@techreport{oai:kindai.repo.nii.ac.jp:00020693,
 author = {田中, 宏和 and 松村, 到 and 森田, 泰慶 and 賴, 晋也 and 芹澤, 憲太郎},
 month = {},
 note = {https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16K09862/, 研究成果の概要（和文）：申請者らは、54例の多発性骨髄腫(MM)症例の骨髄サンプルを用いた解析を行い、CD38+CD138+CD19-CD45-で定義されるMM細胞(PhMCs)からをMMの起源となる細胞を分離した。PhMCsには、CD34+のわずかな分画が存在し、in vitroおよびin vivoでのMM発症、抗腫瘍薬抵抗性に寄与した。骨髄中のCD34+PhMCsの割合は、初発例よりも再発難治例で有意に高かった。遺伝子発現解析の結果、CD34-PhMCsでは一般的なMM細胞の遺伝子発現様式を示し、CD34+PhMCsではより未分化な胚中心以前の発現様式を示した。研究成果の概要（英文）：We isolated myeloma initiating cells from phenotypically defined CD38+ CD138+ CD19-CD45- multiple myeloma (MM) cells (PhMCs) from a set of 54 bone marrow MM patient samples. And we found PhMCs contains a minor CD34+ fraction that possess myeloma-propagating activities in vitro and in vivo, as well as resistance to anticancer drugs. The percent of CD34+ PhMCs was significantly higher in relapse/refractory than in newly diagnosed samples. Gene expression profiling revealed that CD34-PhMCs had a general myeloma cell signature, whereas CD34+ PhMCs exhibited a more immature pre-germinal center like signature. The presence of e cancer stem cells in MM was proposed for a few decades, however the identity of these cells remains controversial. The identification of these MM propagating cells provides a basis for better understanding the pathogenesis of MM and for designing novel therapeutic strategies aimed to eradicate total MM cells., 研究種目：基盤研究(C);  研究期間：2016～2018;   課題番号：16K09862;   研究分野：医歯薬学;   科研費の分科・細目：, application/pdf},
 title = {未分化造血細胞の異常に起因する多発性骨髄腫の新たな発生機構についての解析},
 year = {2019},
 yomi = {タナカ, ヒロカズ and マツムラ, イタル and モリタ, ヤスヨシ and ライ, シンヤ and セリザワ, ケンタロウ}
}