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Methylation data from biological replicates of imatinib and nilotinib resistant K-562 cells

ABSTRACT: Methylation data from biological replicates of imatinib and nilotinib resistant K-562 cells

PROVIDER: PRJNA840879 | ENA |

REPOSITORIES: ENA

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Methylation data from biological replicates of imatinib and nilotinib resistant K-562 cells

Project description:Resistant cells were generated by stepwise exposure to increasing concentrations of imatinib or nilotinib to establish 0.5 and 2 µM imatinib and 0.1 µM nilotinib resistant cells. This procedure was performed twice independently to establish biological replicates of TKI resistance. We analyzed genome-wide methylation to investigate changes in methylation during the development of TKI resistance.

2022-05-21 | GSE203443 | GEO

Gene expression data from biological replicates of imatinib and nilotinib resistant K-562 cells

Project description:Resistant cells were generated by stepwise exposure to increasing concentrations of imatinib or nilotinib to establish 0.5 and 2 µM imatinib and 0.1 µM nilotinib resistant cells. This procedure was performed twice independently to establish biological replicates of TKI resistance. We performed microarrays to analyze the changes in gene expression during the development of TKI resistance.

2022-05-21 | GSE203442 | GEO

Gene expression data from biological replicates of imatinib and nilotinib resistant K-562 cells.

Project description:Resistant cells were generated by stepwise exposure to increasing concentrations of imatinib or nilotinib to establish 0.5 and 2 µM imatinib and 0.05 µM nilotinib resistant cells. This procedure was performed twice independently to establish biological replicates of TKI resistance. We performed microarrays (Clariom S) to analyze the changes in gene expression during the development of TKI resistance.

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Gene expression data from biological replicates of imatinib and nilotinib resistant K-562 cells

Project description:Gene expression data from biological replicates of imatinib and nilotinib resistant K-562 cells

| PRJNA840878 | ENA

Imatinib and Nilotinib induced molecular changes in Philadelphia chromosome-positive Chronic Myelogenous Leukemia

Project description:Chronic myelogenous leukemia (CML) is a malignant stem cell disease characterized by a reciprocal translocation between chromosome 9 and 22. The selective bcr-abl tyrosine-kinase inhibitor Imatinib has become the therapy of choice for patients with newly diagnosed CML including those previously considered candidates for allogeneic haematopoietic stem cell transplantation. The tyrosine-kinase inhibitor Nilotinib is a derivate of Imatinib with higher potency. To examine the molecular and functional effects of Nilotinib and Imatinib in chronic myelogenous leukemia, we performed gene expression and functional analyses in K562 cells following treatment with the two tyrosine kinase inhibitors.

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Transcription profiling of human K562 cells reveals Imatinib and Nilotinib induced molecular changes in Philadelphia chromosome-positive Chronic Myelogenous Leukemia

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Transcription profiling of human lung cancer cells treated with dasatinib, imatinib, nilotinib or PD0325901

Project description:Cell Line: This experiment was designed to measure the transcriptional responses to four kinase inhibitors across a five-logarithm dose range. The A549 human lung cancer cell line was treated with dasatinib, imatinib or nilotinib (4 hours and 20 hours) or PD0325901 (4 hours). Treatments used a 12-point dose range (30 uM with 3-fold dilutions down to 0.17 nM; 0.5% DMSO vehicle for all treatments). Experimental design prevented row or column handling effects being confounded with dose effect.

2008-12-31 | E-TABM-585 | biostudies-arrayexpress

A MALDI-TOF assay identifies nilotinib as an inhibitor of inflammation

Project description:Inflammatory responses are important in cancer, particularly in the context of monocyte-rich aggressive myeloid neoplasm. We developed a label-free cellular phenotypic drug discovery assay to identify anti-inflammatory drugs in human monocytes derived from acute myeloid leukemia (AML), by quantifying several biological features ionizing from only 2,500 cells using matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometry. A proof-of-concept screening showed that the BCR-ABL inhibitor nilotinib, but not the structurally similar imatinib, blocks inflammatory responses in AML and multiple myeloma. In order to identify the cellular (off-)targets for nilotinib, we performed thermal proteome profiling (TPP) over a range of temperatures and compound concentrations. Unlike imatinib, nilotinib inhibits p38 alpha MAP Kinase (MAPK14) and its downstream signaling pathway. This suppressed the expression of inflammatory cytokines, cell adhesion, and innate immunity markers in activated human monocytes derived from AML. Thus, our study provides a tool for the discovery of new anti-inflammatory drugs, which could potentially contribute to the treatment of inflammation in myeloid neoplasms and other diseases.

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K-562 cell lines

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