Friday, March 22, 2013

Nature Reviews Cancer content April 2013 Volume 13 Number 4 pp 219-290

Nature Reviews Cancer


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TABLE OF CONTENTS
 
April 2013 Volume 13 Number 4
Nature Reviews Cancer cover
Impact Factor 37.545 *
In this issue
Research Highlights
Progress
Reviews
Perspectives

Also this month
 Featured article:
Mechanistic links between COPD and lung cancer
A. McGarry Houghton


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BEATSON INTERNATIONAL CANCER CONFERENCE
Targeting the Tumour Stroma
7 - 10 July 2013 Glasgow University
This meeting will highlight recent exciting research into the role played by the tumour stroma in cancer progression and how stromal tissue may be targeted to treat the disease.
Deadline for registration, payment and abstract submission - 6 May 2013

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RESEARCH HIGHLIGHTS
Top

Tumour evolution: Weighed down by passengers?
p219 | doi:10.1038/nrc3488
A new study combines evolutionary simulations with clinical mutation data to suggest that passenger mutations in cancers might have more functional consequences than is often assumed.

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Leukaemia: Knowing left from right
p220 | doi:10.1038/nrc3487
A paper published in Science delves further into the mechanisms through which mutations in isocitrate dehydrogenase contribute to leukaemogenesis.

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Genomic instability: DNA transitions
p220 | doi:10.1038/nrc3490
Burns, Lackey and colleagues find that the cytosine deaminase APOBEC3B seems to be important for the mutation rate in breast cancer.

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Melanoma: Horses for courses
p222 | doi:10.1038/nrc3491
A subset of melanoma cells express high levels of PGC1α, which alters their metabolic phenotype compared with melanoma cells that do not express PGC1α.

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Microenvironment: Making connections
p222 | doi:10.1038/nrc3492
Tumorigenic genetic and epigenetic changes in epithelial cells occur as a result of increased inflammation following the loss of transforming growth factor-β receptor 2 in stromal fibroblasts.

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Medulloblastoma: Fuelling the debate
p222 | doi:10.1038/nrc3494
In medulloblastoma, placental growth factor (PLGF) may signal through a non-tyrosine kinase receptor, neuropilin 1 (NRP1), to promote tumour cell survival without having a substantial effect on angiogenesis, thus providing a rationale for targeting this pathway in these tumours.

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TRIAL WATCH
Oncolytics in the clinic | Avoiding relapse

p223 | doi:10.1038/nrc3501
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Non-coding RNAs: The cancer X factor
p224 | doi:10.1038/nrc3489
Eda Yildirim, Jeannie Lee and colleagues present intriguing evidence that the long non-coding RNA X-inactive specific transcript (Xist) is required for maintaining X-chromosome inactivation, and that the loss of Xist after X inactivation can cause haematopoietic cancers in mice.

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Leukaemia: Holding back
p224 | doi:10.1038/nrc3493
A recent paper published in Blood indicates that the interaction between AML1-ETO and the transcriptional co-repressor NCOR1 is partly responsible for limiting the leukaemogenic capacity of this fusion gene.

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Tumour heterogeneity: The rise of the minority
p225 | doi:10.1038/nrc3499
Landau, Carter, Stojanov and colleagues characterize genetic clonal evolution in chronic lymphocytic leukaemia and connect the occurrence of clonal evolution to therapy and prognosis.

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IN BRIEF

Breast cancer: Channelling oncogenicity | Signalling: A smooth alternative? | Immunotherapy: A vehicle for inflammation | Signalling: Chemokine underpinnings of a tumour
PDF

Cancer
JOBS of the week
Postdoctoral Fellow in Cancer Epigenetics
University of Texas M. D. Anderson Cancer
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Centre for Genomic Regulation (CRG)
Mouse Liver Cancer Models
National University of Singapore
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Barts Cancer Institute, Queen Mary University of London
Assistant Researcher
UCLA Department of Urology
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Molecular Pathology and Diagnosis of Cancer
11.10.13
Cambridge, UK
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PROGRESS
Top
Cancer metabolism: fatty acid oxidation in the limelight
Arkaitz Carracedo, Lewis C. Cantley & Pier Paolo Pandolfi
p227 | doi:10.1038/nrc3483
The vast majority of the research into cancer metabolism has been limited to a handful of metabolic pathways, with other pathways being sidelined. This Progress article brings to light the potential contribution of fatty acid oxidation to cancer cell function.

Abstract | Full Text | PDF
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REVIEWS
Top
Mechanistic links between COPD and lung cancer
A. McGarry Houghton
p233 | doi:10.1038/nrc3477
The presence of chronic obstructive pulmonary disease (COPD) is linked to an increased risk of developing lung cancer, independently of cigarette smoking dosage. This Review discusses the nature of the link between the two diseases and considers specific mechanisms that operate in both COPD and lung cancer.
Abstract | Full Text | PDF

The Hippo pathway and human cancer
Kieran F. Harvey, Xiaomeng Zhang & David M. Thomas
p246 | doi:10.1038/nrc3458
A wealth of recent studies has characterized roles for the Hippo pathway in diverse cancer-relevant processes. This Review discusses our latest understanding of Hippo pathway signalling in cancer, including mechanisms of pathway disruption in cancer, and the opportunities and challenges for therapeutic intervention.
Abstract | Full Text | PDF | Supplementary information

The effects of PEDF on cancer biology: mechanisms of action and therapeutic potential
S. Patricia Becerra & Vicente Notario
p258 | doi:10.1038/nrc3484
Pigment epithelium-derived factor (PEDF) has anti-angiogenic, antitumorigenic and antimetastatic properties. If PEDF is to be used for cancer management, a deeper appreciation of its many functions and mechanisms of action is needed, as discussed in this Review.
Abstract | Full Text | PDF

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PERSPECTIVES
Top
OPINION
Meeting the challenge of ascites in ovarian cancer: new avenues for therapy and research
Emma Kipps, David S. P. Tan & Stan B. Kaye
p273 | doi:10.1038/nrc3432
Malignant ascites presents a considerable clinical challenge to the management of ovarian cancer. This Opinion article discusses recent advances in our understanding of its pathophysiology, the development of new methods to characterize its molecular features and how these findings can be used to improve the treatment of malignant ascites.
Abstract | Full Text | PDF

OPINION
Translational control of cell growth and malignancy by the CPEBs
Andrea D'Ambrogio, Kentaro Nagaoka & Joel D. Richter
p283 | doi:10.1038/nrc3485
The CPEBs regulate polyadenylation — and thus expression — of certain RNAs, including those encoding oncogenes and tumour suppressors. This Opinion article analyses whether the CPEBs are deregulated in cancer and discusses the possible implications for cancer biology.
Abstract | Full Text | PDF | Supplementary information

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September 25-27, 2013

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