Carcinogenesis

Dietary selenium fails to influence cigarette smoke-induced lung tumorigenesis in A/J mice.

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Higher dietary sodium selenite did not inhibit the induction of lung tumors. • Higher dietary selenium increased selenium and GPx protein levels in the lung. • Dietary selenium did not affect lung SOD levels.

Abstract

The goal of the study was to determine if dietary selenium inhibited the induction of lung tumorigenesis by cigarette smoke in A/J mice. Purified diets containing 0.15, 0.5, or 2.0mg/kg selenium in the form of sodium selenite were fed to female A/J mice. Half of the mice in each dietary group were exposed to cigarette smoke 6h/day, 5days/week for five months followed by a four month recovery period in ambient air, while the other half were used as controls. After the recovery period, the mice were euthanized, and their lungs were removed for further analysis. Mice exposed to smoke had a higher tumor incidence and a higher tumor multiplicity, whereas dietary Se did not affect either the tumor incidence or tumor multiplicity. An increase in dietary selenium led to increased levels of selenium in the lung as well as GPx protein levels, but dietary Se did not affect lung SOD protein levels. In conclusion, these data confirm the carcinogenic activity of cigarette smoke in mice but show that dietary Se provided as sodium selenite does not affect smoke-induced carcinogenesis in this model.

Source: cancer letters

 

 

 

 

 

Metabolic syndrome: A novel high-risk state for colorectal cancer

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Metabolic syndrome (MS) and related disorders, including cancer, are steadily increasing in most countries of the world. However, mechanisms underlying the link between MS and colon carcinogenesis have yet to be fully elucidated. In this review article we focus on the relationships between various individual associated conditions (obesity, dyslipidemia, diabetes mellitus type 2 and hypertension) and colon cancer development, and demonstrate probable related factors revealed by in vivo and in vitrostudies. Furthermore, molecules suggested to be involved in cancer promotion are addressed, and the potential for cancer prevention by targeting these molecules is discussed.

 

Source: cancer letters

 

 

 

 

DNA methylome alterations in chemical carcinogenesis.

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Alteration of the DNA methylome is one of the major changes in all types of cancer. ► Exposure to genotoxic and non-genotoxic carcinogens causes DNA methylation changes. ► DNA methylation alterations may be used for carcinogen risk assessment.

Abstract

Carcinogenesis, a complex multifactorial process of the transformation of normal cells into malignant cells, is characterized by many biologically significant and interdependent alterations triggered by the mutational and/or non-mutational (i.e., epigenetic) events. One of these events, specific to all types of cancer, is alterations in DNA methylation. This review summarizes the current knowledge of the role of DNA methylation changes induced by various genotoxic chemicals (carcinogenic agents that interact with DNA) and non-genotoxic carcinogens (chemicals causing tumor by mechanisms other than directly damaging DNA) in the lung, colorectal, liver, and hematologic carcinogenesis. It also emphasizes the potential role for epigenetic changes to serve as markers for carcinogen exposure and carcinogen risk assessment.

Source: cancer letters