Deciphering the Intricate Roles of Radiation Therapy and Complement Activation in Cancer.
Journal
International journal of radiation oncology, biology, physics
ISSN: 1879-355X
Titre abrégé: Int J Radiat Oncol Biol Phys
Pays: United States
ID NLM: 7603616
Informations de publication
Date de publication:
01 09 2020
01 09 2020
Historique:
received:
11
05
2020
revised:
29
06
2020
accepted:
30
06
2020
pubmed:
7
7
2020
medline:
7
4
2021
entrez:
7
7
2020
Statut:
ppublish
Résumé
The complement system consists of a collection of serum proteins that act as the main frontline effector arm of the innate immune system. Activation of complement can occur through 3 individual induction pathways: the classical, mannose-binding lectin, and alternative pathways. Activation results in opsonization, recruitment of effector cells through potent immune mediators known as anaphylatoxins, and cell lysis via the formation of the membrane attack complex. Stringent regulation of complement is required to protect against inappropriate activation of the complement cascade. Complement activation within the tumor microenvironment does not increase antitumoral action; instead, it enhances tumor growth and disease progression. Radiation therapy (RT) is a staple in the treatment of malignancies and controls tumor growth through direct DNA damage and the influx of immune cells, reshaping the makeup of the tumor microenvironment. The relationship between RT and complement activity in the tumor microenvironment is uncertain at best. The following review will focus on the complex interaction of complement activation and the immune-modulating effects of RT and the overall effect on tumor progression. The clinical implications of complement activation in cancer and the use of therapeutics and potential biomarkers will also be covered.
Identifiants
pubmed: 32629082
pii: S0360-3016(20)31366-3
doi: 10.1016/j.ijrobp.2020.06.067
pmc: PMC7857091
mid: NIHMS1615610
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
46-55Subventions
Organisme : NIDCR NIH HHS
ID : R01 DE028282
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE028529
Pays : United States
Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
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