Early-stage breast cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: SeungHyun Jung
PROVIDER: E-GEOD-37839 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Copy number alteration profiling of human early-stage (stage I and II) breast cancers. We aimed to describe the commonly occurred chromosome alterations in early-stage breast cancer (stage I and II) and to explore the implications of the recurrently altered regions (RAR) on the patient prognosis. For this purpose, we analyzed the DNA copy number alterations (CNAs) across the whole genome using oligoarray-comparative genomic hybridization (CGH) in the discovery set of EBC patients.
2012-05-09 | GSE37839 | GEO
Project description:Search for copy number imbalances and allelotype in 971 early stage breast cancer using molecular inversion probe arrays Affymetrix MIP arrays were performed according to the manufacturer's directions on DNA extracted from paraffin embedded formalin fixed Stage I and II Breast Cancers Copy number analysis of Affymetrix Oncoscan Version 1 MIP arrays was performed for 971 Stage I and II breast cancers.
2011-08-16 | E-GEOD-31424 | biostudies-arrayexpress
Project description:We developed a novel approach to isolate tumor cells with high purity from blood via immunomagnetic enrichment followed by fluorescence activated cell sorting (IE/FACS) and examined copy number alterations in these cells. Magnetic beads coated with EpCAM mAb were added to blood to enrich for tumor cells. Enriched samples were then subjected to FACS analysis using differentially labeled mAbs to distinguish tumor cells (EpCAM+) from leukocytes (CD45+) during sorting. DNA from isolated tumor cells was subjected to whole genome amplification (WGA) and copy number analysis via array comparative genomic hybridization (CGH). The assay was evaluated using BT474 and MCF7 breast cancer cell lines and in CTCs from 5 metastatic breast cancer (MBC) patients with matched archival primary tumors and later extended to an additional 97 MBC patients. Evaluation of the assay on isolated breast cancer cell lines spiked into blood correctly identified the known genomic alterations with high reproducibility. In clinical studies, comparison of CTCs with matched archival primary tumors confirmed shared lineage with notable divergence. In addition, serial testing of CTCs confirmed reproducibility, and indicated genomic change over time. Analysis of genomic profiles of CTCs from 102 MBC patients revealed common copy number alterations including gains in 1q and 8q and losses in 8p and 11q. Comparison with a published CGH dataset of primary breast tumors revealed similar frequencies of recurrent genomic copy number aberrations.
2012-12-31 | E-GEOD-27511 | biostudies-arrayexpress
Project description:Purpose: MET is a receptor tyrosine kinase (RTK) that has been considered a druggable target in non-small cell lung cancer (NSCLC). To understand the mechanisms of resistance to MET-TKIs and establish therapeutic strategies, we developed an in vitro model using capmatinib-resistant cell lines (EBC-CR1, CR2, and CR3) derived from the MET-amplified NSCLC cell line EBC-1. Methods: We established capmatinib-resistant NSCLC cell lines from the MET-amplified NSCLC cell line EBC-1 and identified alternative signaling pathways using 3’mRNA sequencing and human phospho-RTK arrays. Copy number alterations were evaluated by quantitative PCR and cell proliferation assay; activation of RTKs and downstream effectors were compared between the parental cell line EBC-1 and the EBC-CR1, -CR2, and -CR3 resistant cell lines. Results: We found that epidermal growth factor (EGFR) mRNA expression and protein activation were increased in EBC-CR1–3 cells compared to EBC-1 cells. EBC-CR1 cells showed EGFR-dependent growth and sensitivity to afatinib, an irreversible EGFR TKI. EBC-CR2 cells, which overexpressed the EGFR-MET heterodimer, responded dramatically to the combination of capmatinib and the phosphoinositide-3 kinase catalytic subunit α (PIK3CA) inhibitor afatinib. In addition, EBC-CR3 cells, which had activated EGFR along with amplified PIK3CA, were sensitive to the combination of afatinib and the PI3Kα inhibitor. Conclusions: Our in vitro studies suggested that activation of EGFR signaling and/or genetic alteration of downstream effectors like PIK3CA were alternative resistance mechanisms used by capmatinib-resistant NSCLC cell lines. In addition, combined treatments with MET, EGFR, and PI3Kα inhibitors may be an effective therapeutic strategy in MET-TKI-resistant NSCLC patients.
