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March 2015 Volume 15 Number 3 | ||||||||||||||||||||||||||||||||||||||||||||||
In this issue Comment Research Highlights Reviews Correspondence Analysis Perspectives
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Article series: Clinical insights Comment: Understanding allergy and cancer risk: what are the barriers? Esther Hoste, Sara Cipolat & Fiona M. Watt p131 | doi:10.1038/nrc3909 Hoste et al. discuss whether allergic immune responses, which have been observed to be protective against some types of cancer, can be activated to target cancer, and what the mechanism of antitumour allergic responses might be. Abstract | Full Text | PDF | ||||||||||||||||||||||||||||||||||||||||||||||
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REVIEWS | Top | |||||||||||||||||||||||||||||||||||||||||||||
Topoisomerase-mediated chromosomal break repair: an emerging player in many games Mohamed E. Ashour, Reham Atteya & Sherif F. El-Khamisy p137 | doi:10.1038/nrc3892 Protein-linked DNA breaks can be formed through the abortive activity of topoisomerases — this Review discusses the roles of such breaks during transcription and in triggering gene deletions and translocations in cancer. Abstract | Full Text | PDF | ||||||||||||||||||||||||||||||||||||||||||||||
DNMT3A in haematological malignancies Liubin Yang, Rachel Rau & Margaret A. Goodell p152 | doi:10.1038/nrc3895 Mutations in the gene encoding DNA methyltransferase 3A (DNMT3A) have been reported in patients with various haematological malignancies, suggesting that DNMT3A could be a tumour suppressor. In this Review, Yang et al. put data from basic science studies into clinical context, opening stimulating discussions regarding possible new therapeutic avenues. Abstract | Full Text | PDF | Supplementary information | ||||||||||||||||||||||||||||||||||||||||||||||
CORRESPONDENCE | Top | |||||||||||||||||||||||||||||||||||||||||||||
Correspondence: Integrative oncology — strong science is needed for better patient care Heather Greenlee et al. p165 | doi:10.1038/nrc3822-c1 Full Text | PDF | ||||||||||||||||||||||||||||||||||||||||||||||
REPLY | Top | |||||||||||||||||||||||||||||||||||||||||||||
Reply: Integrative oncology — strong science is needed for better patient care David H. Gorski p165 | doi:10.1038/nrc3822-c2 Full Text | PDF | ||||||||||||||||||||||||||||||||||||||||||||||
ANALYSIS | Top | |||||||||||||||||||||||||||||||||||||||||||||
Therapeutic opportunities within the DNA damage response Laurence H. Pearl et al. p166 | doi:10.1038/nrc3891 This Analysis uses the published literature to form a DNA damage response network and then uses this to identify potential synthetic lethal interactions and to assess the druggability of proteins in the DNA damage response network. Abstract | Full Text | PDF | Supplementary information | ||||||||||||||||||||||||||||||||||||||||||||||
PERSPECTIVES | Top | |||||||||||||||||||||||||||||||||||||||||||||
TIMELINE Milestones of Lynch syndrome: 1895–2015 Henry T. Lynch et al. p181 | doi:10.1038/nrc3878 Lynch syndrome is caused by heterozygous mutations and epimutations in mismatch repair genes, which lead to specific pathologies, including increased risk of multiple types of cancer and microsatellite instability. Lynch syndrome has been pivotal to the history of understanding hereditary cancer-prone syndromes and continues to lead the way in our understanding of the risk and treatment of familial cancers. Abstract | Full Text | PDF | ||||||||||||||||||||||||||||||||||||||||||||||
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*2013 Journal Citation Report (Thomson Reuters, 2014) |
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