Profiling of indolent and aggressive mammary lesions
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PROVIDER: PRJNA680303 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional profiling of indolent and aggressive mammary lesions
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Project description:We performed transcriptional profiling of tumor cells from indolent and aggressive lesions isolated from a mouse model of breast cancer. To initiate formation of mammary lesions, we delivered lentiviral particles carrying constitutively-activated Erbb2 tagged with HA and GFP (caErbB2) through the lactiferous glands of adult virgin female. Mammary glands bearing lesions were visualized under a fluorescence stereoscope, and regions harboring aggressive (>2mm, comprised of invasive lesions) and indolent (<2mm, enriched for in situ lesions) lesions were dissected away from each other. Lesions from multiple animals were pooled to obtain sufficient material for downstream analysis. Following tissue digestion, GFP-expressing epithelial cells were isolated by fluorescence-activated cell sorting (FACS), and then subjected to bulk RNA-seq.
2021-06-17 | GSE162005 | GEO
Project description:We performed transcriptional profiling of tumor cells from indolent and aggressive lesions isolated from a mouse model of breast cancer. To initiate formation of mammary lesions, we delivered lentiviral particles carrying constitutively-activated Erbb2 tagged with HA and GFP (caErbB2) through the lactiferous glands of adult virgin female. Mammary glands bearing lesions were visualized under a fluorescence stereoscope, and regions harboring aggressive (>2mm, comprised of invasive lesions) and indolent (<2mm, enriched for in situ lesions) lesions were dissected away from each other. Lesions from multiple animals were pooled to obtain sufficient material for downstream analysis. Following tissue digestion, GFP-expressing epithelial cells and CD45+ immune cells were isolated by fluorescence-activated cell sorting (FACS), and then subjected to single-cell RNA-sequencing.
2021-06-17 | GSE161983 | GEO
Project description:Single-cell transcriptional profiling of indolent and aggressive mammary lesions
| PRJNA680255 | ENA
Project description:Title: Gene expression analysis of indolent and aggressive forms of Chronic Myeloid Leukaemia (CML). Description: Chronic Myeloid Leukaemia presents in chronic phase (CP) and terminates in 'blast crisis'. Despite a common abnormality, the duration of CP is variable. The aim is to compare the gene expression profiles of the indolent and aggressive forms of CML. All samples were taken within 3 months of first diagnosis. Indolent patients were defined by chronic phase CML, duration minimum 7 years. Aggressive patients were defined by chronic phase, duration maximum 3 years.
2013-01-30 | E-MIMR-17 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-06-17 | GSE162006 | GEO
Project description:Transcriptomic profiling of dermatomyositis lesions.
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Project description:Clinical management of prostate cancer remains a significant challenge due to the lack of available tests for guiding treatment decisions. The blood Prostate-Specific Antigen (PSA) test has facilitated early detection and intervention of prostate cancer. However, blood PSA levels are less effective in distinguishing aggressive from indolent prostate cancers and other benign prostatic diseases. Thus, the development of novel approaches specific for prostate cancer that can differentiate aggressive from indolent disease remains an urgent medical need. In the current study, we evaluated urine specimens from prostate cancer patients instead of serum using liquid chromatography-tandem mass spectrometry (LC-MS/MS), with the aim of identifying effective prostate cancer biomarkers. Glycoproteins from urine samples of prostate cancer patients with different Gleason scores were characterized via solid phase extraction of N-linked glycosite-containing peptides and LC-MS/MS. In total, 2923 unique glycosite-containing peptides were identified. Comparison of urine-based glycoproteins with those identified from aggressive and non-aggressive prostate cancer tissues as well as sera from prostate cancer patients revealed that the majority of aggressive prostate cancer-associated glycoproteins were more readily detected in patient urine than serum samples. Our data collectively indicate that urine provides a highly reliable source for biomarker testing in patients with aggressive prostate cancer.
2022-02-28 | PXD004495 | Pride
Project description:Transcriptomic profiling of LP lesions, hypertrophic LP (HLP) lesions, and healthy controls
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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.
2014-05-20 | GSE50003 | GEO