中文摘要：

瞄准：从胰腺的腺癌房间线 PANC-1 探索隔离的方法和肿瘤干细胞的生物分析。方法：PANC-1 房间在修改的鹰媒介 F12 (1:1 体积)(DMEM-F12 ) 与 20% 胎儿的牛的浆液(FBS ) 补充了的 Dulbecco 是有教养的。有肿瘤干细胞的性质的 Subpopulation 房间被流动血细胞计数根据房间表面标记 CD44 和 CD24 从胰腺的腺癌房间线 PANC-1 孤立。这些房间在试管内的增生的能力被 3- 估计[4,5-dimehyl-2-thiazolyl ]-2, 5-diphenyl-2H-tetrazolium 溴化物(MTT ) 方法。并且被注入裸体老鼠的正确、左的腋窝的皮下组织的不同潜水艇人口房间的肿瘤生长被学习，并且 CD44 的表示和 CD44+CD24+ 形成房间的小瘤和 PANC-1 房间的 CD24 被 avidin-biotin-peroxidase 检测建筑群(ABC ) 免疫组织化学的染色。结果：排序的 PANC-1 房间的 5.1%-17.5% 表示了房间表面标记 CD44， 57.8%-70.1% 表示了 CD24，仅仅房间的 2.1%-3.5% 是 CD44+CD24+ 。与 CD44-CD24- 房间相比， CD44+CD24+ 房间有更低的生长率在试管内。在裸体老鼠的 104 个 CD44-CD24- 细胞的培植没在 wk 显示出明显的肿瘤生长 12。相反，大肿瘤在在 wk 与 103 个 CD44+CD24+ 房间植入的裸体老鼠被发现 4 (2/8 ) ，致瘤的潜力的 20 褶层增加(P 【 0.05 或 P 【 0.01 ) 。CD44+CD24+ 形成房间的小瘤的房间和 PANC-1 房间之间没有明显的组织学的差别。结论：CD44 和 CD24 可以从胰腺的腺癌房间线 PANC-1 为胰腺的癌症干细胞的隔离被用作房间表面标记。Subpopulation 房间 CD44+CD24+ 有肿瘤的性质干细胞。因为癌症干细胞被认为在对化疗的起始的回答以后为肿瘤开始和它的复发负责，它可以是为新药开发的一个很有希望的目标。

英文摘要：

AIM： To explore the method of isolation and biological analysis of tumor stem cells from pancreatic adenocarcinoma cell line PANC-1. METHODS： The PANC-1 cells were cultured in Dulbecco modified eagle medium F12 （1：1 volume） （DMEM-F12） supplemented with 20% fetal bovine serum （FBS）. Subpopulation cells with properties of tumor stem cells were isolated from pancreatic adenocarcinoma cell line PANC-1 according to the cell surface markers CD44 and CD24 by flow cytometry. The proliferative capability of these cells in vitro were estimated by 3-[4,5-dimehyl-2-thiazolyl]-2, 5-diphenyl- 2H-tetrazolium bromide （MTT） method. And the tumor growth of different subpopulation cells which were injected into the hypodermisof right and left armpit of nude mice was studied, and expression of CD44 and CD24 of the CD44^＋CD24^＋ cell-formed nodules and PANC-1 cells were detected by avidin-biotin-peroxidase complex （ABC） immunohistochemical staining. RESULTS： The 5.1%-17.5% of sorted PANC-1 cells expressed the cell surface marker CD44, 57.8% -70.1% expressed CD24, only 2.1%-3.5% of cells were CD44^＋ CD24^＋. Compared with CD44-CD24- cells, CD44^＋CD24^＋ cells had a lower growth rate in vitro. Implantation of 104 CD44 CD24 cells in nude mice showed no evidenttumor growth at wk 12. In contrast, large tumors were found in nude mice implanted with 103 CD44^＋CD24^＋ cells at wk 4 （2/8）, a 20-fold increase in tumorigenic potential （P 〈 0.05 or P 〈 0.01）. There was no obvious histological difference between the cells of the CD44^＋CD24^＋ cell-formed nodules and PANC-1 cells. CONCLUSION： CD44 and CD24 may be used as the cell surface markers for isolation of pancreatic cancer stem cells from pancreatic adenocarcinoma cell line PANC-1. Subpopulation cells CD44^＋CD24^＋ have properties of tumor stem cells. Because cancer stem cells are thought to be responsible for tumor initiation and its recurrence after an initial response to chemotherapy, it may be a very promising target for new dr