Tuesday, February 24, 2015

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

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Nature Reviews Cancer


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TABLE OF CONTENTS
 
March 2015 Volume 15 Number 3
Nature Reviews Cancer cover
Impact Factor 37.912 *
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. 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
RESEARCH HIGHLIGHTSTop

Metastasis: Feeding the beast
p134 | doi:10.1038/nrc3913
Two 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/nrc3914
This 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/nrc3917
Stites 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/nrc3919
Two 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 shock
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Cancer
JOBS of the week
Pediatric Cancer Reseracher
University of Calgary
Postdoc in Cancer Biology
Baylor Collge of Medicine
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University of Pennsylvania
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Cleveland Clinic Lerner Research Institute
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REVIEWSTop
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
 
CORRESPONDENCETop
Correspondence: Integrative oncology — strong science is needed for better patient care
Heather Greenlee et al.
p165 | doi:10.1038/nrc3822-c1
Full Text | PDF
 
REPLYTop
Reply: Integrative oncology — strong science is needed for better patient care
David H. Gorski
p165 | doi:10.1038/nrc3822-c2
Full Text | PDF
 
ANALYSISTop
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
 
PERSPECTIVESTop
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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