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应用递增阿霉素剂量的方法，体外诱导建立了一株人膀胱移行细胞癌耐药亚株ＢＩＵ－８７／ＡＤＭ。此细胞株对阿霉素的相对耐受度较亲本细胞提高了６．３倍；对阿霉素类似物柔红霉素、表阿霉素及天然生物碱类如长春新碱、鬼臼乙叉忒有明显的交叉耐药性，对顺铂、丝裂霉素无明显的交叉耐药性。与亲本细胞相比，耐药亚株生长速度减慢，倍增期延长，汇合密度降低，细胞异形性明显，有巨细胞形成。进一步研究表明，耐药亚株对柔红霉素聚集显著减少；免疫细胞化学研究显示，约７５％的耐药亚株Ｐ－ｇｐ过表达，而亲本细胞均为阴性；ＲＴ／ＰＣＲ发现，耐药亚株ｍｄｒ１基因表达，而亲本细胞无ｍｄｒ１基因扩增产物。结果证明，ＢＩＵ－８７／ＡＤＭ耐药性的产生与Ｐ－ｇｐ介导产生的细胞内药物外溢增多有关。由于并非所有ＢＩＵ－８７／ＡＤＭ均表达Ｐ－ｇｐ，所以其它耐药机制的共存是可能的。
A dose-dependent dose of doxorubicin was used to induce a BIU-87 / ADM resistant human bladder transitional cell carcinoma in vitro. The relative resistance of this cell line to doxorubicin was 6.3 times higher than that of the parental cells; the doxorubicin analogue of daunorubicin, epirubicin and natural alkaloids such as vincristine, Cross Intuit has obvious cross-resistance, cisplatin, mitomycin no significant cross-resistance. Compared with the parental cells, drug-resistant sub-strains slowed down, the doubling period was prolonged, confluence density was reduced, cells were abnormal, with giant cells. Further studies showed that drug-resistant subunits significantly decreased the concentration of daunorubicin; immunocytochemistry showed that about 75% of the resistant subline P-gp was overexpressed while the parental cells were negative; RT / PCR was found to be resistant Drug subunit mdr1 gene expression, while the parental cells without mdr1 gene amplification product. The results show that, BIU-87 / ADM drug resistance and P-gp-mediated intracellular drug-spill-related increase. As not all BIU-87 / ADM express P-gp, the coexistence of other resistance mechanisms is possible.