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Increased P‐glycoprotein expression and multidrug‐resistant gene (mdr1) amplification are infrequently found in fresh acute leukemia cells. Sequential analysis of 15 cases at initial presentation and relapsed stage
Author(s) -
Ito Yoshinori,
Tanimoto Mitsune,
Kumazawa Takao,
Okumura Masao,
Morishima Yasuo,
Ohno Ryuzo,
Saito Hidehiko
Publication year - 1989
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19890415)63:8<1534::aid-cncr2820630813>3.0.co;2-n
Subject(s) - leukemia , medicine , p glycoprotein , acute leukemia , microbiology and biotechnology , stage (stratigraphy) , antibody , monoclonal antibody , pathology , cancer research , immunology , biology , multiple drug resistance , genetics , drug resistance , paleontology
Using a DNA probe of mdrl and an anti‐P‐glycoprotein monoclonal antibody (MRK16), the authors investigated 19 cases of adult acute leukemia patients (one M1, six M2, three M3, one M4, three M5, two L1, and three L2), comparing leukemia cells at the initial presentation (I) with those at the relapsed stage (R). By Southern hybridization analysis mdr1 DNA levels were not amplified in 32 samples from 19 patients (I:14, R: 18). By Northern hybridization analysis mdrl mRNA levels were not expressed in ten samples from seven patients (I:4, R: 6). By indirect immunofluorescent assay with MRK16 antibody P‐glycoprotein was not detected in 30 samples from 18 patients (I: 13, R: 17). Thus, P‐glycoprotein expression and mdr1 gene amplification occurred infrequently not only in leukemia cells at the initial presentation but also in those at the relapsed cases and may not be a major cause of refractoriness to antileukemia drugs in adult acute leukemia.