Personalized synthetic lethality induced by targeting RAD52 in leukemias identified by gene mutation and expression profile-Reference-Cited by-同舟云学术

Personalized synthetic lethality induced by targeting RAD52 in leukemias identified by gene mutation and expression profile

Published:2013-08-15 Issue:7 Volume:122 Page:1293-1304
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Cramer-Morales Kimberly¹,Nieborowska-Skorska Margaret¹,Scheibner Kara²,Padget Michelle²,Irvine David A.³,Sliwinski Tomasz¹⁴,Haas Kimberly⁵,Lee Jaewoong⁶,Geng Huimin⁶,Roy Darshan⁷,Slupianek Artur¹,Rassool Feyruz V.⁸,Wasik Mariusz A.⁷,Childers Wayne⁵,Copland Mhairi³,Müschen Markus⁶,Civin Curt I.²,Skorski Tomasz¹

Affiliation:

1. Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA;

2. Center for Stem Cell Biology and Regenerative Medicine, University of Maryland School of Medicine, Baltimore, MD;

3. Paul O'Gorman Leukemia Research Centre, University of Glasgow, Glasgow, UK;

4. Department of Molecular Genetics, University of Lodz, 90–236 Lodz, Poland;

5. Moulder Center for Drug Discovery Research, Temple University School of Pharmacy, Philadelphia, PA;

6. Department of Laboratory Medicine, University of California San Francisco, San Francisco, CA;

7. Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA; and

8. Department of Radiation Oncology, University of Maryland School of Medicine, Baltimore, MD

Abstract

Key Points Targeting RAD52 DNA binding domain I by peptide aptamer induces synthetic lethality in BRCA-deficient leukemias. Individual patients with BRCA-deficient leukemias could be identified by genetic and epigenetic profiling.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/122/7/1293/1373781/1293.pdf

Reference50 articles.

1. Cancer stem cells, models of study and implications of therapy resistance mechanisms.;Frame;Adv Exp Med Biol,2011

2. Genomic instability in myeloid malignancies: increased reactive oxygen species (ROS), DNA double strand breaks (DSBs) and error-prone repair.;Sallmyr;Cancer Lett,2008

3. ATM prevents the persistence and propagation of chromosome breaks in lymphocytes.;Callén;Cell,2007

4. Widespread genomic breaks generated by activation-induced cytidine deaminase are prevented by homologous recombination.;Hasham;Nat Immunol,2010

5. DNA repair dysregulation from cancer driver to therapeutic target.;Curtin;Nat Rev Cancer,2012

Cited by 126 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. Methylation synthetic lethality: Exploiting selective drug targets for cancer therapy;Cancer Letters;2024-08

2. PARG is essential for Polθ-mediated DNA end-joining by removing repressive poly-ADP-ribose marks;Nature Communications;2024-07-11

3. New Horizons of Synthetic Lethality in Cancer: Current Development and Future Perspectives;Journal of Medicinal Chemistry;2024-07-02

4. A novel role for the peptidyl-prolyl cis-trans isomerase Cyclophilin A in DNA-repair following replication fork stalling via the MRE11-RAD50-NBS1 complex;EMBO Reports;2024-06-28

5. Mechanism of single-stranded DNA annealing by RAD52–RPA complex;Nature;2024-04-24