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Gene expression in DCIS.COM and SUM225 MIND xenografts during transition from 2 to 6 to 10 weeks

ABSTRACT: We utilized DCIS mouse intraductal (MIND) models with both SUM225 and DCIS.COM cell lines to characterize the sequential and temporal changes in mRNA expression over a time course of 2, 6, and 10 weeks during in vivo progression in the epithelial cells from DCIS to invasive cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE65890 | GEO | 2015/02/12

SECONDARY ACCESSION(S): PRJNA275313

REPOSITORIES: GEO

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Gene expression in DCIS.COM and SUM225 MIND xenografts during transition from 2 to 6 to 10 weeks

Project description:We utilized DCIS mouse intraductal (MIND) models with both SUM225 and DCIS.COM cell lines to characterize the sequential and temporal changes in mRNA expression over a time course of 2, 6, and 10 weeks during in vivo progression in the epithelial cells from DCIS to invasive cancer. DCIS cell lines: DCIS.COM and SUM225 were injected intraductally into the MIND model as triplicates. At 2, 6, and 10 weeks post-injection, the mammary glands were collected and magnetically sorted for the epithelial cells. Affymetrix microarray was utilized to analyze gene expression profiles from RNA isolated from these cells.

2015-02-12 | E-GEOD-65890 | biostudies-arrayexpress

A living biobank of patient-derived ductal carcinoma in situ Mouse-INtraDuctal xenografts identifies factors associated with risk of invasive progression

Project description:Create a living biobank of patient-derived ductal carcinoma in situ (DCIS) Mouse-INtraDuctal (MIND) xenografts to find factors explaining invasive growth. Samples exist of both primary and pdx samples. Invasive growth was scored in the pdx.

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cee7cea1-8503-43fd-80c2-0ec4304363c7 - samples

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Immune escape in breast cancer during in situ to invasive carcinoma transition

Project description:To dissect mechanisms of immune escape during breast tumor progression, we analyzed the composition of leukocytes in normal breast tissues, ductal carcinomas in situ (DCIS), and HER2+ and triple negative invasive ductal carcinomas (IDC). We found significant tissue and tumor subtype-specific differences in multiple cell types including T cells and neutrophils. Analysis of gene expression profiles of T cells demonstrated enrichment for activated GZMB+MKI67+CD8+ effector T cell signatures in DCIS. TCR clonotypes also showed highest diversity in DCIS. Naïve T cell signatures predominated IDCs, especially triple negative subtypes. TIGIT and PDL1 immune checkpoint proteins showed differential expression between DCIS and IDCs with amplification of CD274 (encoding PDL1) only detected in triple negative IDCs. Our results imply that DCIS progression is limited by an anti-tumor immune response that becomes muted in invasive tumors due to selection for cancer cells and microenvironment that suppress activated T cells or no longer trigger their activation.

2017-06-28 | GSE87517 | GEO

cDNA aCGH study of pure DCIS without invasive tumor, DCIS associated with IDC and its IDC component

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

2009-02-01 | GSE10197 | GEO

Transcription profiling of human ductal carcinoma in situ (DCIS) and invasive component (IDC) from 9 breast cancers to identify novel molecular markers characterizing the transition from DCIS to IDC.

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.

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Short and long-term effects of CDK4/6 inhibition on early stage breast cancer

Project description:CDK4/6 inhibitors are used in the treatment of advanced estrogen receptor (ER)(+) breast cancer (BC). Their efficacy in ER(-) and early stage BC is currently under investigation. Here, we show that palbociclib, a CDK4/6 inhibitor, can inhibit both progression of ductal carcinoma in situ (DCIS) and growth of invasive disease in both an ER(-) basal BC model (MCFDCIS) and an ER(+) luminal model (MCF7 intraductal injection). In MCFDCIS cells palbociclib repressed cell cycle gene expression, inhibited proliferation, induced senescence and normalized tumorspheres formed in Matrigel whilst the formation of acini by normal mammary epithelial cells (MCF10A) was not affected. Palbociclib treatment of mice with MCFDCIS tumors inhibited their malignant progression and reduced proliferation of invasive lesions. Transcriptomic analysis of the tumor and stromal cell compartments showed that cell cycle and senescence genes, and MUC16, an ovarian cancer biomarker gene, were repressed during treatment. Knockdown of MUC16 in MCFDCIS cells inhibited proliferation of invasive lesions but not progression of DCIS. After cessation of palbociclib treatment genes associated with differentiation, e.g. p63, inflammation, IFNγ response and antigen processing and presentation remained suppressed in the tumor and surrounding stroma. We conclude that palbociclib can prevent progression of DCIS and is anti-proliferative in ER(-) invasive disease mediated in part via MUC16. Lasting effects of CDK4/6 inhibition after drug withdrawal on differentiation and the immune response could impact the approach to treatment of early stage ER(-) breast cancer.

2019-08-30 | GSE130903 | GEO

Expression profiling of murine DCIS and invasive ductal breast carcinoma

Project description:Murine healthy tissue samples, DCIS and invasive mammary tumors were analyzed in order to identify marker genes which show enhanced expresssion in DCIS and invasive ductal carcinomas. Using this approach, we were able to identify a set of genes which might allow a better detection of DCIS and invasive carcinomas in the future.

2011-04-11 | GSE21444 | GEO

Expression profiling of human DCIS and invasive ductal breast carcinoma

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