Laura F Mendez Luque1, Amanda L Blackmon2, Gajalakshmi Ramanathan2, Angela G Fleischman3,4,5. 1. Department of Biological Chemistry, University of California Irvine, 839 Medical Sciences Rd, Sprague Hall 126, Irvine, CA, 92617, USA. 2. Division of Hematology/Oncology, Department of Medicine, University of California Irvine, 839 Medical Sciences Rd, Sprague Hall 126, Irvine, CA, 92617, USA. 3. Department of Biological Chemistry, University of California Irvine, 839 Medical Sciences Rd, Sprague Hall 126, Irvine, CA, 92617, USA. agf@uci.edu. 4. Division of Hematology/Oncology, Department of Medicine, University of California Irvine, 839 Medical Sciences Rd, Sprague Hall 126, Irvine, CA, 92617, USA. agf@uci.edu. 5. Chao Family Comprehensive Cancer Center, University of California Irvine, 839 Medical Sciences Rd, Sprague Hall 126, Irvine, CA, 92617, USA. agf@uci.edu.
Abstract
PURPOSE OF REVIEW: Chronic inflammation is a characteristic feature of myeloproliferative neoplasm (MPN) and impacts many aspects of the disease including initiation, progression, and symptomatology. RECENT FINDINGS: The chronic inflammatory state of MPN results from disruption of immune signaling pathways leading to overproduction of inflammatory cytokines by both the neoplastic clones and bystander immune cells. This chronic inflammation may allow for the neoplastic clone to gain a selective advantage. The symptomatic burden felt by MPN patients may be a result of the chronic inflammation associated with MPN, as several cytokines have been linked with different symptoms. Pharmacologic as well as nonpharmacologic treatments of the inflammatory component of this disease may lead to decreased symptomatic burden, prevention of disease progression, and improvement in overall disease trajectory. Inflammation plays a key role in the pathogenesis of MPN and represents an important therapeutic target.
PURPOSE OF REVIEW: Chronic inflammation is a characteristic feature of myeloproliferative neoplasm (MPN) and impacts many aspects of the disease including initiation, progression, and symptomatology. RECENT FINDINGS: The chronic inflammatory state of MPN results from disruption of immune signaling pathways leading to overproduction of inflammatory cytokines by both the neoplastic clones and bystander immune cells. This chronic inflammation may allow for the neoplastic clone to gain a selective advantage. The symptomatic burden felt by MPN patients may be a result of the chronic inflammation associated with MPN, as several cytokines have been linked with different symptoms. Pharmacologic as well as nonpharmacologic treatments of the inflammatory component of this disease may lead to decreased symptomatic burden, prevention of disease progression, and improvement in overall disease trajectory. Inflammation plays a key role in the pathogenesis of MPN and represents an important therapeutic target.
Entities:
Keywords:
Diet in cancer; Fatigue; Inflammation in cancer; Inflammatory cytokines; JAK/STAT signaling; Lifestyle in cancer; Myeloproliferative neoplasm; Nonpharmacological approaches; Quality of life
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