{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"submitter":["Adriana Petrazzuolo"],"organism":["Homo sapiens"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-15866"],"description":["Tyrosine kinase receptor anaplastic lymphoma kinase (ALK) is physiologically expressed during embryogenesis. However, chromosomal rearrangements, especially translocations, cause expression of pathogenic ALK fusion proteins that drive tumor formation and maintenance. For instance, the translocation between chromosomes 2 and 5 (t(2;5)) fuses the nucleophosmin 1 (NPM1) gene with ALK, leading to anaplastic large cell lymphoma (ALCL). The constitutive active NPM1::ALK tyrosine kinase drives tumor transformation and tumor cells inevitably depend on ALK kinase activity for survival. For this reason, ALK kinase inhibitors showed great success in treating ALK-positive ALCL. Here, we explored gene expression changes induced by ceritinib, second generation ALK inhibitor, on a representative cell line, SUDHL-1."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Sample Collection - Cells were harvested after treatment and washed 1x with PBS prior to RNA extraction.","Growth Protocol - Human NPM1::ALK-positive anaplastic large cell lymphoma (ALCL) SU-DHL-1 cell line was cultured in RPMI 1640 supplemented with 100 units/mL of penicillin, 100 µg/mL of streptomycin (Pen/Strep) and 10% fetal bovine serum (FBS). Cells were grown in standard conditions (37°C and 5% CO2) and routinely checked for mycoplasma contamination.","Sample Treatment - Cells were treated with 50nM of ceritinib (Selleck Chemicals) or vehicle (DMSO) diluted in culture medium for 48 hours.","Library Construction - To construct the libraries, 1 µg of high-quality total RNA sample (RIN>8) was processed using TruSeq Stranded mRNA kit (Illumina) according to manufacturer instructions. Briefly, after purification of poly-A containing mRNA molecules, mRNA molecules were fragmented and reverse- transcribed using random primers. Replacement of dTTP by dUTP during the second strand synthesis permitted to achieve strand specificity. Addition of a single A base to the cDNA was followed by ligation of Illumina adapters.  Libraries were quantified by qPCR using the KAPA Library Quantification Kit for Illumina Libraries (KapaBiosystems, Wilmington, MA) and library profiles were assessed using the DNA High Sensitivity LabChip kit on an Agilent Bioanalyzer.","Sequencing - Libraries were sequenced on an Illumina Nextseq 500 instrument using 75 base-lengths read V2 chemistry in a paired-end mode.","Nucleic Acid Extraction - RNA was extracted using the RNeasy plus mini kit (Qiagen) following manufacturer's instruction"],"figure_sub":["Organization","MINSEQE Score","Assays and Data","Processed Data","MAGE-TAB Files"],"data_protocol":["Data Transformation - A primary analysis based on AOZAN software (ENS, Paris) was applied to demultiplex and control raw data quality (based of FastQC modules / version 0.11.5). Then, files were aligned using STAR algorithm (version 2.5.2b) and quality control of the alignment realized with Picard tools (version 2.8.1). Reads were then counted using Featurecount (version Rsubread 1.24.1)."],"omics_type":["Metabolomics","Unknown","Transcriptomics","Genomics","Proteomics"],"instrument_platform":["NextSeq 500"],"study_type":["RNA-seq of coding RNA"],"species":["Homo sapiens"],"pubmed_authors":["Adriana Petrazzuolo"],"additional_accession":[]},"is_claimable":false,"name":"Effect of ALK kinase inhibitor, ceritinib, on the gene expression profile of SUDHL-1 cell line","description":"Tyrosine kinase receptor anaplastic lymphoma kinase (ALK) is physiologically expressed during embryogenesis. However, chromosomal rearrangements, especially translocations, cause expression of pathogenic ALK fusion proteins that drive tumor formation and maintenance. For instance, the translocation between chromosomes 2 and 5 (t(2;5)) fuses the nucleophosmin 1 (NPM1) gene with ALK, leading to anaplastic large cell lymphoma (ALCL). The constitutive active NPM1::ALK tyrosine kinase drives tumor transformation and tumor cells inevitably depend on ALK kinase activity for survival. For this reason, ALK kinase inhibitors showed great success in treating ALK-positive ALCL. Here, we explored gene expression changes induced by ceritinib, second generation ALK inhibitor, on a representative cell line, SUDHL-1.","dates":{"release":"2026-01-01T00:00:00Z","modification":"2026-05-27T16:32:22.359Z","creation":"2025-10-24T16:02:53.445Z"},"accession":"E-MTAB-15866","cross_references":{"ENA":["ERP182996"],"EFO":["EFO_0002944","EFO_0004170","EFO_0003789","EFO_0005518","EFO_0003816","EFO_0003738","EFO_0004184","EFO_0003969"]}}