RM-1小鼠前列腺癌細(xì)胞(附鑒
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產(chǎn)品名稱:RM-1小鼠前列腺癌細(xì)胞、RM-1小鼠前列腺癌細(xì)胞、RM-1小鼠前列腺癌細(xì)胞、RM-1小鼠前列腺癌細(xì)胞
種屬 | 小鼠 |
別稱 | RM1 |
組織來源 | 前列腺 |
疾病 | 小鼠前列腺癌 |
傳代比例/細(xì)胞消化 | 1:2傳代,消化2-3分鐘 |
培養(yǎng)基配置 | RPMI1640培養(yǎng)基;10%胎牛血清;1%雙抗 |
簡(jiǎn)介 | 用Zipras/myc9逆轉(zhuǎn)錄病毒感染17日齡C57BL/6胚胎泌尿生殖竇細(xì)胞 ,移植到等基因成年雄性小鼠腎包膜下 |
形態(tài) | 成纖維細(xì)胞樣 |
生長(zhǎng)特征 | 貼壁生長(zhǎng) |
倍增時(shí)間 | 每周 2 至 3 次 |
保藏機(jī)構(gòu) | ATCC; CRL-3310 |
is NKp46 and IFN-gamma dependent. Thus, we present in this study a novel NKp46-lkdiated lkchanism of tumor editing.Although common evolutionary principles drive the growth of cancer cells regardless of the tissue of origin, the microenvironlknt in which tumours arise suaktantially diklers across various organ sites. Recent studies have
axis inhibition will define a robust field of clinical research.Background: Immune infiltration of the tumor microenvironment has been associated with improved survival for some patients with solid tumors. The precise makeup and prognostic relevance of immune infiltrates across a broad spectrum of tumors remain unclear.