P170 GLYCOPROTEIN EXPRESSION AND IMPAIRED ANTHRACYCLINE RETENTION IN CHRONIC MYELOID-LEUKEMIA

被引：11

作者：

DAMIANI, D ^{[1
]}

MICHIELI, M ^{[1
]}

MICHELUTTI, A ^{[1
]}

FANIN, R ^{[1
]}

RUSSO, D ^{[1
]}

BACCARANI, M ^{[1
]}

机构：

[1] UNIV UDINE,SCH MED,DEPT MORPHOL & CLIN RES,CHAIR HAEMATOL,I-33100 UDINE,ITALY

来源：

LEUKEMIA & LYMPHOMA | 1995年 / 17卷 / 3-4期

关键词：

CHRONIC MYELOID LEUKEMIA; CHEMOTHERAPY; ANTHRACYCLINE; MULTIDRUG RESISTANCE;

D O I：

10.3109/10428199509056834

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Chronic myeloid leukaemia (CML) is a well known model of a disease refractory to chemotherapy, including anthracyclines and other drugs that are believed to be pumped out of the cells by a 170 Kd transmembrane glycoprotein (P170). In 35 cases of Ph+ CML we investigated the reactivity of leukaemic cells to a P170-directed monoclonal antibody (MRK-16), by means of flow cytometry. P170 overexpression was found in 4/14 (29%) chronic phase CML cases and in 16/23 (70%) accelerated and blastic phase CML cases (P = 0.01). The same cells were assayed for their ability to retain Daunorubicin and Idarubicin after 2-hours in vitro incubation with 1000 ng/ml of either drug. It was found that anthracycline cell concentration was negatively related with the degree of the reactivity to MRK-16. In accelerated and blastic phase, CML cells simultaneously expressed P170 and the stem cell related marker, CD34. These data confirm that Ph+ leukaemic cells overexpress P170, show that P170 overexpression is functionally relevant, and suggest that P170-related multidrug resistance may be an important factor for chemotherapy failure in Ph+ CML.

引用

页码：289 / 294

页数：6

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