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Philadelphia chromosome (Ph) is the result of a chromosomal translocation leads to malignant transformation of hematopoietic cells . The reason is oncogenic tyrosine kinase activity of the BCR / ABL fusion gene resulting from following the transfer of a fragment of chromosome 9 to chromosome 22 [ t ( 9 , 22 )] . There is a whole family of tyrosine kinases fusion ( FTKs ) related to BCR / ABL , such as the TEL / ABL , TEL/JAK2 , TEL / TRKC (L) , TEL / PDGFâR and NPM / ALK , which induce both acute and chronic myelogenous leukemias and lymphomas. FTKs activate intracellular signal transduction pathways stimulate the cells to divide and protect them from apoptosis and activate mechanisms leading to drug resistance . Various FTKs have the ability to activate STAT transcription factors . STAT5 is necessary for dependent FTKs RAD51 regulation mechanism by homologous recombination repair ( HRR ) . Moreover, when drug therapy FTKs cells exhibit altered by the cell cycle delay in G2 / M. He finds in them also elevated levels of anti-apoptotic proteins . Most likely, the interaction of all these processes underlies the phenomenon of drug resistance, and is the main problem of the effective therapy of leukemia .

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The Editorial Board
Andrzej Łukaszyk - przewodniczący, Zofia Bielańska-Osuchowska, Szczepan Biliński, Mieczysław Chorąży, Aleksander Koj, Włodzimierz Korochoda, Leszek Kuźnicki, Aleksandra Stojałowska, Lech Wojtczak

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Katedra i Zakład Histologii i Embriologii Uniwersytetu Medycznego w Poznaniu, ul. Święcickiego 6, 60-781 Poznań, tel. +48 61 8546453, fax. +48 61 8546440, email:

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