» Articles » PMID: 26543328

Cytokine Regulation of Microenvironmental Cells in Myeloproliferative Neoplasms

Overview
Publisher Wiley
Specialties Biochemistry
Pathology
Date 2015 Nov 7
PMID 26543328
Citations 32
Authors
Affiliations
Soon will be listed here.
Abstract

The term myeloproliferative neoplasms (MPN) refers to a heterogeneous group of diseases including not only polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF), but also chronic myeloid leukemia (CML), and systemic mastocytosis (SM). Despite the clinical and biological differences between these diseases, common pathophysiological mechanisms have been identified in MPN. First, aberrant tyrosine kinase signaling due to somatic mutations in certain driver genes is common to these MPN. Second, alterations of the bone marrow microenvironment are found in all MPN types and have been implicated in the pathogenesis of the diseases. Finally, elevated levels of proinflammatory and microenvironment-regulating cytokines are commonly found in all MPN-variants. In this paper, we review the effects of MPN-related oncogenes on cytokine expression and release and describe common as well as distinct pathogenetic mechanisms underlying microenvironmental changes in various MPN. Furthermore, targeting of the microenvironment in MPN is discussed. Such novel therapies may enhance the efficacy and may overcome resistance to established tyrosine kinase inhibitor treatment in these patients. Nevertheless, additional basic studies on the complex interplay of neoplastic and stromal cells are required in order to optimize targeting strategies and to translate these concepts into clinical application.

Citing Articles

Myeloproliferative Neoplasms and Cardiovascular Disease: A Review.

Leiva O, Liu O, Zhou S, How J, Lee M, Hobbs G Curr Treat Options Oncol. 2024; 25(10):1257-1267.

PMID: 39278999 DOI: 10.1007/s11864-024-01255-8.


Neutrophil-specific expression of JAK2-V617F or CALRmut induces distinct inflammatory profiles in myeloproliferative neoplasia.

Haage T, Charakopoulos E, Bhuria V, Baldauf C, Korthals M, Handschuh J J Hematol Oncol. 2024; 17(1):43.

PMID: 38853260 PMC: 11163796. DOI: 10.1186/s13045-024-01562-5.


Exploring the molecular mechanisms between lymphoma and myelofibrosis.

Wang J, Li Y Am J Transl Res. 2024; 16(3):730-737.

PMID: 38586105 PMC: 10994807. DOI: 10.62347/NWJO7078.


The impact of gut microbial signals on hematopoietic stem cells and the bone marrow microenvironment.

Liu X, Zhang H, Shi G, Zheng X, Chang J, Lin Q Front Immunol. 2024; 15:1338178.

PMID: 38415259 PMC: 10896826. DOI: 10.3389/fimmu.2024.1338178.


Revisiting Circulating Extracellular Matrix Fragments as Disease Markers in Myelofibrosis and Related Neoplasms.

Hasselbalch H, Junker P, Skov V, Kjaer L, Knudsen T, Larsen M Cancers (Basel). 2023; 15(17).

PMID: 37686599 PMC: 10486581. DOI: 10.3390/cancers15174323.


References
1.
Miyazono K . Tumour promoting functions of TGF-β in CML-initiating cells. J Biochem. 2012; 152(5):383-5. DOI: 10.1093/jb/mvs106. View

2.
Ni H, Barosi G, Hoffman R . Quantitative evaluation of bone marrow angiogenesis in idiopathic myelofibrosis. Am J Clin Pathol. 2006; 126(2):241-7. DOI: 10.1309/4YGK-ED5L-WFW4-AVDV. View

3.
Okayama Y, Kawakami T . Development, migration, and survival of mast cells. Immunol Res. 2006; 34(2):97-115. PMC: 1490026. DOI: 10.1385/IR:34:2:97. View

4.
Di Raimondo F, Palumbo G, Molica S, Giustolisi R . Angiogenesis in chronic myeloproliferative diseases. Acta Haematol. 2002; 106(4):177-83. DOI: 10.1159/000046614. View

5.
Gabillot-Carre M, Lepelletier Y, Humbert M, de Sepuvelda P, Ben Hamouda N, Zappulla J . Rapamycin inhibits growth and survival of D816V-mutated c-kit mast cells. Blood. 2006; 108(3):1065-72. DOI: 10.1182/blood-2005-06-2433. View