PARP1-Driven Apoptosis in Chronic Lymphocytic LeukemiaReport as inadecuate

PARP1-Driven Apoptosis in Chronic Lymphocytic Leukemia - Download this document for free, or read online. Document in PDF available to download.

BioMed Research International - Volume 2014 2014, Article ID 106713, 6 pages -

Research ArticleDepartment of Internal Medicine, Hematology Unit, Laikon General Hospital, National and Kapodistrian University of Athens, 11527 Athens, Greece

Received 30 March 2014; Accepted 19 July 2014; Published 3 August 2014

Academic Editor: Marie-Christine Kyrtsonis

Copyright © 2014 Panagiotis T. Diamantopoulos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Chronic lymphocytic leukemia CLL is considered a malignancy resulting from defects in apoptosis. For this reason, targeting apoptotic pathways in CLL may be valuable for its management. Poly ADP-ribose polymerase 1 PARP1 is the main member of a family of nuclear enzymes that act as DNA damage sensors. Through binding on DNA damaged structures, PARP1 recruits repair enzymes and serves as a survival factor, but if the damage is severe enough, its action may lead the cell to apoptosis through caspase activation, or necrosis. We measured the PARP1 mRNA and protein pretreatment levels in 26 patients with CLL and the corresponding posttreatment levels in 15 patients after 3 cycles of immunochemotherapy, as well as in 15 healthy blood donors. No difference was found between the pre- and posttreatment levels of PARP1, but we found a statistically significant relative increase of the 89 kDa fragment of PARP1 that is cleaved by caspases in the posttreatment samples, indicating PARP1-related apoptosis in CLL patients after treatment. Our findings constitute an important step in the field, especially in the era of PARP1 inhibitors, and may serve as a base for future clinical trials with these agents in CLL.

Author: Panagiotis T. Diamantopoulos, Maria Sofotasiou, Vasiliki Papadopoulou, Katerina Polonyfi, Theodoros Iliakis, and Nora-Athina



Related documents