MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives
In recent years the evidence is increasing that chronic inflammation may be an important driving force for clonal evolution and disease progression in the Philadelphia-negative myeloproliferative neoplasms (MPNs), essential thrombocythemia (ET), polycythemia vera (PV), and myelofibrosis (MF). Abnorm...
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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/10.1155/2015/102476 |
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| _version_ | 1832556757087420416 |
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| author | Hans Carl Hasselbalch Mads Emil Bjørn |
| author_facet | Hans Carl Hasselbalch Mads Emil Bjørn |
| author_sort | Hans Carl Hasselbalch |
| collection | DOAJ |
| description | In recent years the evidence is increasing that chronic inflammation may be an important driving force for clonal evolution and disease progression in the Philadelphia-negative myeloproliferative neoplasms (MPNs), essential thrombocythemia (ET), polycythemia vera (PV), and myelofibrosis (MF). Abnormal expression and activity of a number of proinflammatory cytokines are associated with MPNs, in particular MF, in which immune dysregulation is pronounced as evidenced by dysregulation of several immune and inflammation genes. In addition, chronic inflammation has been suggested to contribute to the development of premature atherosclerosis and may drive the development of other cancers in MPNs, both nonhematologic and hematologic. The MPN population has a substantial inflammation-mediated comorbidity burden. This review describes the evidence for considering the MPNs as inflammatory diseases, A Human Inflammation Model of Cancer Development, and the role of cytokines in disease initiation and progression. The consequences of this model are discussed, including the increased risk of second cancers and other inflammation-mediated diseases, emphasizing the urgent need for rethinking our therapeutic approach. Early intervention with interferon-alpha2, which as monotherapy has been shown to be able to induce minimal residual disease, in combination with potent anti-inflammatory agents such as JAK-inhibitors is foreseen as the most promising new treatment modality in the years to come. |
| format | Article |
| id | doaj-art-8dccc94d34844457813df905b0b3a409 |
| 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-8dccc94d34844457813df905b0b3a4092025-02-03T05:44:25ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/102476102476MPNs as Inflammatory Diseases: The Evidence, Consequences, and PerspectivesHans Carl Hasselbalch0Mads Emil Bjørn1Department of Hematology, Roskilde Hospital, University of Copenhagen, Køgevej 7-13, 4000 Roskilde, DenmarkDepartment of Hematology, Roskilde Hospital, University of Copenhagen, Køgevej 7-13, 4000 Roskilde, DenmarkIn recent years the evidence is increasing that chronic inflammation may be an important driving force for clonal evolution and disease progression in the Philadelphia-negative myeloproliferative neoplasms (MPNs), essential thrombocythemia (ET), polycythemia vera (PV), and myelofibrosis (MF). Abnormal expression and activity of a number of proinflammatory cytokines are associated with MPNs, in particular MF, in which immune dysregulation is pronounced as evidenced by dysregulation of several immune and inflammation genes. In addition, chronic inflammation has been suggested to contribute to the development of premature atherosclerosis and may drive the development of other cancers in MPNs, both nonhematologic and hematologic. The MPN population has a substantial inflammation-mediated comorbidity burden. This review describes the evidence for considering the MPNs as inflammatory diseases, A Human Inflammation Model of Cancer Development, and the role of cytokines in disease initiation and progression. The consequences of this model are discussed, including the increased risk of second cancers and other inflammation-mediated diseases, emphasizing the urgent need for rethinking our therapeutic approach. Early intervention with interferon-alpha2, which as monotherapy has been shown to be able to induce minimal residual disease, in combination with potent anti-inflammatory agents such as JAK-inhibitors is foreseen as the most promising new treatment modality in the years to come.http://dx.doi.org/10.1155/2015/102476 |
| spellingShingle | Hans Carl Hasselbalch Mads Emil Bjørn MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives Mediators of Inflammation |
| title | MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives |
| title_full | MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives |
| title_fullStr | MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives |
| title_full_unstemmed | MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives |
| title_short | MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives |
| title_sort | mpns as inflammatory diseases the evidence consequences and perspectives |
| url | http://dx.doi.org/10.1155/2015/102476 |
| work_keys_str_mv | AT hanscarlhasselbalch mpnsasinflammatorydiseasestheevidenceconsequencesandperspectives AT madsemilbjørn mpnsasinflammatorydiseasestheevidenceconsequencesandperspectives |