Tumor necrosis factor is dispensable for the success of immunogenic anticancer chemotherapy

Ma, Yuting, Yamazaki, Takahiro, Yang, Heng, Kepp, Oliver, Galluzzi, Lorenzo, Zitvogel, Laurence, Smyth, Mark J. and Kroemer, Guido (2013) Tumor necrosis factor is dispensable for the success of immunogenic anticancer chemotherapy. Oncoimmunology, 2 6: e24786.1-e24786.7. doi:10.4161/onci.24786

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Author Ma, Yuting
Yamazaki, Takahiro
Yang, Heng
Kepp, Oliver
Galluzzi, Lorenzo
Zitvogel, Laurence
Smyth, Mark J.
Kroemer, Guido
Title Tumor necrosis factor is dispensable for the success of immunogenic anticancer chemotherapy
Journal name Oncoimmunology   Check publisher's open access policy
ISSN 2162-4011
2162-402X
Publication date 2013-06
Sub-type Article (original research)
DOI 10.4161/onci.24786
Open Access Status DOI
Volume 2
Issue 6
Start page e24786.1
End page e24786.7
Total pages 7
Place of publication Austin, TX, United States
Publisher Landes Bioscience
Collection year 2014
Language eng
Abstract The antineoplastic effects of anthracyclines have been shown to rely, at least in part, on a local immune response that involves dendritic cells (DCs) and several distinct subsets of T lymphocytes. Here, we show that the administration of anthracyclines to mice bearing established neoplasms stimulates the intratumoral secretion of tumor necrosis factor a (TNF α). However, blocking the TNF α/TNF receptor (TNFR) system by three different strategies-namely, (1) neutralizing antibodies, (2) etanercept, a recombinant protein in which TNFR is fused to the constant domain of an IgG1 molecule, and (3) gene knockout-failed to negatively affect the therapeutic efficacy of anthracyclines in three distinct tumor models. In particular, TNF α-blocking strategies did not influence the antineoplastic effects of doxorubicin (a prototypic anthracycline) against MCA 205 fibrosarcomas growing in C57BL/6 mice, F244 sarcomas developing in 129/Sv hosts and H2N100 mammary carcinomas arising in BALB/c mice. These findings imply that, in contrast to other cytokines (such as interleukin-1β, interleukin-17 and interferon γ), TNFαis not required for anthracyclines to elicit therapeutic anticancer immune responses.
Keyword Apoptosis
Calreticulin
Dendritic cell
Immunogenic cell death
Interferon gamma
T cells
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2014 Collection
School of Medicine Publications
 
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Created: Sun, 18 Aug 2013, 00:04:47 EST by System User on behalf of School of Medicine