ABI1-based 7-gene expression signature predicts breast cancer metastasis and survival
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE159956 | GEO | 2021/08/18
REPOSITORIES: GEO
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Project description:ABI1-based 7-gene expression signature predicts breast cancer metastasis and survival
| PRJNA670946 | ENA
Project description:subpopulation of breat cancer using gene expression data and clinical data Keywords: breast cancer survival and metastasis analysis
2006-06-28 | GSE2845 | GEO
Project description:Introduction: A gene expression signature indicative of active wound responses is common to more than 90% of non-neoplastic tissues adjacent to breast cancer, but these tissues also show substantial heterogeneity, suggesting different microenvironmental subtypes. Genomic variation in the extratumoral microenvironment has received limited study. Methods: Gene expression analysis from 72 patient-derived samples adjacent to invasive breast cancer or ductal carcinoma in situ was evaluated. Unsupervised clustering identified two distinct gene expression subgroups that differed substantially in expression of genes associated with epithelial-to-mesenchymal transition (EMT). We evaluated the prognostic and biological relevance of this extratumoral EMT-like signature using clinical and experimental approaches. Results: We found that the extratumoral EMT-like signature was not significantly associated with overall survival among all patients [Hazard Ratio (HR) = 1.4, 95% CI 0.6 - 2.8, p=0.337], but there was a strong association with overall survival among estrogen receptor (ER)-positive patients [HR = 2.5, 95% CI 0.9 – 6.7, p=0.062] or hormone-treated patients [HR=2.6, 95% CI 1.0 – 7.0, p=0.045]. In addition, co-culturing of ER-positive MCF-7 cells with cells undergoing EMT increased migration of MCF7 cells in a TGF-β1 dependent manner. Conclusion: Together, these results suggest that the presence of an EMT-like signature in the cancer-adjacent extratumoral microenvironment may influence the aggressiveness of the ER-positive tumors and that ER-positive patients with these extratumoral signatures may require additional treatments or more aggressive surgeries. Reference vs. test sample. 74 test samples (12 breast tumors, 62 normal tissue adjacent to breast tumor) from 72 patients.
2011-12-31 | E-GEOD-31589 | biostudies-arrayexpress
Project description:To execute RNA-Seq analysis of PyMT breast tumors studied in animals with and heterozygous and homozygous states of Abi1 gene
2020-12-08 | GSE162815 | GEO
Project description:Purpose:The Vimentin gene plays a pivotal role in epithelial-to-mesenchymal transition (EMT) and is known to be over-expressed in the prognostically poor basal-like breast cancer subtype. Recent studies have reported Vimentin DNA methylation in association with poor clinical outcomes in other solid tumors, but not in breast cancer. We therefore quantified Vimentin DNA methylation in breast tumors and matched normal pairs in association with gene expression and survival in a cohort of 83 breast cancer patients. Materials and Methods:Vimentin methylation was quantified in 14 breast cell lines, 83 breast tumors, and 57 matched normal pairs using MALDI-TOF mass spectrometry. Gene expression data via qRT-PCR in cell lines, and oligo microarray data from breast tissues was correlated with percent methylation in the Vimentin promoter. A threshold of 20 percent average methylation was set for bivariate and multivariate tests of association between methylation and tumor subtype, tumor histopathology, and survival. Results:Vimentin was differentially methylated in luminal breast cancer cell lines, and in luminal A, luminal B and HER2+ breast tumor subtypes, but was rare in basal-like cell lines and tumors. Increased methylation was strongly correlated with decreased mRNA expression in cell lines, and had a moderate inverse correlation in breast tumors. Importantly, Vimentin methylation predicted poor overall survival independent of race, subtype, stage, nodal status or estrogen receptor positivity. Conclusion:Vimentin methylation predicts overall survival in breast cancer patients and holds promise as a prognostic biomarker for guiding treatment and prophylaxis. reference x sample
2013-02-19 | E-GEOD-35629 | biostudies-arrayexpress
Project description:Cell motility and invasion initiate metastasis. However, only a subpopulation of cancer cells within a tumor will ultimately become invasive. Due to this stochastic and transient nature, in an experimental setting, migrating and invading cells need to be isolated from the general population in order to study the gene expression profiles linked to these processes. This report describes microarray analysis on RNA derived from migrated or invaded subpopulations of triple negative breast cancer cells in a Transwell set-up, at two different time points during motility and invasion, pre-determined as “early” and “late” in real-time kinetic assessments. Invasion- and migration-related gene expression signatures were generated through comparison with non-invasive cells, remaining at the upper side of the Transwell membranes. Late-phase signatures of both invasion and migration indicated poor prognosis in a series of breast cancer data sets. Furthermore, evaluation of the genes constituting the prognostic invasion-related gene signature revealed Krüppel-like factor 9 (KLF9) as a putative suppressor of invasive growth in breast cancer. Next to loss in invasive vs non-invasive cell lines, KLF9 also showed significantly lower expression levels in the “early” invasive cell population, in several public expression data sets and in clinical breast cancer samples when compared to normal tissue. Overexpression of EGFP-KLF9 fusion protein significantly altered morphology and blocked invasion and growth of MDA-MB-231 cells in vitro. In addition, KLF9 expression correlated inversely with mitotic activity in clinical samples, indicating anti-proliferative effects.
