[Multiple medication resistance of apoptosis-resistant tumoral cells].
A4 clone cells, received by CD95-mediated selection from the parental line of Jurkat T-lymphoblast human leukosis, lost their ability of apoptosis as a result of programmed cell death mechanism breakdown. The complex of their acquired phenotypic properties meets tumor progression criteria: oxidative stress resistance, active immune suppression, and low requirement for growth factors. The loss of A4 cell ability of apoptosis is accompanied by acquisition of the phenotype of multiple medication resistance to a wide spectrum of antineoplastic chemotherapeutic drugs and cytotoxins.
Blokhin
D Iu
DIu
Sokolovskaia
A A
AA
Vlasenkova
N K
NK
Mikhaĭlov
A D
AD
Baryshnikov
A Iu
AIu
D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D004273:DNA, Neoplasm / Q000235:genetics; D018432:Drug Resistance, Multiple; D019008:Drug Resistance, Neoplasm; D006801:Humans; D015459:Leukemia-Lymphoma, Adult T-Cell / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D009336:Necrosis / Q000473:pathology*; D014407:Tumor Cells, Cultured / Q000473:pathology
D000970:Antineoplastic Agents; D004273:DNA, Neoplasm