Widespread parainflammation in human cancer

Chronic inflammation has been recognized as one of the hallmarks of cancer. We recently showed that parainflammation, a unique variant of inflammation between homeostasis and chronic inflammation, strongly promotes mouse gut tumorigenesis upon p53 loss. Here we explore the prevalence of parainflamma...

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Bibliographic Details
Published in:Genome Biology 2016-07, Vol.17 (1), p.145, Article 145
Main Authors: Aran, Dvir, Lasry, Audrey, Zinger, Adar, Biton, Moshe, Pikarsky, Eli, Hellman, Asaf, Butte, Atul J, Ben-Neriah, Yinon
Format: Article
Language:English
Subjects:
Animals
Anti-Inflammatory Agents, Non-Steroidal - therapeutic use
Assaults
Bioinformatics
Cancer
Carcinogenesis - genetics
DNA damage
Gene expression
Genome, Human
Genomes
Homeostasis
Humans
Inflammation
Inflammation - complications
Inflammation - drug therapy
Inflammation - genetics
Information sources
Medical prognosis
Mice
Mutagenesis
Mutation
Neoplasms - complications
Neoplasms - drug therapy
Neoplasms - genetics
Nonsteroidal anti-inflammatory drugs
p53 Protein
Prognosis
Rodents
Senescence
Transcriptome - genetics
Tumor cell lines
Tumor Suppressor Protein p53 - genetics
Tumorigenesis
Tumors
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Summary:Chronic inflammation has been recognized as one of the hallmarks of cancer. We recently showed that parainflammation, a unique variant of inflammation between homeostasis and chronic inflammation, strongly promotes mouse gut tumorigenesis upon p53 loss. Here we explore the prevalence of parainflammation in human cancer and determine its relationship to certain molecular and clinical parameters affecting treatment and prognosis. We generated a transcriptome signature to identify parainflammation in many primary human tumors and carcinoma cell lines as distinct from their normal tissue counterparts and the tumor microenvironment and show that parainflammation-positive tumors are enriched for p53 mutations and associated with poor prognosis. Non-steroidal anti-inflammatory drug (NSAID) treatment suppresses parainflammation in both murine and human cancers, possibly explaining a protective effect of NSAIDs against cancer. We conclude that parainflammation, a low-grade form of inflammation, is widely prevalent in human cancer, particularly in cancer types commonly harboring p53 mutations. Our data suggest that parainflammation may be a driver for p53 mutagenesis and a guide for cancer prevention by NSAID treatment.
ISSN:1474-760X
1474-7596
1474-760X
DOI:10.1186/s13059-016-0995-z