Microbiome, Inflammation, and Cancer

Francescone, Ralph; Hou, Vivianty; Grivennikov, Sergei I.

doi:10.1097/ppo.0000000000000048

Cited by 202 publications

(156 citation statements)

References 95 publications

(112 reference statements)

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“…A distinctive characteristic of inflammation is the activation of cellular components that participate in tumorigenesis (Elinav et al, 2013). However, the role of inflammation is not limited to initiation, but is also relevant to tumour growth (Francescone et al, 2014). Tumour-infiltrating myeloid cells produce proinflammatory cytokines, such as IL-6, that induce STAT3 and NRkB signalling to increase cellular proliferation and to suppress apoptosis (Elinav et al, 2013).…”

Section: Mediated By the Immune System Effectmentioning

confidence: 99%

“…Generally, more than 20 % of cancers are preceded by chronic inflammation, such as in hepatocellular carcinoma (HCC) and CRC (Francescone et al, 2014). A distinctive characteristic of inflammation is the activation of cellular components that participate in tumorigenesis (Elinav et al, 2013).…”

Section: Mediated By the Immune System Effectmentioning

confidence: 99%

“…It is debatable whether cancer is the product of variations in the microbiota, or whether modifications in the normal microbiome are the result of cancer progression; there is strong evidence of both (Blumberg & Powrie, 2012;Francescone et al, 2014). On the one hand, tumour cells exhibit differential profiles when compared with untransformed progenitors, and this may favour the selective adherence of some members of the microflora.…”

Section: Introductionmentioning

confidence: 99%

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Microbiota dysbiosis: a new piece in the understanding of the carcinogenesis puzzle

García-Castillo

Sanhueza

McNerney

et al. 2016

Journal of Medical Microbiology

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Cancer is defined as an uncontrolled proliferation of malignant cells in a host and it is one of the main causes of death worldwide. Genetic and environmental factors play an important role in its development, and the involvement of microbial communities has also recently been recognized. The close relationship that characterizes the colonization by human commensal communities involves health risks, particularly when the homeostasis is disturbed. It has been hypothesized that this process may lead to cancer by modulating the inflammatory response of the host, by the production of carcinogenic metabolic products or by the production of toxins, which disrupt the cell cycle. The metabolic effects of the intestinal microbiota have been studied in greater detail in the gastrointestinal tract, and it has been recognized that microbial communities of other body surfaces can cause effects either locally or at a distance. In vitro and in vivo studies have allowed the characterization of the microbiota and the establishment of a cause and effect relationship with some types of cancer. Nevertheless, despite the results, representative studies are necessary to validate the findings and definitively establish the role of microbiota in cancer development in order to open the possibility of promising therapeutic and diagnostic applications. Thus, the aims of this review are to briefly examine the available evidence, and to analyse the mechanisms described for pancreatic, lung, colorectal cancer , oral squamous cell carcinoma and hepatocellular carcinoma and the impact of the current knowledge about the effects of the microbiota on carcinogenesis.

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Section: Mediated By the Immune System Effectmentioning

confidence: 99%

Section: Mediated By the Immune System Effectmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Microbiota dysbiosis: a new piece in the understanding of the carcinogenesis puzzle

García-Castillo

Sanhueza

McNerney

et al. 2016

Journal of Medical Microbiology

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“…While only up to 20% of all tumors arise under the context of preceding chronic inflammation and/or autoimmunity, the majority of solid malignancies have the ability to recruit immune and inflammatory cells and upregulate inflammatory mediators, such as cytokines and chemokines, after tumor initiation, a phenomenon known as tumor-elicited inflammation (11,12). Evidence for the involvement of inflammation in tumor development has been demonstrated in studies showing that the regular use of nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, is associated with decreased risk for CRC development and mortality (13,14).…”

Section: Introductionmentioning

confidence: 99%

Anti-inflammatory natural product goniothalamin reduces colitis-associated and sporadic colorectal tumorigenesis

