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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Alectinib-resistant NSCLC harboring EML4-ALK cells: Parental vs. Alectinib-resistant

ABSTRACT: Transcriptional profiling of NSCLC harboring EML4-ALK comparing parental H2228 cells with alectinib resistant H2228 cells. Two-condition experiment, H2228 vs. H2228/CHR cells. Biological replicates: 1 parental replicates, 3 alectinib-resistant replicates.

ORGANISM(S): Homo sapiens

SUBMITTER: Hideko Isozaki

PROVIDER: E-GEOD-73167 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Alectinib-resistant NSCLC harboring EML4-ALK cells: Parental vs. Alectinib-resistant

Project description:Transcriptional profiling of NSCLC harboring EML4-ALK comparing parental H2228 cells with alectinib resistant H2228 cells.

2015-09-18 | GSE73167 | GEO

Analysis of ALK TKI sensitive and ALK TKI resistant isogenic pairs of H3122 (EML4-ALK E13;A20) cells

Project description:Starting with H3122 cells, which harbor the EML4-ALK E13;A20 fusion and are known to be sensitive to ALK tyrosine kinase inhibitors, we generated isogenic pairs of ALK TKI sensitive and ALK TKI resistant cell lines using established methods (see Chmeliecki, J et al Science Trans Med 2011). We modeled resistance against the currently FDA approved ALK TKI, crizotinib (also called PF-1066). We also modeled resistance against a novel more potent ALK inhibitor, X-376 (ref: Lovly, CM et al Cancer Research 2011). We compared gene expression profiles between the 'parental' (ALK TKI sensitive) H3122 cells and the drug resistant cells (H3122 CR for Crizotinib resistant cells and H3122 XR for X-376 resistant cells).

2014-07-14 | GSE49508 | GEO

Vulnerability of drug-resistant EML4-ALK rearranged lung cancer to transcriptional inhibition

Project description:A subset of lung adenocarcinomas is driven by the EML4-ALK translocation. Despite excellent initial responses in patients, acquired resistance to ALK inhibitors occurs. Exploring these mechanisms of resistance, we found that EML4-ALK cells resistant to ALK inhibitors are remarkably sensitive to THZ1, alvocidib or dinaciclib. These compounds robustly induce apoptosis through transcriptional inhibition and downregulation of anti-apoptotic genes. In conclusion, this study shows that THZ1, alvocidib or dinaciclib could be a therapeutic option for a subset of patients with acquired resistance to first, second and third-generation ALK inhibitors.

2019-12-15 | E-MTAB-8563 | biostudies-arrayexpress

Vulnerability of drug-resistant EML4-ALK rearranged lung cancer to transcriptional inhibition

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RNA-seq of human NSCL cell lines with induced fusion genes; ALK-EML4-V1, ALK-EML4-V3, ALK-TFG, ALK-KIF5B

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2022-12-18 | E-MTAB-11304 | biostudies-arrayexpress

Expression data from EML4-ALK overexpression in HEK293 cell line and EML4-ALK knockdown in H2228 lung cancer cell line.

Project description:We demonstrate that EML4-ALK siRNAs significantly reduced cell viability in EML4-ALK postive lung cancer cell lines,while overexpression of EML4-ALK increased cell viability in HEK293 cells in vitro. The aim of this study was to analyze the EML4-ALK regulated gene expression in lung cancer.

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Transcription profiling of QUB HCT116 sensitive and resistant colorectal cancer time series

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Expression data from IL4 treatment in EML4-ALK-positive lung cancer cells.

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Project description:First line treatment for EML4-ALK fusion-positive lung cancer patient is the use of an ALK tyrosine kinase inhibitor (TKI), such as alectinib. While most patients initially respond to this therapy, many patients often develop relapse, and efficacious therapies for patients with relapse disease are limited. To study EML4-ALK fusion-positive lung cancer, novel murine lung cancer cell lines were generated from C57BL/6 mice using an intratracheally injected Adeno-virus that contains Cas9 and guide RNAs for the EML4-ALK translocation, which leads to the development of lung tumors. Cell lines were derived from these tumors. In an effort to better understand how cells respond to alectinib, we treated EML4-ALK-positive murine cell lines (EA1, EA2, and EA3 cells) in vitro for 1-7 days with either 100nM alectinib or DMSO-control. At each time point, RNA was isolated from each condition. RNA was submitted to RNA-seq. Differential analysis on the RNA-seq data was performed to determine and track gene changes over time between control and treated cells. These data will allow us to better develop novel therapeutics to use in conjunction with alectinib when treating EML4-ALK fusion-positive patients.

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EML4-ALK transgenic mouse lung normal tissue vs. lung tumor tissue

Project description:Gene expression profile of lung tumor tissues from EML4-ALK transgenic mouse (generous gift from Prof. H. Mano, Univ. of Tokyo) compared with lung normal tissues

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