ScRNA-seq profiling of breast cancer tumors, BRCA1 mutant pre-neoplastic mammary gland cells and normal mammary gland cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA678650 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Women with germline mtuation in BRCA1 have increased risk for developing hereditary breast cancer. The role of the epitheilum-assocaited niche during BRCA1-driven tumor intiation remains unclear. Here, we show that the pre-malignant stromal niche promotes epithelial prolifeation and BRCA1-driven cancer intiation in trans. Using single-cell RNA seq analysis of human pre-neoplastic BRCA1 and control breast tissue, we show that stromal cells provide numerous pro-proliferative paracrine signals inducing epithelial proliferation.
2021-11-17 | GSE174588 | GEO
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.
2022-02-20 | PXD030355 | Pride
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.
2022-02-20 | PXD030328 | Pride
Project description:Pre-neoplastic stromal cells drive BRCA1-mediated breast tumorigenesis
| PRJNA730582 | ENA
Project description:This study presents a single cell transcriptome map of nearly 430,000 cells encompassing normal breast at different hormonal stages, preneoplastic BRCA1+/- tissue, the major clinical subtypes of breast cancer, and matching pairs of tumors and involved axillary lymph nodes. Comparison of normal tissue specimens according to menopausal status primarily revealed changes in the stroma. Although there were modest changes in the microenvironment of preneoplastic BRCA1+/- versus normal tissue, a profound increase in infiltrating immune cells and a concomitant decrease in fibroblasts accompanied the transition to neoplasia. Single cell profiling of 32 tumors representing treatment-naive ER+, HER2+, triple negative (TN) breast cancers revealed equivalent diversity between tumor cells across the subtypes, each comprising a broad cluster and a prominent subset of cycling cells. In the immune landscape of tumors, highly proliferative T cells characterize TN and HER2+ tumors, whereas cycling tumor-associated macrophages featured in ER+ tumors. Copy number variant and scRNA-seq analysis of paired ER+ tumors and lymph node (LN) samples revealed either collective migration of primary tumor cells into LNs or seeding by genetically distinct clones. This large-scale integration of patient samples provides a high resolution map of cell diversity for normal and cancerous human breast.
2021-03-19 | GSE161529 | GEO
Project description:The present experiments were performed to determine the roles of estrogen receptors α and β (ERα and ERβ) in normal and neoplastic development in the mouse mammary gland. In wild-type mice, in vivo administration of estradiol (E) + progesterone (P) stimulated mammary ductal growth and alveolar differentiation. Mammary glands from mice in which the ERβ gene has been deleted (βERKO mice) demonstrated normal ductal growth and differentiation in response to E + P. By contrast, mammary glands from mice in which the ERα gene has been deleted (αERKO mice) demonstrated only rudimentary ductal structures that did not differentiate in response to E + P. EGF demonstrates estrogen-like activity in the mammary glands of αERKO mice: treatment of αERKO mice with EGF + P (without E) supported normal mammary gland development, induced expression of progesterone receptor (PR), and increased levels of G- protein-coupled receptor (GPR30) protein. Mammary gland development in βERKO mice treated with EGF + P was comparable to that of wild-type mice receiving EGF + P; EGF had no statistically significant effects on the induction of PR or expression of GPR30 in mammary glands harvested from either wild-type mice or βERKO mice. In vitro exposure of mammary glands to 7,12-dimethylbenz[a]anthracene (DMBA) induced preneoplastic mammary alveolar lesions (MAL) in glands from wild-type mice and βERKO mice, but failed to induce MAL in mammary glands from αERKO mice. Microarray analysis of DMBA-treated mammary glands identified 28 functional pathways whose expression was significantly different in αERKO mice versus both βERKO and wild-type mice; key functions that were differentially expressed in αERKO mice included cell division, cell proliferation, and apoptosis. The data demonstrate distinct roles for ERα and ERβ in normal and neoplastic development in the mouse mammary gland, and suggest that EGF can mimic the ERα-mediated effects of E in this organ.
2014-10-18 | GSE62451 | GEO
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
2020-06-22 | GSE151197 | GEO
Project description:The present experiments were performed to determine the roles of estrogen receptors M-NM-1 and M-NM-2 (ERM-NM-1 and ERM-NM-2) in normal and neoplastic development in the mouse mammary gland. In wild-type mice, in vivo administration of estradiol (E) + progesterone (P) stimulated mammary ductal growth and alveolar differentiation. Mammary glands from mice in which the ERM-NM-2 gene has been deleted (M-NM-2ERKO mice) demonstrated normal ductal growth and differentiation in response to E + P. By contrast, mammary glands from mice in which the ERM-NM-1 gene has been deleted (M-NM-1ERKO mice) demonstrated only rudimentary ductal structures that did not differentiate in response to E + P. EGF demonstrates estrogen-like activity in the mammary glands of M-NM-1ERKO mice: treatment of M-NM-1ERKO mice with EGF + P (without E) supported normal mammary gland development, induced expression of progesterone receptor (PR), and increased levels of G- protein-coupled receptor (GPR30) protein. Mammary gland development in M-NM-2ERKO mice treated with EGF + P was comparable to that of wild-type mice receiving EGF + P; EGF had no statistically significant effects on the induction of PR or expression of GPR30 in mammary glands harvested from either wild-type mice or M-NM-2ERKO mice. In vitro exposure of mammary glands to 7,12-dimethylbenz[a]anthracene (DMBA) induced preneoplastic mammary alveolar lesions (MAL) in glands from wild-type mice and M-NM-2ERKO mice, but failed to induce MAL in mammary glands from M-NM-1ERKO mice. Microarray analysis of DMBA-treated mammary glands identified 28 functional pathways whose expression was significantly different in M-NM-1ERKO mice versus both M-NM-2ERKO and wild-type mice; key functions that were differentially expressed in M-NM-1ERKO mice included cell division, cell proliferation, and apoptosis. The data demonstrate distinct roles for ERM-NM-1 and ERM-NM-2 in normal and neoplastic development in the mouse mammary gland, and suggest that EGF can mimic the ERM-NM-1-mediated effects of E in this organ. Gene expression of mammary gland organ culture and DMBA-induced lesions from 4 mouse strains.
2014-10-18 | E-GEOD-62451 | biostudies-arrayexpress
Project description:Brca1 mutation predisposes women to early onset of breast and ovarian cancers.Through its diverse functions in DNA damage repair, cell cycle control, transcription regulation, ubiquitination and so on, BRCA1 acts as a very significant tumor suppressor and genomic safeguard. Brca1 deficiency induces severe cellular stress, when occurring in the mammary glands, it impairs the regular developmental process and eventually causes tumorigenesis due to accumulation of genome instability and other mechanisms. The Brca1-defiencient mouse mammary tumor were characterized with great tumoral heterogeneity, which is in line with the human breast cancers carrying BRCA1 mutations. Here we studied the molecular complexicity of Brca1-deficient mouse mammary tumors vie RNA sequencing.
2021-11-17 | GSE148565 | GEO