Nature Reviews Cancer contents March 2015 Volume 15 Number 3 pp131-194

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TABLE OF CONTENTS
March 2015 Volume 15 Number 3
Impact Factor37.912 *	In this issue Comment Research Highlights Reviews Correspondence Analysis Perspectives Also this month  Article series: Clinical insights  Featured article: Milestones of Lynch syndrome: 1895–2015 Henry T. Lynch, Carrie L. Snyder, Trudy G. Shaw, Christopher D. Heinen & Megan P. Hitchins
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Article series: Clinical insights Comment: Understanding allergy and cancer risk: what are the barriers? Esther Hoste, Sara Cipolat & Fiona M. Wattp131 | doi:10.1038/nrc3909Hoste 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
RESEARCH HIGHLIGHTS Top Metastasis: Feeding the beast p134 | doi:10.1038/nrc3913Two studies have examined how manipulation of energy availability by cancer cells, mediated by changes in microRNAs (miRNAs), can fuel metastatic colonization. PDF Angiogenesis: A sudden rush of blood to the tumour p135 | doi:10.1038/nrc3914This study describes a novel approach to increase blood vessels in tumours to enhance drug delivery, uptake and metabolism. PDF Tumorigenesis: Mutant relationships p135 | doi:10.1038/nrc3917Stites and Trampont et al. used mathematical modelling with verification in cells and cancer genome data to understand the effects of weakly activating RAS mutations. They found that pairs of mutations within the RAS pathway might be able to act together to create a selective advantage in human tumours. PDF DNA repair: A new tool to target DNA repair p136 | doi:10.1038/nrc3919Two studies have shown that DNA polymerase-&thgr; (POLQ) promotes an alternative form of non-homologous end-joining (alt-NHEJ) and suppresses homologous recombination (HR) in mammalian cells. The activity of alt-NHEJ is essential for the survival of cells deficient in HR. PDF IN BRIEF Breast cancer: The importance of recycling | Tumour heterogeneity: A free ride | Radiotherapy: Healing the brain| Therapeutics: Give it a shockPDF Cancer  JOBS of the week Pediatric Cancer Reseracher University of Calgary Postdoc in Cancer Biology Baylor Collge of Medicine Head Bioinformatician for the Centre for Evolution and Cancer Closing Institute of Cancer Research (ICR) Postdoctoral Researcher Position in Cancer Biology University of Pennsylvania Postdoctoral Fellowship - Cancer Stem Cell Biology Cleveland Clinic Lerner Research Institute More Science jobs from Cancer EVENT 2nd International Symposium of the Cancer Research Center of Lyon (CRCL) 21.09.15 Lyon, France More science events from
REVIEWS
Topoisomerase-mediated chromosomal break repair: an emerging player in many games Mohamed E. Ashour, Reham Atteya & Sherif F. El-Khamisyp137 | doi:10.1038/nrc3892Protein-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. Goodellp152 | doi:10.1038/nrc3895Mutations 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
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
Reply: Integrative oncology — strong science is needed for better patient care David H. Gorskip165 | doi:10.1038/nrc3822-c2 Full Text | PDF
ANALYSIS
Therapeutic opportunities within the DNA damage response Laurence H. Pearl et al.p166 | doi:10.1038/nrc3891This 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
TIMELINE Milestones of Lynch syndrome: 1895–2015 Henry T. Lynch et al.p181 | doi:10.1038/nrc3878Lynch 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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