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On Tuesday 4th April, at the 107th American Association for Cancer Research (AACR) annual meeting in Washington, DC, USA, there was a poster session focused on “Combination Therapies and Approaches to Sensitize Cancer Cells to Drugs”. During this session, a poster (4059/29) titled “KPC34: a co-drug that combines a DNA damaging agent with a targeted therapy for the treatment of AML” by Gregory L. Kucera and colleagues from Wake Forest School of Medicine, North Carolina, was on display.
Standard chemotherapy with Cytarabine (Ara-C) in Acute Myeloid Leukemia (AML) is hindered by chemoresistance which leads to relapse in patients. Chemoresistance can occur due to several mechanisms including reduced activation of Ara-C via down-regulated Deoxycytidine Kinase (dCK) levels or decreased uptake via lowered Equilibrative Nucleoside Transporter 1 (ENT-1) levels. Kucera et al. aimed to assess the efficacy of KPC34, a novel synthetic phospholipid/deoxycytidine analog conjugate, in AML.
In summary, KPC34 can inhibit PKC and cause DNA termination. The authors concluded by suggesting that KPC34 has the “potential to replace Ara-C-based leukemia treatment regimens as a single agent or in combination” therapy for AML.
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