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The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Oncogenic Ras Diverts a Host TNF Tumor Suppressor Activity into Tumor Promoter

Open access
Cordero, Julia B., Macagno, Juan P., Stefanatos, Rhoda K., Strathdee, Karen E., Cagan, Ross L., Vidal, Marcos·2010·Developmental Cell

Abstract

SUMMARY The roles of inflammatory cytokines and the immune response in cancer remain paradoxical. In the case of tumor necrosis factor (TNF), there is undisputed evidence indicating both protumor and antitumor activities. Recent work in Drosophila indicated that a TNF-dependent mechanism eliminates cells deficient for the polarity tumor suppressors dlg or scrib. In this study, however, we show that in tumors deficient for scrib that also expressed the Ras oncoprotein, the TNF signal was diverted into a protumor signal that enhanced tumor growth through larval arrest and stimulated invasive migration. In this case, TNF promoted malignancy and was detrimental to host survival. TNF was expressed at high levels by tumor-associated hemocytes recruited from the circulation. The expression of TNF by hemocytes was both necessary and sufficient to trigger TNF signaling in tumor cells. Our evidence suggests that tumors can evolve into malignancy through oncogenic Ras activation and the hijacking of TNF signaling.

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Crossref · 10.1016/j.devcel.2010.05.014

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Metadata

Authors
Cordero, J. B., Macagno, J. P., Stefanatos, R. K., Strathdee, K. E., Cagan, R. L., & Vidal, M.
Venue
Developmental Cell
Publisher
Elsevier BV
Published
2010-06
Volume
18
Issue
6
Pages
999-1011
ISSN
1534-5807 (ISSN-L)
OpenAlex
W1996137175
Cited by
239
References
4
FWCI
5.78
Type
journal article
Language
en
Open access
bronze

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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