Here we describe the comprehensive gene expression profiles of each cell type composing normal breast tissue and in situ and invasive breast carcinomas using serial analysis of gene expression. Based on these data, we determined that extensive gene expression changes occur in all cell types during cancer progression and that a significant fraction of altered genes encode secreted proteins and receptors. Despite the dramatic gene expression changes in all cell types, genetic alterations were detected only in cancer epithelial cells. The CXCL14 and CXCL12 chemokines overexpressed in tumor myoepithelial cells and myofibroblasts, respectively, bind to receptors on epithelial cells and enhance their proliferation, migration, and invasion. Thus, chemokines may play a role in breast tumorigenesis by acting as paracrine factors.

The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression. Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors. Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells. Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.

BackgroundStress has been associated with poor eating behaviors and diet quality, as well as high body mass index (BMI). Low-income women may be particularly vulnerable to stress and severe obesity. Yet it is unknown how stress increases the risk of severe obesity through disordered eating behaviors and poor diet quality or through mechanisms independent of diet.MethodsWe examined cross-sectional data from women (n = 101) with a child enrolled in the Special Supplemental Nutrition Program for Women, Infants, and Children in Cumberland County, North Carolina (spring 2012). We collected measured heights and weights to calculate BMI. Using structural equation modeling, we differentiated pathways from stress to weight status: (1) indirectly through eating behaviors (cognitive restraint, emotional eating, and uncontrolled eating) and diet quality, which we examined with the Healthy Eating Index 2010 and 24-h dietary recalls, and (2) directly through possible unmeasured risk factors independent of diet. The analysis controlled for race/ethnicity, income, age, whether the dietary recall day was typical, and whether the respondent completed one or two 24-h dietary recalls.ResultsPerceived stress was positively associated with uncontrolled eating (β = 0.38, p < 0.001) and emotional eating (β = 0.50, p < 0.001). However, higher stress was not associated with weight status through eating behaviors and diet quality. Independent of eating behaviors and diet quality, stress was positively associated with severe obesity (β = 0.26, p = 0.007).ConclusionsImproving stress coping strategies for low-income women may improve eating behaviors and reduce severe obesity.Electronic supplementary materialThe online version of this article (doi:10.1186/s12937-015-0110-4) contains supplementary material, which is available to authorized users.