Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation
Myeloproliferative neoplasms (MPNs) are a heterogeneous group of clonal diseases characterized by the excessive and chronic production of mature cells from one or several of the myeloid lineages. Recent advances in the biology of MPNs have greatly facilitated their molecular diagnosis since most pat...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/145293 |
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| author | Sylvie Hermouet Edith Bigot-Corbel Betty Gardie |
| author_facet | Sylvie Hermouet Edith Bigot-Corbel Betty Gardie |
| author_sort | Sylvie Hermouet |
| collection | DOAJ |
| description | Myeloproliferative neoplasms (MPNs) are a heterogeneous group of clonal diseases characterized by the excessive and chronic production of mature cells from one or several of the myeloid lineages. Recent advances in the biology of MPNs have greatly facilitated their molecular diagnosis since most patients present with mutation(s) in the JAK2, MPL, or CALR genes. Yet the roles played by these mutations in the pathogenesis and main complications of the different subtypes of MPNs are not fully elucidated. Importantly, chronic inflammation has long been associated with MPN disease and some of the symptoms and complications can be linked to inflammation. Moreover, the JAK inhibitor clinical trials showed that the reduction of symptoms linked to inflammation was beneficial to patients even in the absence of significant decrease in the JAK2-V617F mutant load. These observations suggested that part of the inflammation observed in patients with JAK2-mutated MPNs may not be the consequence of JAK2 mutation. The aim of this paper is to review the different aspects of inflammation in MPNs, the molecular mechanisms involved, the role of specific genetic defects, and the evidence that increased production of certain cytokines depends or not on MPN-associated mutations, and to discuss possible nongenetic causes of inflammation. |
| format | Article |
| id | doaj-art-ff2059dd8e484175ba6de8421637fffd |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-ff2059dd8e484175ba6de8421637fffd2025-02-03T01:23:29ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/145293145293Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic InflammationSylvie Hermouet0Edith Bigot-Corbel1Betty Gardie2Inserm UMR 892, CNRS UMR 6299, Centre de Recherche en Cancérologie Nantes-Angers, Institut de Recherche en Santé, Université de Nantes, 44007 Nantes, FranceInserm UMR 892, CNRS UMR 6299, Centre de Recherche en Cancérologie Nantes-Angers, Institut de Recherche en Santé, Université de Nantes, 44007 Nantes, FranceInserm UMR 892, CNRS UMR 6299, Centre de Recherche en Cancérologie Nantes-Angers, Institut de Recherche en Santé, Université de Nantes, 44007 Nantes, FranceMyeloproliferative neoplasms (MPNs) are a heterogeneous group of clonal diseases characterized by the excessive and chronic production of mature cells from one or several of the myeloid lineages. Recent advances in the biology of MPNs have greatly facilitated their molecular diagnosis since most patients present with mutation(s) in the JAK2, MPL, or CALR genes. Yet the roles played by these mutations in the pathogenesis and main complications of the different subtypes of MPNs are not fully elucidated. Importantly, chronic inflammation has long been associated with MPN disease and some of the symptoms and complications can be linked to inflammation. Moreover, the JAK inhibitor clinical trials showed that the reduction of symptoms linked to inflammation was beneficial to patients even in the absence of significant decrease in the JAK2-V617F mutant load. These observations suggested that part of the inflammation observed in patients with JAK2-mutated MPNs may not be the consequence of JAK2 mutation. The aim of this paper is to review the different aspects of inflammation in MPNs, the molecular mechanisms involved, the role of specific genetic defects, and the evidence that increased production of certain cytokines depends or not on MPN-associated mutations, and to discuss possible nongenetic causes of inflammation.http://dx.doi.org/10.1155/2015/145293 |
| spellingShingle | Sylvie Hermouet Edith Bigot-Corbel Betty Gardie Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation Mediators of Inflammation |
| title | Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation |
| title_full | Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation |
| title_fullStr | Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation |
| title_full_unstemmed | Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation |
| title_short | Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation |
| title_sort | pathogenesis of myeloproliferative neoplasms role and mechanisms of chronic inflammation |
| url | http://dx.doi.org/10.1155/2015/145293 |
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