TY - JOUR
T1 - Bone marrow microenvironment
T2 - roles and therapeutic implications in obesity-associated cancer
AU - Cheng, Feifei
AU - He, Jin
AU - Yang, Jing
N1 - Funding Information:
This work was supported by the National Institutes of Health/National Cancer Institute (R01 CA193362) and the Cancer Prevention & Research Institute of Texas (RP220639). We would like to thank Yuhong Liu, Department of Chemistry, The University of Tokyo, for her support in the development and illustration of figures. We also gratefully acknowledge Drs Shaefali P. Rodgers and James M. Kasper, Houston Methodist Hospital, who edited the manuscript. F.C. and J.Y. designed the study and discussed the content. F.C. and J.H. researched data for the article. F.C. wrote the article. J.Y. revised the article. All authors reviewed the article before submission. The authors declare no competing interests.
Funding Information:
This work was supported by the National Institutes of Health/National Cancer Institute ( R01 CA193362 ) and the Cancer Prevention & Research Institute of Texas ( RP220639 ). We would like to thank Yuhong Liu, Department of Chemistry, The University of Tokyo, for her support in the development and illustration of figures. We also gratefully acknowledge Drs Shaefali P. Rodgers and James M. Kasper, Houston Methodist Hospital, who edited the manuscript.
Publisher Copyright:
© 2023 Elsevier Inc.
PY - 2023/7
Y1 - 2023/7
N2 - Obesity is increasing globally and has been closely linked to the initiation and progression of multiple human cancers. These relationships, to a large degree, are mediated through obesity-driven disruption of physiological homeostasis characterized by local and systemic endocrinologic, inflammatory, and metabolic changes. Bone marrow microenvironment (BMME), which evolves during obesity, has been implicated in multiple types of cancer. Growing evidence shows that physiological dysfunction of BMME with altered cellular composition, stromal and immune cell function, and energy metabolism, as well as inflammation and hypoxia, in the context of obesity contributes to cancer initiation and progression. Nonetheless, the mechanisms underlying the obesity–BMME–cancer axis remain elusive. In this review, we discuss the recent advances in understanding the evolution of BMME during obesity, its contributions to cancer initiation and progression, and the implications for cancer therapy.
AB - Obesity is increasing globally and has been closely linked to the initiation and progression of multiple human cancers. These relationships, to a large degree, are mediated through obesity-driven disruption of physiological homeostasis characterized by local and systemic endocrinologic, inflammatory, and metabolic changes. Bone marrow microenvironment (BMME), which evolves during obesity, has been implicated in multiple types of cancer. Growing evidence shows that physiological dysfunction of BMME with altered cellular composition, stromal and immune cell function, and energy metabolism, as well as inflammation and hypoxia, in the context of obesity contributes to cancer initiation and progression. Nonetheless, the mechanisms underlying the obesity–BMME–cancer axis remain elusive. In this review, we discuss the recent advances in understanding the evolution of BMME during obesity, its contributions to cancer initiation and progression, and the implications for cancer therapy.
KW - bone marrow microenvironment
KW - cancer
KW - obesity
KW - targeted therapy
KW - Neoplasms/etiology
KW - Bone Marrow/metabolism
KW - Humans
KW - Obesity/complications
KW - Inflammation/metabolism
KW - Tumor Microenvironment
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U2 - 10.1016/j.trecan.2023.03.007
DO - 10.1016/j.trecan.2023.03.007
M3 - Review article
C2 - 37087397
AN - SCOPUS:85153352539
VL - 9
SP - 566
EP - 577
JO - Trends in Cancer
JF - Trends in Cancer
SN - 2405-8033
IS - 7
ER -