- Tytuł:
- Reactive oxygen species in BCR-ABL1-expressing cells - relevance to chronic myeloid leukemia
- Autorzy:
-
Antoszewska-Smith, Joanna
Pawlowska, Elzbieta
Blasiak, Janusz - Powiązania:
- https://bibliotekanauki.pl/articles/1038675.pdf
- Data publikacji:
- 2017
- Wydawca:
- Polskie Towarzystwo Biochemiczne
- Tematy:
-
chronic myeloid leukemia
reactive oxygen species
DNA damage
DNA repair
cancer stem cells
imatinib resistance - Opis:
- Chronic myeloid leukemia (CML) results from the t(9;22) reciprocal chromosomal translocation producing the BCR-ABL1 gene, conferring growth and proliferation advantages in the CML cells. CML progresses from chronic, often syndrome-free, to blast phase, fatal if not treated. Although the involvement of BCR-ABL1 in some signaling pathways is considered as the cause of CML, the mechanisms resulting in its progression are not completely known. However, BCR-ABL1 stimulates the production of reactive oxygen species (ROS), which levels increase with CML progression and induce BCR-ABL1 self-mutagenesis. Introducing imatinib and other tyrosine kinase inhibitors (TKIs) to CML therapy radically improved its outcome, but TKIs-resistance became an emerging problem. TKI resistance can be associated with even higher ROS production than in TKI-sensitive cells. Therefore, ROS-induced self-mutagenesis of BCR-ABL1 can be crucial for CML progression and TKI resistance and in this way should be taken into account in therapeutic strategies. As a continuous production of ROS by BCR-ABL1 would lead to its self-destruction and death of CML cells, there must be mechanisms controlling this phenomenon. These can be dependent on DNA repair, which is modulated by BCR-ABL1 and can be different in CML stem and progenitor cells. Altogether, the mechanisms of the involvement of BCR-ABL1 in ROS signaling can be engaged in CML progression and TKI-resistance and warrant further study.
- Źródło:
-
Acta Biochimica Polonica; 2017, 64, 1; 1-10
0001-527X - Pojawia się w:
- Acta Biochimica Polonica
- Dostawca treści:
- Biblioteka Nauki
Artykuł