Project description:The main goal of this experiment was to contrast the gene expression of mammary gland tissues at three different tumoral stages : M/D-driven mammary gland small tumors vs mammary gland tissues that have been exposed to M/D but they did not develop a tumor (hyperplastic mammary gland) vs mammary gland tissues that were NOT expossed to M/D (normal mammary gland). Expression profile of 18 mice mammary gland tissues at 3 differents neoplastic stages before and after M/D expossure
Project description:WT mammary gland(WTMG),mutant-MG(MTMG),WT breast tumors(WTBT),MTBT and MTBT-adjacent MG were collected to do data-independent acquisiton(DIA)mass to find the intrinsic factors that is associated with Brca1-deficiency induced breast cancer.
Project description:WT mammary gland(WTMG),mutant-MG(MTMG),WT breast tumors(WTBT),MTBT and MTBT-adjacent MG were collected to do data-independent acquisiton(DIA)mass to find the intrinsic factors that is associated with Brca1-deficiency induced breast cancer.
Project description:Different doses of glucose were inused into dairy goat mammary gland. The mammary gland tissues were biopsied to analyze the changes of transcriptome responding to glucose infusion.
Project description:In this study, two small RNA libraries were constructed using dry period and peak lactation dairy goat mammary gland tissues and sequenced by the Illumina Solexa high-throughput sequencing system. A total of 346 conserved and 95 novel miRNAs were identified in the dairy goat. The expression of miRNAs was confirmed by qRT-PCR in nine tissues and the mammary gland during development cycles. In addition, several candidate miRNAs that may be involved in mammary gland development and lactation were found by the comparison of miRNA expression profiles among different tissue and developmental stages of the mammary gland. This study provides the identification and profile of miRNAs related to the biology of the mammary gland in the dairy goat. The identification of these miRNAs could contribute to understanding the molecular mechanisms of lactation physiology and the development of the mammary gland in the dairy goat.
Project description:The goal of this study is to investigate the role of deregulated c-MYC in cooperation with activated NeuNT (mutated rat HER2) in mammary tumor molecular heterogeneity. We monitored female mice through two cycles of pregnancy/lactation in order to activate Blg-Cre expression in mammary gland after the second cycle. MYC-NeuNT mice develop tumors between 4 and 12 weeks post Blg-Cre activation, H&E images from these tumors showed histologic heterogeneity. NeuNT mice developed tumors between 28 to 44 weeks post Blg-Cre activation that also showed histologic heterogeneity.
Project description:Clinical studies have linked use of progestins (synthetic progesterone (P4)) to breast cancer risk. However, little is understood regarding the role native P4, signaling through the progesterone receptor (PR), plays in formation of breast tumors. Studies published by our lab highlighted a link between PR and immune signaling pathways, suggesting PR induces PR to repress the interferon signaling pathway. Given these findings, we sought to investigate whether P4/PR drive immunomodulation in the mammary gland and development of mammary gland tumors. We found that mice treated with P4 displayed changes in the mammary gland suggesting inhibited immune response compared to placebo-treated mice. Furthermore, transgenic mice with PR overexpression demonstrated decreased numbers of immune cell populations in their mammary gland, lymph nodes, and spleens. Upon long-term monitoring, we determined that multi-parous PR overexpressing mice developed significantly more mammary gland tumors than control mice. Additionally, tumors of PR overexpressing mice contained fewer infiltrating immune cells. Finally, RNA sequencing analysis of tumor samples revealed that immune-related gene signatures were enriched in tumors of control mice compared to tumors of PR overexpressing mice. Together, these findings provide a novel mechanism behind P4-mediated promotion of mammary gland tumor development and provide rationale to investigate anti-progestin treatment to promote immune-mediated elimination of mammary gland tumors.