Stress and catecholamines modulate the bone marrow microenvironment to promote tumorigenesis

Affiliations:

¹ Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.

² Division of Clinical Hematology, University Hospital Basel, Basel, Switzerland.

Keywords: 

bone marrow, cancer, metastasis, leukemia, catecholamines, CXCL12/CXCR4, angiogenesis, stress.

Abbreviatons:

ALL – acute lymphoblastic leukemia,

AML – acute myeloid leukemia,

AR – adrenergic receptor,

BCL-2 – B-cell lymphoma 2,

bFGF – basic fibroblast growth factor,

BM – bone marrow,

cAMP – cyclic adenosine monophosphate,

COX2 – cyclooxygenase 2,

DA – dopamine,

DTC – disseminated tumor cells,

EPI – epinephrine,

FAK – focal adhesion kinase,

GM-CSF – granulocyte-macrophage colony-stimulating factor,

HSC – hematopoietic stem cell,

HSPC – hematopoietic stem and progenitor cell,

IL-6 – interleukin 6,

LSC – leukemic stem cell,

MDS – myelodysplastic syndrome,

MSC – mesenchymal stromal cell,

NK – natural killer,

NOR – norepinephrine,

PGE2 – prostaglandin E2,

PKA – protein kinase A,

RANK – receptor activator of NF-κB,

RANKL – RANK ligand,

SNS – sympathetic nervous system,

TAM – tumor associated macrophage,

TNF – tumor necrosis factor,

VCAM-1 – vascular cell adhesion molecule 1,

VEGF – vascular endothelial growth factor,

VEGF-R – VEGF receptor.

Corresponding Author(s):

Conflict of interest statement:

The authors declare no conflict of financial interest.

Please cite this article as:

Pauline Hanns, Anna M. Paczulla, Michael Medinger, Martina Konantz and Claudia Lengerke (2019). Stress and cate-cholamines modulate the bone marrow microenvironment to promote tumorigenesis. Cell Stress 3(7): 221-235. doi: 10.15698/cst2019.07.192

© 2019 Hanns 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.