Effects of doxorubicin dosages on gene copy number variations in MCF-7 cell line
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ABSTRACT: Anti-cancer drugs, particularly doxorubicin may trigger alterations in the copy numbers of genes. The data present the results of array comperative genomic hybridization of two different MCF-7 cell lines that are resistant to diverse concentration of the doxorubicin in the presence of the sentive control. Although the submission options were chosen as SurePrint G3 Human CGH Microarray 8x60K (G4450A; Agilent Technologies, USA) for all data, a resistant cell line, so called aCGH_400DOX, was studied by the GenetiSure Cyto 8 x 60K CGH Microarrays (G5982A; Agilent Technologies, USA). The results underlined that resistance to the doxorubicin at diverse drug dosages critically altered the copy numbers of some of the fundamental genes.
Project description:Copy number variation analysis between BJ cells and BJ cells derived iPS cells which were established by using non-transmissible measles virus vector DNA derived from BJ cell and iPS cells were extracted and analysis using CGH array
Project description:Cells of the osteoblast lineage affect homing, number of long term repopulating hematopoietic stem cells (HSCs) HSC mobilization and lineage determination and Blymphopoiesis . More recently osteoblasts were implicated in pre-leukemic conditions in mice. Yet, it has not been shown that a single genetic event taking place in osteoblastscan induce leukemogenesis. We show here that in mice, an activating mutation of β-catenin leading to development of acute myeloid leukemia (AML) with common chromosomal aberrationsand cell autonomous progression. Activated β-catenin stimulates expression of the Notch ligand Jagged-1 in osteoblasts. Subsequent activation of Notch signaling in HSCprogenitors induces the malignant changes. Demonstrating the pathogenetic role of theNotch pathway, genetic or pharmacological inhibition of Notch signaling ameliorates AML. Nuclear accumulation and increased β-catenin signaling in osteoblasts was also identified in 38% ofpatients with MDS/AML. These patients showed increased Notch signaling in hematopoietic cells. These findings demonstrate that genetic alterations in osteoblasts can induce AML, identify molecular signals leading to this transformation and suggest a potential novel pharmacotherapeuticapproach to AML. The present entry describes a comparison of copy numbers of DNA from βcat(ex3)osb mice from the mouse spleen with that of WT (C57BL/J Mice) mice. DNA from spleen myeloid cells from βcat(ex3)osb mice and WT mice were hybridized to Agilent CGH 244A arrays. DNA from spleen myeloid cells from βcat(ex3)osb mice in C57BL/J background was labeled with red dye. DNA from spleen myeloid cells from WT (C57BL/J) mice were labeled with green dye. There were five arrays with DNA from 1 mouse of each genotype per array.
Project description:In this work the objective is identify chromosomal alterations in ependymoma in pediatric patients, we used CGH microarray were performed through the Agilent platform.
Project description:CMT-Stylo is a canine mammary gland adenocarcinoma cell line. From this cell line, a doxorubicin resistant subline called CMT-Star was developed by culturing the cells in the presence of doxorubicin from low concentration to 100 nM doxorubicin (to induce drug resistance). The CMT-Stylo cells were maintained in Dulbecco’s modified eagles medium (DMEM) supplemented with 10% Foetal bovine serum (FBS) and 1% Penicillin-Streptomycin (ThermoFisher Scientific, USA) in 5% CO2 at 370C. The CMT-Star cell line was maintained in additional 5 nM doxorubicin to maintain its resistant phenotype.
Project description:CMT-Stylo is a canine mammary gland adenocarcinoma cell line. From this cell line, a doxorubicin resistant subline called CMT-Star was developed by culturing the cells in the presence of doxorubicin from low concentration to 100 nM doxorubicin (to induce drug resistance). The CMT-Stylo cells were maintained in Dulbecco’s modified eagles medium (DMEM) supplemented with 10% Foetal bovine serum (FBS) and 1% Penicillin-Streptomycin (ThermoFisher Scientific, USA) in 5% CO2 at 370C. The CMT-Star cell line was maintained in additional 5 nM doxorubicin to maintain its resistant phenotype.
Project description:Between 2004 and 2012, patients with pT1-3, pN0-3, M0 breast tumors were randomised between adjuvant dose-dense doxorubicin-cyclophosphamide (ddAC) versus docetaxel-doxorubicin-cyclophosphamide (TAC). Trial registration numbers: ISRCTN61893718 and BOOG 2004-04.
Project description:Array CGH analysis of paired blood and tumor DNA samples from 14 patients with sporadic Wilms tumor. Previously array CGH studies in WT have only been performed in tumor tissue samples. We herein describe a novel set of constitutional abnormalities and point to candidate genes that might be associated with WT development. 28 paired DNA samples of peripheral blood/fresh tumor tissue from 14 patients (10 males, 4 females) with histologically confirmed WT. All tumor samples were collected from primary tumors from patients treated with the same neoadjuvant chemotherapy following the International Society of Paediatric Oncology (SIOP) WT 2001 trial protocol.
Project description:CGH array of MA1 and MA2 variant cells as compared to the parental SUM149-Luc breast cancer cell line. The MA1 and MA2 variants were isolated based on the ability of rare cancer cells to survive and grow without adding glutamine in culture medium. To gain insight into the characteristic of metabolically adaptable MA cells that enables them to survive severe metabolic challenge, i.e., prolonged lack of glutamine and other challenges [Singh et al., PLoS ONE 7: e36510, 2012], we analyzed CGH array to compare these cells with the parental SUM149-Luc (luciferase-transfected) cells. We analyzed two independently selected cell populations, one from 0.5 million parental cells (designated MA1) and one from 1 million parental cells (designated MA2). Comparing the MA1 and MA2 variants to the common parental SUM149-Luc cell line. One sample each.
Project description:Aneuploidy, a state of having uneven numbers of chromosomes, is a form of large-effect mutation able to confer adaptive phenotypes under diverse stress conditions. Here we investigate whether pleiotropic stresses could in turn induce aneuploidy in budding yeast. Cells exposed to radicicol, an Hsp90 inhibitor, exhibit chromosomal instability. To assess the karyotype of cells with an acquired resistance to radicicol, array CGH was used to compare three stably resistant yeast colonies to a WT strain.
Project description:We performed array-CGH and targeted massive parallel sequencing using the commercial gene panel design ClearSeq Inherited Disease (Agilent Technologies) to identify the pathogenic sequence variants in a girl presenting an apparent microcephaly with mild dysmorphic facial features, delayed psychomotoric development and central hypotonia.