Anticancer drug clustering in lung cancer based on gene expression profiles and sensitivity database
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE4127 | GEO | 2006/02/10
SECONDARY ACCESSION(S): PRJNA95007
REPOSITORIES: GEO
Similar Datasets
Project description:Anticancer drug clustering in lung cancer based on gene expression profiles. We performed gene expression analysis in lung cancer cell lines. (used: Affymetrix GeneChip Human Genome U133 Array Set HG-U133A). We also examines the sensitivity of these cell lines to commonly used anti-cancer agents (docetaxel, paclitaxel, gemcitabine, vinorelbine, 5-FU, SN38, cisplatin, and carboplatin) via MTT assay. We related the cytoxic activity of each of these agents to corresponding expression pattern in each of the cell lines using modified NCI program. Experiment Overall Design: gene expression analysis in lung cancer cell lines
2007-12-12 | E-GEOD-4127 | biostudies-arrayexpress
Project description:We evaluted the synergyistic interactions of cannabidiol (CBD) with standard chemotherapeutic agents such as Docetaxel (DOC), doxorubicin (DOX), paclitaxel (PTX), vinorelbine (VIN), and 7-Ethyl-10-hydroxycamptothecin (SN38) in MCf7 cells ultising different synergy metrics. Then we explored the synergistic mechanisms on the proteome level of the most synergistic combination (CBD and SN38 in a molar ratio of 371:1, respectively)
2021-11-03 | PXD026587 | Pride
Project description:Bordel2018 - GSMM for Human Metabolic
Reactions (HMR database)
This model is described in the article:
Constraint based modeling of
metabolism allows finding metabolic cancer hallmarks and
identifying personalized therapeutic windows
Sergio Bordel
Oncotarget. 2018; 9:19716-19729
Abstract:
In order to choose optimal personalized anticancer
treatments, transcriptomic data should be analyzed within the
frame of biological networks. The best known human biological
network (in terms of the interactions between its different
components) is metabolism. Cancer cells have been known to have
specific metabolic features for a long time and currently there
is a growing interest in characterizing new cancer specific
metabolic hallmarks. In this article it is presented a method
to find personalized therapeutic windows using RNA-seq data and
Genome Scale Metabolic Models. This method is implemented in
the python library, pyTARG. Our predictions showed that the
most anticancer selective (affecting 27 out of 34 considered
cancer cell lines and only 1 out of 6 healthy mesenchymal stem
cell lines) single metabolic reactions are those involved in
cholesterol biosynthesis. Excluding cholesterol biosynthesis,
all the considered cell lines can be selectively affected by
targeting different combinations (from 1 to 5 reactions) of
only 18 metabolic reactions, which suggests that a small subset
of drugs or siRNAs combined in patient specific manners could
be at the core of metabolism based personalized treatments.
This model is hosted on
BioModels Database
and identified by:
MODEL1707250000.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
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| MODEL1707250000 | BioModels
Project description:Six non- and drug-resistant colorectal cancer cell lines were selected in this study, which were non-resistant cell lines: HCT116 and LoVo, four drug-resistant cell lines: HCT116-OxPt, HCT116-SN38, LoVo-OxPt, LoVo-SN38.Proteins extraced from three HCT116 related cell lines were labled and pooled together, and proteins from other three LoVo related cell lines were labled and pooled together.
2022-03-04 | PXD004070 | Pride
Project description:Methylating agents of SN1 type constitute a widely used class of anticancer drugs, the effect of which on human non-small-cell lung cancer (NSCLC) has not been adequately studied. We thus studied the effect of N-methyl-N-nitrosourea (MNU), a model SN1 methylating agent, on two human NSCLC cell lines: A549 (p53wt) and H157 (p53null). We investigated the mechanism of MNU-induced cell death through a time course gene expression profiling study, 24, 48 and 72h following treatment. Two human NSCLC cell lines (A549, H157) were treated with MNU or DMSO for 24h, 48h, or 72h. 34 total samples were analyzed.
