Project description:Human Promyelocytic Leukemia Cell Line HL60 has been used extensively as a model for myeloid differentiation and leukemia. HL60-RG cell is its sub-line and shows a higher growth rate. In this study, we carried out a genome scan using SNP 10k mapping array on both cells. Comparative study on chromosomal changes of these cells will give us information on mechanism of tumor progression. Keywords: cell type comparison
Project description:The Fanconi anemia (FA) pathway is a network of proteins critical to the preservation of genomic integrity and the prevention of cancer. FA proteins safeguard the genome by regulating the cell cycle and facilitating error-free repair of DNA damage. Bi-allelic mutation of genes encoding FA pathway proteins causes the cancer predisposition syndrome Fanconi anemia (FA), which is associated with a high incidence of acute myeloid leukemia (AML). Individuals with mono-allelic mutation of a subset FA genes do not develop FA but suffer increased lifetime risk of solid and hematological malignancies. Within the general population, approximately 14% of sporadic AMLs harbor damaging mutations within the FA pathway. Our previous work demonstrated that inhibition of the mitotic kinase PLK1 induced synthetic lethality in cells deficient for FANCA, the gene most frequently lost in FA. This finding corroborates work from others that have identified synthetic lethal interactions between PLK1 and additional FA genes (FANCG, BRCA1, and BRCA2). Together, these findings suggest that FA pathway mutations may serve as biomarkers for sensitivity to PLK1 inhibitors, which have demonstrated therapeutic efficacy in an undefined subset of AML patients. Here, HL60 AML cells were generated with shControl or shFANCA and treated with 10nM volasertib for 24 h prior to kinome profiling.
Project description:Human Promyelocytic Leukemia Cell Line HL60 has been used extensively as a model for myeloid differentiation and leukemia. HL60-RG cell is its sub-line and shows a higher growth rate. In this study, we carried out a genome scan using SNP 10k mapping array on both cells. Comparative study on chromosomal changes of these cells will give us information on mechanism of tumor progression. Experiment Overall Design: Two samples HL60-NG cell and HL60-RG cel were analyzed by SNP 10k mapping array.
Project description:Expression data from untreated or Dll4-Fc treated THP1 cell line. We used Dll4-Fc stimulation of AML cells to study whether Notch activation has an impact on AML. We analyzed THP1 cell line in vitro treated with Dll4-Fc or vehicle control to determine genes affected by Notch activation.
Project description:Radiation-resistant of acute myeloid leukemia cell present challenges to treatment, and the acquisition of resistance to ionizing radiation (IR) is a matter of clinical concern. However, little information is available on the behavior of radio-resistant leukemia in terms of gene expression profiles and intercellular communication. In this study, mRNA microarray was used to analyze the intracellular genetic network in the established radio-resistant HL60 (Res-HL60) cell line. Significant changes in the expression of 7,309 known mRNAs were observed in Res-HL60 relative to control. In addition, 7 mRNAs were determined as targets because significant changes in the expression were observed using Ingenuity analysis software, confirming the quantitative RT-PCR. However, extracellular vesicles from Res-HL60 cells did not include these target mRNAs. These results suggest that radio-resistant leukemia model is regulated by the expression and suppression of specific mRNAs, and these molecules are not transferred between cells by extracellular vesicles.
Project description:We performed quantitative metabolomics and 13C-glucose isotopic profiling experiments on AML MOLM14 cell line following 24h of treatment with venetoclax (50 nM) and aracytine (25 uM) or combination compared to untreated samples. In addition, we also performed quantitative metabolomic experiments on MOLM14 silenced for BCL2 (shRNA).
