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Cancer Metastasis Rev. 2018 Sep;37(2-3):203-211. doi: 10.1007/s10555-018-9741-1.

Stress, inflammation, and eicosanoids: an emerging perspective.

Author information

1
Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Unit 1362, 1515 Holcombe Blvd., Houston, TX, 77030, USA.
2
Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
3
Department of Palliative, Rehabilitation and Integrative Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
4
Department of Psychological and Brain Sciences, University of Iowa, Iowa City, IA, USA.
5
Department of Obstetrics and Gynecology, University of Iowa, Iowa City, IA, USA.
6
Department of Urology, University of Iowa, Iowa City, IA, USA.
7
Holden Comprehensive Cancer Center, University of Iowa, Iowa City, IA, USA.
8
Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Unit 1362, 1515 Holcombe Blvd., Houston, TX, 77030, USA. asood@mdanderson.org.
9
Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. asood@mdanderson.org.
10
Center for RNA Interference and Non-coding RNA, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. asood@mdanderson.org.

Abstract

Clinical and experimental studies support the notion that adrenergic stimulation and chronic stress affect inflammation, metabolism, and tumor growth. Eicosanoids are also known to heavily influence inflammation while regulating certain stress responses. However, additional work is needed to understand the full extent of interactions between the stress-related pathways and eicosanoids. Here, we review the potential influences that stress, inflammation, and metabolic pathways have on each other, in the context of eicosanoids. Understanding the intricacies of such interactions could provide insights on how systemic metabolic effects mediated by the stress pathways can be translated into therapies for cancer and other diseases.

KEYWORDS:

Cancer; Eicosanoids; Inflammation; PGE2; Stress

PMID:
29948328
PMCID:
PMC6237279
DOI:
10.1007/s10555-018-9741-1
[Indexed for MEDLINE]
Free PMC Article

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