Similar Datasets
Project description:Human breast cancer cell line MCF-7 is usually sensitive to chemotherapy drug BMS-554417, an insulin receptor (IR) and insulin-like growth factor receptor (IGFR) inhibitor. However, through step-wise increase in BMS-554417 doses in culture media, we were able able to screen and select a single MCF-7 clone that is BMS-554417 resistant. It is cross resistant to BMS-536924. This new line of MCF-7 cells was named as MCF-7R4. The transcriptome profiling of both MCF-7 and MCF-7R4 was performed using Affymetrix HG-U133 plus2.0 GeneChip arrays. Five replicates of MCF-7 and five replicates of MCF-7R4 were profiled.
2009-11-05 | E-GEOD-18912 | biostudies-arrayexpress
Project description:Aims: Congenital heart defect (CHD) account for 25% of all human congenital abnormalities. Very few CHD-causing genes have been identified so far; so, to discover further genes we performed a global transcriptome analysis in mouse models of CHD. Methods and results: By the use of a retinoic acid competitive antagonist (BMS-189453) we caused CHD, thymic abnormalities and neural tube defects in mouse newborns. Transposition of great arteries was the prevalent cardiac defect observed (61%). Recently we were able to partially rescue this abnormal phenotype by oral administration of folic acid. Now we have performed a microarray analysis in mouse embryos (8.5 dpc) treated with BMS-189453 alone and with BMS-189453 plus folic acid (FA). On the basis of microarray and QRT-PCR results, we deeper analysed Hif1α because of its down-regulation in BMS-treated embryos vs WT and its increased expression level in BMS+FA treated embryos compared to BMS-treated ones. Immunofluorescence experiments confirmed the under-expression of Hif1α protein in BMS-treated embryos compared to WT and BMS+FA treated ones and moreover demonstrated that at 8.5 dpc Hif1α is mainly expressed in the embryo’s heart. Conclusion: We propose that Hif1α down-regulation by blocking retinoic acid binding, may contribute to the development of the cardiac defects of mouse newborns. In line with our hypothesis, when Hif1α expression level is restored (by supplementation of folic acid) a decrement of CHD is found. At the best of our knowledge this is the first report that link retinoic acid metabolism to Hif1α regulation and the development of TGA 2 samples w/ 2 dye-swaps
2010-09-20 | E-GEOD-19012 | biostudies-arrayexpress
Project description:BMS oral microbiome
| PRJEB75198 | ENA
Project description:Human breast cancer cell line MCF-7 is usually sensitive to chemotherapy drug BMS-554417, an insulin receptor (IR) and insulin-like growth factor receptor (IGFR) inhibitor. However, through step-wise increase in BMS-554417 doses in culture media, we were able able to screen and select a single MCF-7 clone that is BMS-554417 resistant. It is cross resistant to BMS-536924. This new line of MCF-7 cells was named as MCF-7R4. The transcriptome profiling of both MCF-7 and MCF-7R4 was performed using Affymetrix HG-U133 plus2.0 GeneChip arrays.
2009-11-06 | GSE18912 | GEO
Project description:Bone represents congenial soil for metastatic seeds and is frequently affected by metastasis of multiple cancer types. The histological and molecular characteristics of bone metastases (BMs) are diverse but poorly understood. Herein, we performed single-cell RNA-seq on 34 BMs from 6 cancer types and identified 3 ecosystem archetypes characterized by enrichment of macrophages/osteoclasts (Mφ-OC), regulatory/exhausted T cells (Treg-Tex), and monocytes (Mono), respectively. Breast cancer BMs are mostly the Mφ-OC archetype driven by the osteolytic vicious cycle, whereas kidney cancers BMs mainly belong to the Treg-Tex archetype that lacks osteoclasts. Lung cancers BMs evenly distributed across all archetypes. Further analyses revealed parallel mechanisms of immunosuppression and bone remodeling. Elevated estrogen signaling distinguishes macrophages in the Mφ-OC subtype, which was investigated in a companion study. Together, we elucidated that divergent mechanisms toward bone colonization and that BMs of different origins can adopt the same mechanism through convergent evolution or adaptation.
