Fig 1: Human tumors coexpress LIF and IL-1a, which synergize in mouse models to potentiate EMH. (A–C) In mice with 10 days of LIF overexpression lentivirus or empty vector control lentivirus and 24 hours after treatment with 200 ng IL-1a IV, PMNs in the PB as a percent of total leukocytes (A, n = 7–8), KSL cells as a fraction of total splenic CD45+ cells (B, n = 7–8), GMP cells as a fraction of total splenic CD45+ cells (C, n = 7–8). (D–F) RNA-seq expression of IL1A, LIF, and CSF3 expression in tumor compared to normal tissue for breast (D, 292–1,099), colonic (E, n = 288–349), and pancreatic (F, n = 171–178). (G) Our proposed model of parallel mechanisms for tumor-associated EMH mediated in part by indirect inflammatory changes to HSPCs by tumor-derived IL-1a through local HSPC TNFa expression and direct proliferative effects on splenic ABS cells from tumor-derived LIF. Processed data for this figure can be found in S1 Data. EMH, extramedullary hematopoiesis; GMP, granulocyte–monocyte precursor; HSPC, hematopoietic stem and progenitor cell; IV, intravenous; KSL, Kit+/Sca-1+/Lineage-; LIF, leukemia inhibitory factor; PB, peripheral blood; PMN, polymorphonuclear neutrophil; RNA-seq, RNA-sequencing.