Biomarkers identified for TNBC and ER⁺HER2^-BC.

<p>Biomarkers identified for TNBC and ER⁺HER2^-BC.</p

An approach to select DEGs (protein coding genes) identified by UQ-pgQ2* and <i>DESeq2</i>.

<p>An approach to select DEGs (protein coding genes) identified by UQ-pgQ2* and <i>DESeq2</i>.</p

Summary of normalization methods and software packages used.

<p>Summary of normalization methods and software packages used.</p

Determining an optimal |logFC|** by observed FPR.

<p>An observed FPR based on all of 35203 genes is computed given a |logFC| cutoff in parenthesis.</p

Hierarchical clustering heatmaps of BC based on the DESeq-normalized gene expression levels.

<p>The genes with similar expression patterns are clustered together. The up-regulated genes are in red and the down-regulated genes are in green. (A) A heatmap based on gene expression levels of 1,693 DEGs uniquely identified in TNBC data. (B) A heatmap based on gene expression of 2,299 DEGs uniquely identified in ER⁺HER2^-BC data.</p

The DEGs are associated with cancer biology identified by IPA.

<p>The DEGs are associated with cancer biology identified by IPA.</p

Benzene exposure is associated with cardiovascular disease risk

<div><p>Benzene is a ubiquitous, volatile pollutant present at high concentrations in toxins (e.g. tobacco smoke) known to increase cardiovascular disease (CVD) risk. Despite its prevalence, the cardiovascular effects of benzene have rarely been studied. Hence, we examined whether exposure to benzene is associated with increased CVD risk. The effects of benzene exposure in mice were assessed by direct inhalation, while the effects of benzene exposure in humans was assessed in 210 individuals with mild to high CVD risk by measuring urinary levels of the benzene metabolite <i>trans</i>,<i>trans</i>-muconic acid (<i>t</i>,<i>t</i>-MA). Generalized linear models were used to assess the association between benzene exposure and CVD risk. Mice inhaling volatile benzene had significantly reduced levels of circulating angiogenic cells (Flk-1⁺/Sca-1⁺) as well as an increased levels of plasma low-density lipoprotein (LDL) compared with control mice breathing filtered air. In the human cohort, urinary levels of <i>t</i>,<i>t</i>-MA were inversely associated several populations of circulating angiogenic cells (CD31⁺/34⁺/45⁺, CD31⁺/34⁺/45⁺/AC133^–, CD34⁺/45⁺/AC133⁺). Although <i>t</i>,<i>t</i>-MA was not associated with plasma markers of inflammation or thrombosis, <i>t</i>,<i>t</i>-MA levels were higher in smokers and in individuals with dyslipidemia. In smokers, <i>t</i>,<i>t</i>-MA levels were positively associated with urinary metabolites of nicotine (cotinine) and acrolein (3-hydroxymercapturic acid). Levels of <i>t</i>,<i>t</i>-MA were also associated with CVD risk as assessed using the Framingham Risk Score and this association was independent of smoking. Thus, benzene exposure is associated with increased CVD risk and deficits in circulating angiogenic cells in both smokers and non-smokers.</p></div

Demographics and CVD risk history stratified by <i>t</i>,<i>t</i>-MA.

<p>Demographics and CVD risk history stratified by <i>t</i>,<i>t</i>-MA.</p