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Cancers 2017, 9(4), 28; doi:10.3390/cancers9040028

DNA Repair Pathway Alterations in Bladder Cancer

Department of Radiation Oncology, Dana-Farber Cancer Institute/Brigham & Women’s Hospital, Harvard Medical School, Boston, MA 02215, USA
Academic Editor: Eddy S. Yang
Received: 7 March 2017 / Revised: 22 March 2017 / Accepted: 23 March 2017 / Published: 27 March 2017
(This article belongs to the Special Issue DNA Repair Pathways in Cancer)
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Abstract

Most bladder tumors have complex genomes characterized by a high mutation burden as well as frequent copy number alterations and chromosomal rearrangements. Alterations in DNA repair pathways—including the double-strand break (DSB) and nucleotide excision repair (NER) pathways—are present in bladder tumors and may contribute to genomic instability and drive the tumor phenotype. DNA damaging such as cisplatin, mitomycin C, and radiation are commonly used in the treatment of muscle-invasive or metastatic bladder cancer, and several recent studies have linked specific DNA repair pathway defects with sensitivity to DNA damaging-based therapy. In addition, tumor DNA repair defects have important implications for use of immunotherapy and other targeted agents in bladder cancer. Therefore, efforts to further understand the landscape of DNA repair alterations in bladder cancer will be critical in advancing treatment for bladder cancer. This review summarizes the current understanding of the role of DNA repair pathway alterations in bladder tumor biology and response to therapy. View Full-Text
Keywords: urothelial cancer; bladder cancer; DNA repair; nucleotide excision repair; mutational signature; genomic instability urothelial cancer; bladder cancer; DNA repair; nucleotide excision repair; mutational signature; genomic instability
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Mouw, K.W. DNA Repair Pathway Alterations in Bladder Cancer. Cancers 2017, 9, 28.

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