Project description:Circulating immune cells that have interacted with tumor tissue exhibit distinct characteristics compared to those in healthy individuals, potentially offering critical insights into tumor presence and malignancy. However, the epigenetic mechanisms governing these blood immune cells in cancer patients remain poorly understood. In this study, we investigated chromatin accessibility and transcription factor binding in peripheral blood mononuclear cells (PBMCs) from dogs with mammary gland tumors using ATAC-seq. Our analysis revealed altered chromatin accessibility near genes associated with immune function, neuronal activity, and lipid metabolism in affected dogs. Notably, we identified CEBPD-bound peaks that were upregulated in cancer-affected PBMCs and demonstrated that the transcription of their associated genes, CD47 and MAP4K4, was also upregulated in monocytes under cancer co-culture conditions—an effect that was mitigated following CRISPR interference of these regions. These findings underscore the critical role of chromatin accessibility and transcriptional regulation in the immune response to cancer
Project description:We studied the impact of mammary tumorigenesis on Tregs in tumors and distant organs (CD3+CD4+CD25+). Here we generated RNAseq data from sorted Tregs (CD3+CD4+CD25+) from WT and K14cre;Cdh1F/F;Trp53F/F mice bearing 225mm2 mammary tumors from blood, spleen, lungs, TDLNs, tumor and healthy mammary gland
Project description:Identification of differentially expressed genes in benign and malignant mammary gland tumors of dog and their role in cancers of mammary gland
Project description:Using microarray technology, we aim to identify genes affecting the biology of mammary tumor cancers in dogs. Canine mammary gland tumors (CMGTs) are the most common neoplasms in sexually intact female dogs. CMGTs have been suggested as a model for studying human breast cancer because of several similarities, including the relative age of onset, risk factors, incidence, histological and molecular features, biological behavior, metastatic pattern, and responses to therapy.
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: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:Identify gene expression changes in the absence of Plk2 Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis. Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis.