Genomic instability in cancer
Genomic instability is often associated with cancer and can be indicative of a poor prognosis for some types of cancer. But, is genomic instability a consequence of tumour progression or an active process that drives tumour evolution? The answer to this question has still not been entirely resolved. Many new findings have highlighted certain DNA repair pathways and cell cycle control processes that have important consequences for genomic stability and tumour cell biology. Indeed, there are numerous efforts to manipulate the DNA damage responses to selectively induce tumour cell death through catastrophic genomic instability, and some are already showing promise. Of course, radiotherapy and other existing chemotherapeutic agents should not be overlooked as therapeutic strategies by which DNA damage induces tumour cell death and there are various efforts to improve the response to radiotherapy and to understand responses (and resistance) to current cytotoxic chemotherapeutics. This series takes a look at the progress made in this field and the questions that remain about the role of genomic instability in cancer.
Index
2013
July 2013 Vol 13 No 7
End–joining, translocations and cancer
Samuel F. Bunting & Andre Nussenzweig
doi:10.1038/nrc3537
March 2013 Vol 13 No 3
In the wrong place at the wrong time: does cyclin mislocalization drive oncogenic transformation?
Jonathan D. Moore
doi:10.1038/nrc3468
2012
December 2012 Vol 12 No 12
DNA repair dysregulation from cancer driver to therapeutic target
Nicola J. Curtin
doi:10.1038/nrc3399
October 2012 Vol 12 No 10
Chromothripsis and cancer: causes and consequences of chromosome shattering
Josep V. Forment, Abderrahmane Kaidi & Stephen P. Jackson
doi:10.1038/nrc3352
October 2012 Vol 12 No 10
Crosstalk between chromatin state and DNA damage response in cellular senescence and cancer
Gabriele Sulli, Raffaella Di Micco & Fabrizio d'Adda di Fagagna
doi:10.1038/nrc3342
September 2012 Vol 12 No 9
The effects of deregulated DNA damage signalling on cancer chemotherapy response and resistance
Peter Bouwman & Jos Jonkers
doi:10.1038/nrc3342
March 2012 Vol 12 No 3
RB: mitotic implications of a tumour suppressor
Amity L. Manning and Nicholas J. Dyson
doi:10.1038/nrc3216
February 2012 Vol 12 No 2
Balancing repair and tolerance of DNA damage caused by alkylating agents
Dragony Fu, Jennifer A. Calvo & Leona D. Samson
doi:10.1038/nrc3185
January 2012 Vol 12 No 1
BRCA1 and BRCA2: different roles in a common pathway of genome protection
Rohini Roy, Jarin Chun & Simon N. Powell
doi:10.1038/nrc3181
2011
July 2011 Vol 11 No 7
DNA interstrand crosslink repair and cancer
Andrew J. Deans & Stephen C. West
doi:10.1038/nrc3088
June 2011 Vol 11 No 6
Human cancers express mutator phenotypes: origin, consequences and targeting
Lawrence A. Loeb
doi:10.1038/nrc3063
April 2011 Vol 11 No 4
Strategies to improve radiotherapy with targeted drugs
Adrian C. Begg, Fiona A. Stewart & Conchita Vens
doi:10.1038/nrc3007
March 2011 Vol 11 No 3
Telomeric and extra-telomeric roles for telomerase and the telomere-binding proteins
Paula Martínez & María A. Blasco
doi:10.1038/nrc3025
March 2011 Vol 11 No 3
Transcriptional mutagenesis: causes and involvement in tumour development
Damien Brégeon & Paul W. Doetsch
doi:10.1038/nrc3025
February 2011 Vol 11 No 2
DNA polymerases and cancer
Sabine S. Lange, Kei-ichi Takata & Richard D. Wood
doi:10.1038/nrc2998
2010
December 2010 Vol 10 No 12
Shared and separate functions of polo–like kinases and aurora kinases in cancer
Susanne M. A. Lens, Emile E. Voest & René H. Medema
doi:10.1038/nrc2964