2017-05-01 | GSE94405 | GEO
Project description:Breast cancer is the most prevalent cancer in women 1, and most cases are believed to have a sporadic, rather than heritable basis 2. To identify breast cancer driver genes, we exploited the C3H-Mcm4Chaos3/Chaos3 (“Chaos3”) mouse model that, by virtue of bearing a defective DNA replicative helicase subunit that causes elevated genomic instability (GIN), sustains somatic alterations ultimately causing mammary adenocarcinomas 6. Array Comparative Genomic Hybridization (aCGH) analysis of Chaos3 mammary tumors revealed recurrent copy number alterations (CNAs), most notably deletion of the Neurofibromin 1 (Nf1) tumor suppressor gene in all cases. NF1, a negative regulator of RAS, is traditionally recognized for its role in driving the development of neurofibromas in the context of the human disease Neurofibromatosis Type 1, but not breast cancer. Genomic DNA from tumor and reference samples were hybridized to NimbleGen 3x720K mouse CGH arrays. Two reference samples were used independently. CNAs were visualized using Nimblegen, IGV, and KCsmart software 32. Select genes were validated via qPCR. Critical regions within each Chaos3 CNA were identified as the region with the greatest overlap across multiple Chaos3 tumors. Recurring Copy Number Variations (CNVs) for 12 Chaos3 tumors and 2 MMTV-Neu mammary tumors analyzed by aCGH are indicated. Samples analyzed are primary tumors except where indicated.
2012-10-01 | E-GEOD-37607 | biostudies-arrayexpress
Project description:Alterations in circulating miRNAs following early-stage breast cancer resection
| PRJNA247473 | ENA
Project description:We investigated the CNAs in a four stage tumorigenesis model. This model included copy number analyses in non-transgenic NMRI mice (normal) and in transgenic SVT/t mice: non-malignant hyperplastic mammary glands and breast cancers, as well as breast cancer derived cell lines. We focused our research on copy number analyses to compare the genomic alterations that occur during tumorigenesis. We addressed the question, whether common predisposed chromosomal breakpoints could be seen to promote malignant transformation. We can report a characteristic increase of copy number alterations from normal to tumor stage in our model. Furthermore, we have identified chromosomal segments and found characteristic fragmentations.
2012-09-04 | GSE35873 | GEO
Project description:Search for copy number imbalances and allelotype in 971 early stage breast cancer using molecular inversion probe arrays
2011-08-17 | GSE31424 | GEO
Project description:We investigated the CNAs in a four stage tumorigenesis model. This model included copy number analyses in non-transgenic NMRI mice (normal) and in transgenic SVT/t mice: non-malignant hyperplastic mammary glands and breast cancers, as well as breast cancer derived cell lines. We focused our research on copy number analyses to compare the genomic alterations that occur during tumorigenesis. We addressed the question, whether common predisposed chromosomal breakpoints could be seen to promote malignant transformation. We can report a characteristic increase of copy number alterations from normal to tumor stage in our model. Furthermore, we have identified chromosomal segments and found characteristic fragmentations. Affymetrix SNP array analysis was performed with Mouse Diversity Genotyping Arrays (Affymetrix). DNA was extracted from frozen biopsies of mammary tumor samples of six mice and two cell lines. Normalization and allele summarization were performed with the BRLMM-P algorithm provided and copy number analysis was performed for the each sample using the average signal intensity of both normal samples as the reference for copy number inference.
2012-09-04 | E-GEOD-35873 | biostudies-arrayexpress