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Blood, 1 September 2005, Vol. 106, No. 5, pp. 1817-1823. Prepublished online as a Blood First Edition Paper on May 17, 2005; DOI 10.1182/blood-2004-11-4296. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-11-4296v1 106/5/1817    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Holleman, A. Articles by Pieters, R. Search for Related Content PubMed PubMed Citation Articles by Holleman, A. Articles by Pieters, R. Related Collections Apoptosis Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Decreased PARP and procaspase-2 protein levels are associated with cellular drug resistance in childhood acute lymphoblastic leukemia Amy Holleman, Monique L. den Boer, Karin M. Kazemier, H. Berna Beverloo, Anne R. M. von Bergh, Gritta E. Janka-Schaub, and Rob Pieters From the Departments of Pediatric Oncology/Hematology and Clinical Genetics, Erasmus MC/Sophia Children's Hospital, Rotterdam, The Netherlands; and the Cooperative Acute Lymphoblastic Leukemia (COALL) study group/Children's University Hospital, Hamburg, Germany. Drug resistance in childhood acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) is associated with impaired ability to induce apoptosis. To elucidate causes of apoptotic defects, we studied the protein expression of Apaf-1, procaspases-2, -3, -6, -7, -8, -10, and poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) in cells from children with acute lymphoblastic leukemia (ALL; n = 43) and acute myeloid leukemia (AML; n = 10). PARP expression was present in all B-lineage samples, but absent in 4 of 15 T-lineage ALL samples and 3 of 10 AML cases, which was not caused by genomic deletions. PARP expression was a median 7-fold lower in T-lineage ALL (P < .001) and 10-fold lower in AML (P < .001) compared with B-lineage ALL. PARP expression was 4-fold lower in prednisolone, vincristine and L-asparaginase (PVA)-resistant compared with PVA-sensitive ALL patients (P < .001). Procaspase-2 expression was 3-fold lower in T-lineage ALL (P = .022) and AML (P = .014) compared with B-lineage ALL. In addition, procaspase-2 expression was 2-fold lower in PVA-resistant compared to PVA-sensitive ALL patients (P = .042). No relation between apoptotic protease-activating factor 1 (Apaf-1), procaspases-3, -6, -7, -8, -10, and drug resistance was found. In conclusion, low baseline expression of PARP and procaspase-2 is related to cellular drug resistance in childhood acute lymphoblastic leukemia. (Blood. 2005;106:1817-1823) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: N. Pottier, M. H. Cheok, W. Yang, M. Assem, L. Tracey, J. C. Obenauer, J. C. Panetta, M. V. Relling, and W. E. Evans Expression of SMARCB1 modulates steroid sensitivity in human lymphoblastoid cells: identification of a promoter snp that alters PARP1 binding and SMARCB1 expression Hum. Mol. Genet., October 1, 2007; 16(19): 2261 - 2271. [Abstract] [Full Text] [PDF] U. Testa and R. Riccioni Deregulation of apoptosis in acute myeloid leukemia Haematologica, January 1, 2007; 92(1): 81 - 94. [Abstract] [Full Text] [PDF]

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