Khronicheskiy mieloleykoz (KhML) - naibolee chastoe mieloproliferativnoe zabolevanie, kharakterizuyushcheesya retsiproknoy translokatsiey t(9;22),(q34;q11), privodyashchey k obrazovaniyu onkogennogo khimernogo gena BCR-ABL na 22q-khromosome. Gen BCR-ABL kodiruet tsitoplazmaticheskiy khimernyy protein, obladayushchiy vyrazhennoy tirozinkinaznoy aktivnost'yu. Poyavlenie preparatov, ingibiruyushchikh tirozinkinazy (ITK), korennym obrazom izmenilo taktiku lecheniya KhML, sdelav ee patogeneticheski napravlennoy. Odnako, v 20-30% sluchayakh u bol'nykh, poluchayushchikh lechenie ITK, voznikaet rezistentnost' k terapii. Odnim iz mekhanizmov vozniknoveniya ustoychivosti k imatinibu yavlyaetsya poyavlenie mutatsiy v gene BCR-ABL. Dannaya rabota posvyashchena molekulyarno-geneticheskomu izucheniyu khronicheskogo mieloleykoza v Respublike Bashkortostan, a takzhe obzoru poslednikh dannykh mirovoy literatury ob etiopatogeneze etogo zabolevaniya.