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Proinflammatory cytokines, immune response and tumour progression.

Authors: Michela, Spadaro; Guido, Forni;

Proinflammatory cytokines, immune response and tumour progression.

Abstract

Tumour cells naturally secrete proinflammatory cytokines and chemokines to interact with the microenvironment and regulate neoangiogenesis. The repertoire of factors thus produced shapes tumour progression. However, experiments in the mouse have shown that injection of a low pharmacological dose of a proinflammatory cytokine or chemokine into the microenvironment increases the inflammatory reaction so enormously that locally activated leukocytes inhibit or eradicate the tumour. Massive shrinkage of recurrent head and neck squamous cell carcinomas (SCC) and prevention of recurrences after surgical removal of a primary SCC follow perilymphatic administration of low doses of interleukin (IL)2, while low daily doses of IL12 markedly delay carcinogenesis in transgenic mice predestined to die of mammary carcinomas and keep them tumour-free for long periods. The reaction elicited by proinflammatory cytokines evidently has a great potential in tumour control.

Keywords

Immunity, Cellular, Immune System, Neoplasms, Disease Progression, Animals, Cytokines, Humans

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
0
Average
Average
Average
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