@article{oai:sapmed.repo.nii.ac.jp:00014151,
 author = {Hiroshi, Yasui and Tadao, Ishida and Masanori, Nojima and Yuka, Aoki and Hiroshi, Ikeda and Hiromu, Suzuki and Toshiaki, Hayashi and Yasuhisa, Shinomura and Minoru, Toyota},
 journal = {Tumor Research, Tumor Research},
 month = {},
 note = {Multiple myeloma continues to be a lethal malignancy despite the development of treatments such as high-dose chemotherapy combined with stem cell transplantation. Multiple myeloma arises through an accumulation of multiple genetic anges, including immunoglobulin gene rearrangements involved in Cyclin D. The main difficulties in multiple myeloma treatments are drug-resistance. DNA methylation of the5' CpG islands of genes is often found in multiple myeloma. To screen for he genes involved in tumorigenesis of multiple myeloma, which are silenced by DNA methylation, we performed cDNA microarray analysis using multiple myeloma cell lines treated with demethylating agent5-aza-2-deoxycytidine (DAC), and entified RASD1, a dexamethasone (Dex)-inducible gene, as one of the targets of epigenetic changes. Inactivation of RASD1 was found to correlate with resistance to Dex, and treatment of multiple myeloma cells with DAC restored sensitivity to Dex. These findings suggest the involvement of epigenetic gene silencing in multiple myeloma progression and drug-resistance, and the usefulness of demethylation therapy for multiple myeloma treatment. Furthermore, DNA methylation can be an epigenetic biomarker for multiple myeloma.},
 pages = {21--31},
 title = {Epigenetic biomarkers for prediction of sensitivity to chemotherapeutic drugs in multiple myeloma},
 volume = {45},
 year = {2010}
}