Myelopoiesis, metabolism and therapy: a crucial crossroads in cancer progression
Authors:Antonio Sica1,2, Valentina Guarneri3,4 and Alessandra Gennari5
1 Department of Pharmaceutical Sciences, Università del Piemonte Orientale “Amedeo Avogadro”, via Bovio 6, Novara, Italy.
2 Humanitas Clinical and Research Center, Via Manzoni 56, 20089 Rozzano, Milan, Italy.
3 Department of Surgery, Oncology and Gastroenterology, University of Padova.
4 Istituto Oncologico Veneto IOV I.R.C.C.S, Padova, Italy.
5 Division of Oncology, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.
Keywords:
cancer, emergency myelopoiesis, tumor-associated macrophages, myeloid-derived suppressor cells, immune-metabolism, chemotherapy.
Abbreviatons:
αKG – α-ketoglutarate,
AMPK – adenosine monophosphate kinase,
BC – breast cancer,
BM – bone marrow,
DC – dendritic cell,
G-CSF – granulocyte colony-stimulating factor,
HSC – hematopoietic stem cell,
M-CSF – macrophage colony-stimulating factor,
MDSC – myeloid-derived suppressor cell,
NAMPT – nicotinamide phosphoribosyltransferase,
pCR – pathologic complete response,
TAM – tumor-associated macrophage,
Treg – regulatory T cell.
Corresponding Author(s):
Conflict of interest statement:
There is no conflict of interest.
Please cite this article as:
Antonio Sica, Valentina Guarneri and Alessandra Gennari (2019). Myelopoiesis, metabolism and therapy: a crucial crossroads in cancer progression. Cell Stress 3(9): 284-294. doi: 10.15698/cst2019.09.197
© 2019 Sica et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduc-tion in any medium, provided the original author and source are acknowledged.
Abstract:
Cancers promote immunological stresses that induce alterations of the myelopoietic output, defined as emergency myelopoiesis, which lead to the generation of different myeloid populations endowed with tumor-promoting activities. New evidence indicates that acquisition of this tumor-promoting phenotype by myeloid cells is the result of a multistep process, encompassing initial events originating into the bone marrow and later steps operating in the tumor microenvironment. The careful characterization of these sequential mechanisms is likely to offer new potential therapeutic opportunities. Here, we describe relevant mechanisms of myeloid cells reprogramming that instate immune dysfunctions and limit effective responses to anticancer therapy and discuss the influence that metabolic events, as well as chemotherapy, elicit on such events.