2014-01-29 | GSE54465 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE41971: In vivo NCL-targeting affects breast cancer aggressiveness through miRNA regulation [NanoString] GSE41972: In vivo NCL-targeting affects breast cancer aggressiveness through miRNA regulation [Affymetrix] Refer to individual Series
2012-11-02 | E-GEOD-41973 | biostudies-arrayexpress
Project description:Cell motility and invasion initiate metastasis. However, only a subpopulation of cancer cells within a tumor will ultimately become invasive. Due to this stochastic and transient nature, in an experimental setting, migrating and invading cells need to be isolated from the general population in order to study the gene expression profiles linked to these processes. This report describes microarray analysis on RNA derived from migrated or invaded subpopulations of triple negative breast cancer cells in a Transwell set-up, at two different time points during motility and invasion, pre-determined as M-bM-^@M-^\earlyM-bM-^@M-^] and M-bM-^@M-^\lateM-bM-^@M-^] in real-time kinetic assessments. Invasion- and migration-related gene expression signatures were generated through comparison with non-invasive cells, remaining at the upper side of the Transwell membranes. Late-phase signatures of both invasion and migration indicated poor prognosis in a series of breast cancer data sets. Furthermore, evaluation of the genes constituting the prognostic invasion-related gene signature revealed KruM-LM-^Hppel-like factor 9 (KLF9) as a putative suppressor of invasive growth in breast cancer. Next to loss in invasive vs non-invasive cell lines, KLF9 also showed significantly lower expression levels in the M-bM-^@M-^\earlyM-bM-^@M-^] invasive cell population, in several public expression data sets and in clinical breast cancer samples when compared to normal tissue. Overexpression of EGFP-KLF9 fusion protein significantly altered morphology and blocked invasion and growth of MDA-MB-231 cells in vitro. In addition, KLF9 expression correlated inversely with mitotic activity in clinical samples, indicating anti-proliferative effects. After selection of two time points (M-bM-^@M-^\earlyM-bM-^@M-^] and M-bM-^@M-^\lateM-bM-^@M-^]), RNA from invasive and migratory MDA-MB-231 cells was isolated from Transwell membranes and hybridized onto an Illumina HumanHT-12 v4 Expression beadchip. Gene expressions of migrated/invaded subpopulations vs non-motile cells were compared.
2014-01-29 | E-GEOD-54465 | biostudies-arrayexpress
Project description:Purpose:The Vimentin gene plays a pivotal role in epithelial-to-mesenchymal transition (EMT) and is known to be over-expressed in the prognostically poor basal-like breast cancer subtype. Recent studies have reported Vimentin DNA methylation in association with poor clinical outcomes in other solid tumors, but not in breast cancer. We therefore quantified Vimentin DNA methylation in breast tumors and matched normal pairs in association with gene expression and survival in a cohort of 83 breast cancer patients. Materials and Methods:Vimentin methylation was quantified in 14 breast cell lines, 83 breast tumors, and 57 matched normal pairs using MALDI-TOF mass spectrometry. Gene expression data via qRT-PCR in cell lines, and oligo microarray data from breast tissues was correlated with percent methylation in the Vimentin promoter. A threshold of 20 percent average methylation was set for bivariate and multivariate tests of association between methylation and tumor subtype, tumor histopathology, and survival. Results:Vimentin was differentially methylated in luminal breast cancer cell lines, and in luminal A, luminal B and HER2+ breast tumor subtypes, but was rare in basal-like cell lines and tumors. Increased methylation was strongly correlated with decreased mRNA expression in cell lines, and had a moderate inverse correlation in breast tumors. Importantly, Vimentin methylation predicted poor overall survival independent of race, subtype, stage, nodal status or estrogen receptor positivity. Conclusion:Vimentin methylation predicts overall survival in breast cancer patients and holds promise as a prognostic biomarker for guiding treatment and prophylaxis.
2013-02-19 | GSE35629 | GEO
Project description:Abi1 gene dose study in PyVT breast tumors
| PRJNA683072 | ENA