Genomic mechanisms of p210BCR-ABL signaling: induction of heat shock protein 70 through the GATA response element confers resistance to paclitaxel-induced apoptosis.

@article{Ray2004GenomicMO,
  title={Genomic mechanisms of p210BCR-ABL signaling: induction of heat shock protein 70 through the GATA response element confers resistance to paclitaxel-induced apoptosis.},
  author={Sutapa Ray and Ying Lu and Stefan H E Kaufmann and William Clay Gustafson and Jann Ellen Karp and Istvan Boldogh and Alan P. Fields and Allan R. Brasier},
  journal={The Journal of biological chemistry},
  year={2004},
  volume={279 34},
  pages={
          35604-15
        }
}
Chronic myelogenous leukemia (CML) results from a t(9,22) translocation, producing the p210(BCR-ABL) oncoprotein, a tyrosine kinase that causes transformation and chemotherapy resistance. To further understand mechanisms mediating chemotherapy resistance, we identified 556 differentially regulated genes in HL-60 cells stably expressing p210(BCR-ABL) versus those expressing an empty vector using cDNA macro- and oligonucleotide microarrays. These BCR-ABL-regulated gene products play diverse roles… CONTINUE READING

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