEukarGeneExpr.v20.i1.50
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RÉSUMÉ

Philadelphia negative myeloproliferative neoplasms include essential thrombocythemia, polycythemia vera, and primary myelofibrosis. Altered signaling is a hallmark of myeloproliferative neoplasms, as demonstrated by the presence of activating JAK2 (V617F) mutation in about 70% of patients (95% of polycythemia vera, 50%−60% of essential thrombocythemia, and 50%−60% of primary myelofibrosis). How a unique point mutation can cause three different phenotypes remains to be clarified. The oncogenic potential of this mutation has been documented by mouse models, and different clinical studies have demonstrated an effect of mutant allele burden on phenotype. Mutant allele burden, in fact, directly correlates with hemoglobin value, leukocyte count, and, inversely, with platelet count. The molecular basis of JAK2 (V617F)-negative myeloproliferative neoplasms remains largely unexplained. Additional mutations in MPL, TET2, and CBL genes have been found in a small proportion of these patients. Implications of these mutations in the understanding of the pathogenesis of myeloproliferative neoplasms and in the clinical phenotype are discussed in this review.

CITÉ PAR
  1. Naeim Faramarz, Nagesh Rao P., Song Sophie X., Grody Wayne W., Myeloproliferative Neoplasms Associated with JAK2 Mutation, in Atlas of Hematopathology, 2013. Crossref

  2. Muendlein Axel, Gasser Klaus, Kinz Elena, Stark Nicole, Leiherer Andreas, Rein Philipp, Saely Christoph H., Grallert Harald, Peters Annette, Drexel Heinz, Lang Alois H., Evaluation of the prevalence and prospective clinical impact of theJAK2 V617Fmutation in coronary patients, American Journal of Hematology, 89, 3, 2014. Crossref

  3. Muendlein Axel, Kinz Elena, Gasser Klaus, Leiherer Andreas, Rein Philipp, Saely Christoph H., Grallert Harald, Peters Annette, Fraunberger Peter, Drexel Heinz, Lang Alois H., Occurrence of theJAK2 V617Fmutation in patients with peripheral arterial disease, American Journal of Hematology, 90, 1, 2015. Crossref

  4. Kinz E., Leiherer A., Lang A. H., Drexel H., Muendlein A., Accurate quantitation of JAK2 V617F allele burden by array-based digital PCR, International Journal of Laboratory Hematology, 37, 2, 2015. Crossref

  5. Qian Cui-Juan, Yao Jun, Si Jian-Min, Nuclear JAK2: Form and Function in Cancer, The Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology, 294, 9, 2011. Crossref

  6. Looyenga Brendan D., Hutchings Danielle, Cherni Irene, Kingsley Chris, Weiss Glen J., MacKeigan Jeffrey P., Gelovani Juri G., STAT3 Is Activated by JAK2 Independent of Key Oncogenic Driver Mutations in Non-Small Cell Lung Carcinoma, PLoS ONE, 7, 2, 2012. Crossref

  7. Link-Lenczowska Dorota, Pallisgaard Niels, Cordua Sabrina, Zawada Magdalena, Czekalska Sylwia, Krochmalczyk Dorota, Kanduła Zuzanna, Sacha Tomasz, A comparison of qPCR and ddPCR used for quantification of the JAK2 V617F allele burden in Ph negative MPNs, Annals of Hematology, 97, 12, 2018. Crossref

  8. Zloto Ofira, Lubetsky Aharon, Ben-Bassat Mizrachi Iris, Kesler Anat, Quiros Peter A., Huna-Baron Ruth, Prognostic value of JAK2V617F mutation in pseudotumor cerebri associated with cerebral venous sinus thrombosis, Acta Neurologica Scandinavica, 139, 2, 2019. Crossref

  9. Naeim Faramarz, Nagesh Rao P., Song Sophie X., Phan Ryan T., Myeloproliferative Neoplasms Associated With JAK2 , MPL, and CALR Mutations, in Atlas of Hematopathology, 2018. Crossref

  10. Meloni-Ehrig Aurelia, The Cytogenetics of Hematologic Neoplasms, in The Principles of Clinical Cytogenetics, 2013. Crossref

  11. Ma Qiang, Frequency and characteristics of the JAK2 V617F mutation in 23 cerebral venous sinus thrombosis patients with thrombocytosis, Journal of International Medical Research, 48, 12, 2020. Crossref

  12. Passamonti F, How to manage polycythemia vera, Leukemia, 26, 5, 2012. Crossref

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