Механизмы устойчивости опухолей к цисплатину
цисплатина. Результати цієї роботи вказують на можливість участі
продукту гена v-src в індукції резитентності до цисплатина шляхом
модуляції деяких шляхів репарації ДНК [111].
Ампліфікація гена сорцина (кальцій-звязуючого білка з
молекулярною масою 19-22кД) в деяких модельних системах асоціювалася
з резистентним фенотипом [112]. Важко зараз сказати, чи є
резистентність пов`язаною саме з сорцином чи разом з геном сорцина у
клітинах ампліфіковані і інші, більш важливі для розвитку
резистентності гени.
Таким чином резистентність до цисплатина має комплексний
характер і пов`язана з рядом особливостей клітин на рівні
цитоплазматичної мемрани, внутрішньоклітинних систем детоксикації,
систем репарації та порушення функціональної активності генів p 53,
bcl-2, fos, mdm 2, nm23та інших.
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