2025-05-27 | GSE266330 | GEO
Project description:Three types of BMs from adult human eyes, the inner limiting membrane, the retinal vascular BMs and the lens capsule, were isolated for analysis by 1D-SDS-PAGE and LC-MS/MS.
2017-11-29 | MSV000081772 | MassIVE
Project description:Three types of BMs from adult human eyes, the inner limiting membrane, the retinal vascular BMs and the lens capsule, were isolated for analysis by 1D-SDS-PAGE and LC-MS/MS.
2014-07-16 | PXD001025 | Pride
Project description:Purpose: To identify the aberrant long non-coding RNA (lncRNA) and explore the predictive value of lncRNA on the risk of brain metastases (BMs) for patients with limited-stage small cell lung cancer (SCLC). Patients and Methods: We executed an array of lncRNA and mRNA chip assays on peripheral blood mononuclear cells of SCLC patients with BM comparing to others without BMs to identify the lncRNAs relating to BMs. Then validation was conducted in clinical data to confirm the relationship of lncRNAs and BMs furtherly. We estimated the cumulative incidence of BMs using the Kaplan-Meier method and differences between the groups were analyzed using the log-rank test. Results: The expression of 67 lncRNAs (27 up, 40 down) and 47 mRNAs (20 up, 27 down) were different significantly in BM groups comparing to the group without BMs (fold change ≥ 2.0, p value ≤0.05) which were found by lncRNA and mRNA chip assays initially. Four lncRNAs were verified by qRT-PCR to confirm the accuracy of the microarray data and then the results of 11 pairs of patients (11 patients with BMs, while 11 patients without BMs) showed that low expression of LncRNA XR_429159.1 was the high-risk factor of BM. Further clinical data showed that the BM incidence of 25 patients with low level LncRNA XR_429159.1 was 31% at 1-year, and that was 14.3% in the 18 patients with high level LncRNA XR_429159.1, p = 0.035. Conclusion: Our present study identified that low expression of lncRNA XR_429159.1 was the high-risk factor of BM in patients with limited-stage SCLC.
2021-04-16 | GSE161968 | GEO
Project description:Aims: Congenital heart defect (CHD) account for 25% of all human congenital abnormalities. Very few CHD-causing genes have been identified so far; so, to discover further genes we performed a global transcriptome analysis in mouse models of CHD. Methods and results: By the use of a retinoic acid competitive antagonist (BMS-189453) we caused CHD, thymic abnormalities and neural tube defects in mouse newborns. Transposition of great arteries was the prevalent cardiac defect observed (61%). Recently we were able to partially rescue this abnormal phenotype by oral administration of folic acid. Now we have performed a microarray analysis in mouse embryos (8.5 dpc) treated with BMS-189453 alone and with BMS-189453 plus folic acid (FA). On the basis of microarray and QRT-PCR results, we deeper analysed Hif1α because of its down-regulation in BMS-treated embryos vs WT and its increased expression level in BMS+FA treated embryos compared to BMS-treated ones. Immunofluorescence experiments confirmed the under-expression of Hif1α protein in BMS-treated embryos compared to WT and BMS+FA treated ones and moreover demonstrated that at 8.5 dpc Hif1α is mainly expressed in the embryo's heart. Conclusion: We propose that Hif1α down-regulation by blocking retinoic acid binding, may contribute to the development of the cardiac defects of mouse newborns. In line with our hypothesis, when Hif1α expression level is restored (by supplementation of folic acid) a decrement of CHD is found. At the best of our knowledge this is the first report that link retinoic acid metabolism to Hif1α regulation and the development of TGA
2010-09-20 | GSE19012 | GEO