Oxidative stress as a therapeutic perspective for ATM-deficient chronic lymphocytic leukemia patients
| Authors | |
|---|---|
| Year of publication | 2015 |
| Type | Article in Periodical |
| Magazine / Source | Haematologica |
| MU Faculty or unit | |
| Citation | |
| Web | http://www.haematologica.org/content/100/8/994.full-text.pdf+html |
| Doi | http://dx.doi.org/10.3324/haematol.2015.130260 |
| Field | Oncology and hematology |
| Keywords | ATM protein; ATR protein; doxorubicin; mitogen activated protein kinase p38; olaparib; reactive oxygen metabolite |
| Attached files | |
| Description | Ataxia Telangiectasia Mutated (ATM) kinase co-ordinates a wide spectrum of cellular processes through the phosphorylation of numerous substrates. ATM, which is implicated in cellular response to DNA double strand breaks (DSBs), plays a crucial role in anti-cancer DNA damage response (DDR) pathway, but also represents a key sensor to oxidative stress 1(Figure 1). Germinal ATM mutations lead to recessive inherited Ataxia telangiectasia syndrome characterized by neurodegenerative and immunological symptoms and an increased risk of tumor development. 2 Somatic ATM inactivation is frequently found in lymphoproliferative diseases, contributing to elevated genomic instability and resulting in the defective activation of the p53 pathway and poor patient outcome. Thus,ATM defects represent an important prognostic and potentially predictive marker in chronic lymphocytic leukemia(CLL). Finally, ATM dysfunction also offers the opportunity to develop novel therapeutic strategies |
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