Impact of Host, Lifestyle and Environmental Factors in the Pathogenesis of MPN
- PMID: 32722135
- PMCID: PMC7463688
- DOI: 10.3390/cancers12082038
Impact of Host, Lifestyle and Environmental Factors in the Pathogenesis of MPN
Abstract
Philadelphia-negative myeloproliferative neoplasms (MPNs) occur when there is over-production of myeloid cells stemming from hematopoietic stem cells with constitutive activation of JAK/STAT signaling, with JAK2V617F being the most commonly occurring somatic driver mutation. Chronic inflammation is a hallmark feature of MPNs and it is now evident that inflammation is not only a symptom of MPN but can also provoke development and precipitate progression of disease. Herein we have considered major MPN driver mutation independent host, lifestyle, and environmental factors in the pathogenesis of MPN based upon epidemiological and experimental data. In addition to the traditional risk factors such as advanced age, there is evidence to indicate that inflammatory stimuli such as smoking can promote and drive MPN clone emergence and expansion. Diet induced inflammation could also play a role in MPN clonal expansion. Recognition of factors associated with MPN development support lifestyle modifications as an emerging therapeutic tool to restrain inflammation and diminish MPN progression.
Keywords: inflammatory diet; lifestyle; myeloproliferative neoplasm; prevention; smoking.
Conflict of interest statement
The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results. Research reported in this publication was supported by the National Cancer Institute of the National Institutes of Health under Award Number T32CA009054. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Figures
References
-
- Levine R.L., Wadleigh M., Cools J., Ebert B.L., Wernig G., Huntly B.J., Boggon T.J., Wlodarska I., Clark J.J., Moore S., et al. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. Cancer Cell. 2005;7:387–397. doi: 10.1016/j.ccr.2005.03.023. - DOI - PubMed
-
- Baxter E.J., Scott L.M., Campbell P.J., East C., Fourouclas N., Swanton S., Vassiliou G.S., Bench A.J., Boyd E.M., Curtin N., et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet (Lond. Engl.) 2005;365:1054–1061. doi: 10.1016/S0140-6736(05)71142-9. - DOI - PubMed
Publication types
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Miscellaneous