Vendramini–Costa

Francescone

Posocco

et al. 2016

CARCIN

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The tumor microenvironment offers multiple targets for cancer therapy, including pro-tumorigenic inflammation. Natural compounds represent an enormous source of new anti-inflammatory and anticancer agents. We previously showed that the styryl lactone goniothalamin (GTN) has promising antiproliferative and anti-inflammatory activities. Because inflammation is a major driver of colorectal cancer (CRC), we therefore evaluated the therapeutic and preventive potentials of GTN in colitis, colitis-associated cancer (CAC) and spontaneous CRC. First, in a simplistic model of inflammation in vitro, GTN was able to inhibit cytokine production in bone marrow-derived macrophages induced by lipopolysaccharide. Next, in dextran sulfate sodium (DSS) induced-colitis model, mice treated with GTN displayed restored tissue architecture, increased cell proliferation in the colonic crypts and reduced epithelial damage. Moreover, colon tissue from GTN-treated mice had significantly less expression of the inflammatory genes interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), S100A9, interleukin 23A (IL-23A), IL-22 and IL-17A. In the azoxymethane/DSS model of CAC, GTN reduced tumor multiplicity, load and size. Additionally, GTN suppressed production of IL-6, IL-17 and TNF-α in tumor tissue, as well as abrogated stromal immune cell activation and nuclear translocation of NF-κB. Finally, in a tamoxifen inducible model of sporadic CRC, GTN-treated mice had significantly fewer tumors and decreased levels of IL-17A, IL-6, S100A9 and TNF-α protein within the tumors. These results suggest that GTN possesses anti-inflammatory and antitumor activities and represents a preventive and therapeutic agent modulating the inflammatory environment in the colon during colitis as well as CAC and CRC development.

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“…Approximately 15%-20% of human tumors are initiated by inflammation-driven processes (Francescone et al 2014). …”

Section: Introductionmentioning

confidence: 99%

The oral cavity microbiota: between health, oral disease, and cancers of the aerodigestive tract

et al. 2017

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Many studies show that the human microbiome plays a critical role in the chronic pathologies of obesity, inflammatory bowel diseases, and diabetes. More recently, the interaction between cancer and the microbiome has been highlighted. Most studies have focused on the gut microbiota because it represents the most extensive bacterial community, and the body of evidence correlating it with gut syndromes is increasing. However, in the strict sense, the gastrointestinal (GI) tract begins in the oral cavity, and special attention should be paid to the specific flora of this cavity. This study reviewed the current knowledge about the various microbial ecosystems of the upper part of the GI tract and discussed their potential link to carcinogenesis. The overall composition of the microbial communities, as well as the presence or absence of "key species", in relation to carcinogenesis is addressed. Alterations in the oral microbiota can potentially be used to predict the risk of cancer. Molecular advances and the further monitoring of the microbiota will increase our understanding of the role of the microbiota in carcinogenesis and open new perspectives for future therapeutic and prophylactic modalities.Key words: upper aerodigestive, microbiome, oral cavity, carcinogenesis.Résumé : Plusieurs études montrent que le microbiome humain joue un rôle essentiel dans les pathologies chroniques que sont l'obésité, les maladies inflammatoires de l'intestin et le diabète. Plus récemment, l'interaction entre le cancer et le microbiome a été soulignée. La plupart des études se sont concentrées sur le microbiote intestinal car il représente la communauté bactérienne la plus étendue, et l'ensemble des preuves le corrélant avec les syndromes de l'intestin est en croissance. Cependant, au sens strict, le tractus gastro-intestinal (GI) commence dans la cavité orale et une attention spéciale devrait être portée à la flore spécifique de cette cavité. Cette étude fait la synthèse des connaissances actuelles relatives à divers écosystèmes microbiens de la partie supérieure du tractus GI et discute de leur lien potentiel à la carcinogenèse. La composition globale des communautés microbiennes, de même que la présence ou l'absence « d'espèces clés » relativement à la carcinogenèse sont soulevées. Des modifications du microbiote oral peuvent potentiellement être utilisées pour prédire les risques de cancer. Les percées moléculaires et la surveillance accrue du microbiote accroitront notre compréhension du rôle du microbiote dans la carcinogenèse et ouvriront de nouvelles perspectives en vue de modalités thérapeutiques et prophylactiques futures. [Traduit par la Rédaction]

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Microbiome, Inflammation, and Cancer

Cited by 202 publications

References 95 publications

Microbiota dysbiosis: a new piece in the understanding of the carcinogenesis puzzle

Microbiota dysbiosis: a new piece in the understanding of the carcinogenesis puzzle

Anti-inflammatory natural product goniothalamin reduces colitis-associated and sporadic colorectal tumorigenesis

The oral cavity microbiota: between health, oral disease, and cancers of the aerodigestive tract

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