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Open AccessJournal ArticleDOI

Dietary and Genetic Obesity Promote Liver Inflammation and Tumorigenesis by Enhancing IL-6 and TNF Expression

TLDR
It is demonstrated that either dietary or genetic obesity is a potent bona fide liver tumor promoter in mice and obesity-promoted HCC development was dependent on enhanced production of the tumor-promoting cytokines IL-6 and TNF, which cause hepatic inflammation and activation of the oncogenic transcription factor STAT3.
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This article is published in Cell.The article was published on 2010-01-22 and is currently open access. It has received 1537 citations till now. The article focuses on the topics: Chronic inflammatory response & Liver cancer.

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Immunity, Inflammation, and Cancer

TL;DR: The principal mechanisms that govern the effects of inflammation and immunity on tumor development are outlined and attractive new targets for cancer therapy and prevention are discussed.
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Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis†

TL;DR: Endoplasmic reticulum stress and related signaling networks, (adipo)cytokines, and innate immunity are emerging as central pathways that regulate key features of NASH.
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Diabetes and Cancer: A consensus report

TL;DR: A consensus statement of experts assembled jointly by the American Diabetes Association and the American Cancer Society reviews the state of science concerning the association between diabetes and cancer incidence or prognosis and whether diabetes treatments influence risk of cancer or cancer prognosis.
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Obesity-induced gut microbial metabolite promotes liver cancer through senescence secretome

TL;DR: It is shown that senescence-associated secretory phenotype (SASP) has crucial roles in promoting obesity-associated hepatocellular carcinoma (HCC) development in mice, and a similar pathway may contribute to at least certain aspects of obesity- associated HCC development in humans as well.
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Revisiting STAT3 signalling in cancer: new and unexpected biological functions

TL;DR: Well known for its role in tumour cell proliferation, survival, invasion and immunosuppression, JAK–STAT3 signalling also promotes cancer through inflammation, obesity, stem cells and the pre-metastatic niche.
References
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A simple method for the isolation and purification of total lipides from animal tissues.

TL;DR: In this paper, the authors described a simplified version of the method and reported the results of a study of its application to different tissues, including the efficiency of the washing procedure in terms of the removal from tissue lipides of some non-lipide substances of special biochemical interest.
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Cancer-related inflammation.

TL;DR: The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.
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Inflammation and metabolic disorders

TL;DR: Dysfunction of the immune response and metabolic regulation interface can be viewed as a central homeostatic mechanism, dysfunction of which can lead to a cluster of chronic metabolic disorders, particularly obesity, type 2 diabetes and cardiovascular disease.
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Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults.

TL;DR: Current patterns of overweight and obesity in the United States could account for 14 percent of all deaths from cancer in men and 20 percent of those in women, and increased body weight was associated with increased death rates for all cancers combined and for cancers at multiple specific sites.
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Hepatocellular Carcinoma: Epidemiology and Molecular Carcinogenesis

TL;DR: A detailed understanding of epidemiologic factors and molecular mechanisms associated with HCC ultimately could improve current concepts for screening and treatment of this disease.
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