Patrolling Monocytes Watch Over Relapse.
The latest years greatly enriched our knowledge of monocytes biology. First, the phenotypic, functional and molecular heterogeneity of this cell population has been largely investigated, revealing the existence of multiple subsets displaying distinct functions in response to different stimuli. Second, monocytes have emerged as important regulators of cancer development and progression, with different subsets playing opposing roles in these processes. Yet, so far, the contribution of monocytes to tumor development appeared to be limited to solid tumors. Nevertheless, monocytes/macrophages populations are important components of bone marrow stem cells niches, and during physiological conditions, they regulate normal hematopoietic stem cells retention and maintenance.1 Their role in leukemia development, however, remains unclear. In a recent Cancer Cell paper, Witkowski et al fill some gaps in this scenario, demonstrating that non-classical monocytes play an essential role in the pathogenesis of B-cell acute lymphoblastic leukemia (B-ALL),2 an hematological cancer whereby B-cell progenitors accumulate in the bone marrow (BM). By combining single cells RNA sequencing and CITE sequencing, the authors compared the bone marrow composition of 4 healthy bone marrow and seven primary B-ALL encompassing 2 distinct genetic lesions (Ph+ and ETV6/RUNX1). These analyses revealed that two distinct myeloid clusters were significantly changed in the BM of B-ALL patients as compared to the healthy BM samples. The first one, corresponding to so called classical monocytes (CD14+CD16−), was decreased in diagnostic BM samples. The second one, corresponding to CD14dimCD16+CD115+ non-classical monocytes, was instead increased at diagnosis.
|Journal:||Hemasphere; 2020 Aug ; 4 (4) 451. doi:10.1097/HS9.0000000000000451|
|PubMed:||PMID: 32903316 (Go to PubMed)|