Pro-inflammatory-Related Loss of CXCL12 Niche Promotes Acute Lymphoblastic Leukemic Progression at the Expense of Normal Lymphopoiesis.

摘要: Pediatric oncology, notably childhood acute lymphoblastic leukemia (ALL), is currently one of the health leading concerns worldwide and a biomedical priority. Decreasing overall mortality in children requires comprehensive understanding its pathobiology. It becoming clear that malignant cell-to-niche intercommunication microenvironmental signals control early cell fate decisions are critical for tumor progression. We show here mesenchymal stromal component ALL bone marrow differ from normal counterpart number functional properties may have key role during leukemic development. A decreased proliferation potential, contrasting with strong ability producing pro-inflammatory cytokines an aberrantly loss CXCL12 SCF, suggest lymphoid niches unique exclude hematopoiesis. Cell competence ex vivo assays within tridimensional co-culture structures indicated growth advantage precursor cells their niche remodeling by reduction, resulting progression at expense niche-associated lymphopoiesis.