2016-06-30 | E-GEOD-65933 | biostudies-arrayexpress
Project description:Produces anticancer agents
| PRJNA13658 | ENA
Project description:Purpose: Irinotecan (SN38) and oxaliplatin are chemotherapeutic agents used in the treatment of colorectal cancer. However, the frequent development of resistance to these drugs represents a considerable challenge in the clinic. Alus as retrotransposons comprise 11% of the human genome. Genomic toxicity induced by carcinogens or drugs can reactivate Alus by altering DNA methylation. Whether or not reactivation of Alus occurs in SN38 and oxaliplatin resistance remains unknown. Methods: We applied reduced representation bisulfite sequencing (RRBS) to investigate the DNA methylome in SN38- or oxaliplatin-resistant colorectal cancer cell line models. Moreover, we extended the RRBS analysis to tumor tissue from 14 patients with colorectal cancer who either did or did not benefit from capecitabine + oxaliplatin treatment. For the clinical samples, we applied a concept of DNA methylation entropy to estimate the diversity of DNA methylation states of the identified resistance phenotype-associated methylation loci observed in the cell line models. Results: We identified different loci being characteristic for the different resistant cell lines. Interestingly, 53% of the identified loci were Alu sequences -- especially the Alu Y subfamily. Furthermore, we identified an enrichment of Alu Y sequences that likely results from increased integration of new copies of Alu Y sequence in the drug-resistant cell lines. In the clinical samples, SOX1 and other SOX gene family members were shown to display variable DNA methylation states in their gene regions. The Alu Y sequences showed remarkable variation in DNA methylation states across the clinical samples. Our findings imply a crucial role of Alu Y in colorectal cancer drug resistance. Our study underscores the complexity of colorectal cancer aggravated by mobility of Alu elements and stresses the importance of personalized strategies, using a systematic and dynamic view, for effective cancer therapy. Investigation of the representive methylome of well-established SN38 and Oxaliplatin resistant cell line models and 14 clinical colorectal metastatic samples that have developed resistance to XELOX to review the epigenetic mechnism of the drug resistance.
2015-04-01 | E-GEOD-56269 | biostudies-arrayexpress
Project description:The present study was carried out to determine the bioactivity of polysaccharides extracted from Euglena gracilis (EgPs). These were characterized by FT-IR and GC-MS. Cytotoxicity analyses (MTT) were performed on healthy human gingival fibroblast cell lines (HGF-1), obtaining an IC50 of 228.66 µg mL-1, and cell lines with anticancer activity for colon cancer (HCT-116), breast cancer (MCF-7), human leukemia (U-937, HL-60) and lung cancer (NCl-H460), showing that EgPs have anticancer activity, mainly in HTC-116 cells (IC50 = 26.1 µg mL-1). The immunological assay determined the immunomodulatory capacity of polysaccharides for the production of proinflammatory cytokines IL-6 and TNF-α in murine macrophages (RAW 264.7) and TNF-α in human monocytes (THP-1). It was observed that the EgPs had a stimulating capacity in the synthesis of these interleukins. The antioxidant capacity of polysaccharides and their biomass were analyzed using the ABTS method (18.30 ± 0.14% and (5.40 ± 0.56%, respectively, and the DPPH method for biomass (17.79 ± 0.57%). We quantitatively profiled HGF-1 proteins by liquid chromatography-tandem mass spectrometry analysis, coupled with 2-plex tandem mass tag labelling, in normal cells. In total, 1346 proteins were identified and quantified with high confidence, of which five were considered to be overexpressed. The data is available through ProteomeXchange, under identifier PXD029076.
2022-12-21 | PXD029076 | Pride
Project description:Methylating agents of SN1 type constitute a widely used class of anticancer drugs, the effect of which on human non-small-cell lung cancer (NSCLC) has not been adequately studied. We thus studied the effect of N-methyl-N-nitrosourea (MNU), a model SN1 methylating agent, on two human NSCLC cell lines: A549 (p53wt) and H157 (p53null). We investigated the mechanism of MNU-induced cell death through a time course gene expression profiling study, 24, 48 and 72h following treatment.
2016-06-30 | GSE65933 | GEO
Project description:Purpose: Irinotecan (SN38) and oxaliplatin are chemotherapeutic agents used in the treatment of colorectal cancer. However, the frequent development of resistance to these drugs represents a considerable challenge in the clinic. Alus as retrotransposons comprise 11% of the human genome. Genomic toxicity induced by carcinogens or drugs can reactivate Alus by altering DNA methylation. Whether or not reactivation of Alus occurs in SN38 and oxaliplatin resistance remains unknown. Methods: We applied reduced representation bisulfite sequencing (RRBS) to investigate the DNA methylome in SN38- or oxaliplatin-resistant colorectal cancer cell line models. Moreover, we extended the RRBS analysis to tumor tissue from 14 patients with colorectal cancer who either did or did not benefit from capecitabine + oxaliplatin treatment. For the clinical samples, we applied a concept of DNA methylation entropy to estimate the diversity of DNA methylation states of the identified resistance phenotype-associated methylation loci observed in the cell line models. Results: We identified different loci being characteristic for the different resistant cell lines. Interestingly, 53% of the identified loci were Alu sequences -- especially the Alu Y subfamily. Furthermore, we identified an enrichment of Alu Y sequences that likely results from increased integration of new copies of Alu Y sequence in the drug-resistant cell lines. In the clinical samples, SOX1 and other SOX gene family members were shown to display variable DNA methylation states in their gene regions. The Alu Y sequences showed remarkable variation in DNA methylation states across the clinical samples. Our findings imply a crucial role of Alu Y in colorectal cancer drug resistance. Our study underscores the complexity of colorectal cancer aggravated by mobility of Alu elements and stresses the importance of personalized strategies, using a systematic and dynamic view, for effective cancer therapy.
2015-04-01 | GSE56269 | GEO