Project description:Overweight and obesity are now recognized as established risk factors for breast cancer in postmenopausal women. Reciprocal interactions have been described between adipose and cancer cells. Among the cell types present in the breast, myoepithelial cells (MECs) are considered "tumour suppressor" cells. During the transition from ductal carcinoma in situ to invasive cancer, disorganization or even the disappearance of MECs is observed. As the adipose microenvironment is now considered as a central actor in the progression of breast cancer, our objective was to evaluate if it could be involved in MEC functional modifications, leading to the transition of in situ to invasive carcinoma, particularly in obese patients. Through a co-culture model, we found that adipose cells could decrease the viability of the MECs. The adipose cells could also disrupt the expression of the genes involved in the maintenance of the extracellular matrix and to amplify the expression of leptin and inflammatory markers. The metabolite analyses revealed specific profiles that may be involved in the growth of neoplastic cells. All of these perturbations could thus be responsible for the loss of tumour suppressor status of MECs and promote the transition from in situ to invasive carcinoma.
Project description:This SuperSeries is composed of the following subset Series: GSE41194: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 1) GSE41196: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 2) GSE41197: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 3) GSE41198: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 4 stroma) GSE41227: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 4 Epithelial) Refer to individual Series
Project description:This is a matched-pair analysis of ductal carcinoma in situ (DCIS) and invasive component (IDC) of nine breast ductal carcinoma to identify novel molecular markers characterizing the transition from DCIS to IDC for a better understanding of its molecular biology.
Project description:This study identifies progression in breast ductal carcinoma in situ (DCIS) as it progresses towards triple negative invasive breast cancer (TNBC).
Project description:This study identifies progression in breast ductal carcinoma in situ (DCIS) as it progresses towards triple negative invasive breast cancer (TNBC).
Project description:cDNA aCGH study of pure DCIS (breast duct carcinoma in situ) without invasive tumor, DCIS associated with IDC (breast invasive duct carcinoma) and its IDC component 23 patients: 6 pure DCIS without invasive cancer and no history of invasive cancer, 17 DCIS associated with IDC. Out of the latter 1 tumor had only enough DCIS (#16) for aCGH and one - IDC (#23) Keywords: Comparative clinical study
Project description:The transition from ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC) is an important step during breast tumorgenesis. Understanding its molecular changes may uncover both novel preventive and therapeutic strategies and may help to identify high-risk DCIS that progress to IDC. The mechanisms are unknown and the role of CapG in the nucleus is an enigma. Here, we tested the association between clinicopathological CapG expression in tumor samples and used a cell culture model to test the hypothesis that CapG affects gene expression. Breast cancer samples were analyzed by reverse transcriptase – real time PCR (RT-qPCR). We used microarray analysis to study the transcriptome of the cell culture model and validated changes in gene expression in laser capture micro-dissected formalin-fixed paraffin-embedded (FFPE) invasive ductal carcinoma (IDC) and ductal carcinoma in situ (DCIS), respectively. We were able to associate increased CapG expression with an invasive breast cancer phenotype. In 28.2% of breast cancer samples CapG expression in breast cancer samples revealed in 28.2% a very high CapG expression and statistical significant association (p<0.05) to positive metastasis status (M1) and negative ER status (ER-). In case of CapG overexpression microarray analyses generated a list of differential expressed genes and revealed enhanced expression levels of GPNMB, NRP1, LOXL2, TRIM47 and COL16A1, while ZDHHC11, KIAA1467 were down-regulated. We show here for the first time an effect on the transcriptome by experimental modification of CapG expression. Concluding, CapG is involved in tumor progression.
