OBJECTIVE To investigate the association between changes in the levels of 41 inflammatory factors and 8 common hematological malignancies (HMs), providing a reference for exploring the etiology and early prevention of HMs.

METHODS Genome-wide association study (GWAS) data for 41 inflammatory factors were used as exposures, and GWAS data for eight common HMs were used as outcomes, including acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myeloid leukemia (CML), chronic lymphocytic leukemia (CLL), diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), Hodgkin lymphoma (HL) and multiple myeloma (MM). Univariate Mendelian randomization (MR) analysis was first performed to assess the causal relationship between inflammatory factor levels and the pathogenesis of HMs. Subsequently, multivariate MR analysis was conducted to identify inflammatory factors independently genetically associated with the pathogenesis of HMs. Finally, reverse MR analysis was performed to evaluate the influence of HMs on inflammatory factor levels.

RESULTS The interleukin-16 (IL-16) was identified as a risk factor for the pathogenesis of AML (OR=1.832). The IL-8 was a risk factor for the pathogenesis of CML (OR=4.231) but a protective factor for the pathogenesis of CLL (OR=0.345). The regulated upon activation normal T-cell expressed and secreted (RANTES) were risk factors for the pathogenesis of CLL (OR=2.224). The basic fibroblast growth factor (bFGF) was a protective factor for the pathogenesis of DLBCL (OR=0.220). The vascular endothelial growth factor (VEGF) was a risk factor for the pathogenesis of MM (OR=1.235). Reverse MR analysis did not reveal any genetic association between HMs and inflammatory factors.

CONCLUSION The causal associations between specific inflammatory factors and HM risk suggest that these factors may serve as disease markers and therapeutic targets, providing a reference for early diagnosis and prevention of HMs.