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2012/11/23

Nature Reviews Cancer contents December 2012 Volume 12 Number 12 pp 793-886

Nature Reviews Cancer


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TABLE OF CONTENTS
 
December 2012 Volume 12 Number 12
Nature Reviews Cancer cover
Impact Factor 37.545 *
In this issue
Research Highlights
Reviews
Perspectives

Also this month
Article series:
Genomic instability in cancer
 Featured article:
DNA repair dysregulation from cancer driver to therapeutic target
Nicola J. Curtin


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RESEARCH HIGHLIGHTS
Top

Metastasis: Converging targets
p793 | doi:10.1038/nrc3411
Tavazoie and colleagues show that three microRNAs target apolipoprotein E, which is a suppressor of melanoma metastasis.

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Glioma: Tumour cells in reverse
p794 | doi:10.1038/nrc3404
Inder Verma and colleagues provide evidence that, at least in mice, mature neurons and astrocytes can be transformed and can dedifferentiate to form gliomas.

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Metastasis: Elf represses snail
p795 | doi:10.1038/nrc3406
A recent publication in Nature Cell Biology indicates that the transcription factor ELF5 suppresses epithelial to mesenchymal transition and metastasis through repression of SNAI2.

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IN THE NEWS
Melanoma: Seeing red

p795 | doi:10.1038/nrc3412
A new study suggests that people with red hair and fair skin are at risk from developing melanoma because of a particular pigment in their skin.

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Tumour immunology: Context is key for TSLP
p796 | doi:10.1038/nrc3405
Two new studies published in Cancer Cell characterize a context-dependent tumour suppressive role for the interleukin-like inflammatory protein TSLP.

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Signalling: New roles for TLR2
p796 | doi:10.1038/nrc3407
Jenkins and colleagues identify a non-inflammatory role of TLR2 in gastric tumorigenesis.

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MicroRNAs: Editing changes the meaning
p797 | doi:10.1038/nrc3413
Editing of a microRNA (miRNA) is impaired in gliomas, and the non-edited and edited miRNAs have different gene targets, which promote and suppress invasive activity, respectively.

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Metabolism: Warburg behind the butyrate paradox?
p798 | doi:10.1038/nrc3401
A new study finds that metabolism might converge with epigenetic gene regulation to explain the context-dependent effects of the metabolite butyrate on colon cell proliferation.

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Lymphoma: Epigenetic therapy gains momentum
p798 | doi:10.1038/nrc3402
Two groups have reported the discovery of small-molecule inhibitors of EZH2 that have the ability to selectively kill lymphoma cells with EZH2-activating mutations.

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Leukaemia: Early changes
p799 | doi:10.1038/nrc3403Three groups have used human trisomy 21 fetal liver cells or human trisomy 21 induced pluripotent stem cells (iPSCs) to examine the effects of trisomy 21 on the early stages of haematopoiesis.
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IN BRIEF

Metastasis: The clot thickens | Therapeutics: BET spreading | Leukaemia: Supporting role | Signalling: All together now
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Cancer
JOBS of the week
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Lyon, France
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REVIEWS
Top
Article series: Genomic instability in cancer
DNA repair dysregulation from cancer driver to therapeutic target
Nicola J. Curtin
p801 | doi:10.1038/nrc3399
The DNA damage response (DDR) is often altered in tumour cells and this Review discusses the many strategies to target the pathways that comprise the DDR as single agents and in combination to produce synthetic lethality specifically in tumour cells.
Abstract | Full Text | PDF

Medulloblastomics: the end of the beginning
Paul A. Northcott, David T. W. Jones, Marcel Kool, Giles W. Robinson, Richard J. Gilbertson, Yoon-Jae Cho, Scott L. Pomeroy, Andrey Korshunov, Peter Lichter, Michael D. Taylor & Stefan M. Pfister
p818 | doi:10.1038/nrc3410
Medulloblastoma has been the subject of numerous genomics and transcriptomics studies that have led to this disease being subclassified into various clinically meaningful groups and to advances in understanding the biology of these subgroups, with implications for treatment.
Abstract | Full Text | PDF

Future directions in cancer prevention
Asad Umar, Barbara K. Dunn & Peter Greenwald
p835 | doi:10.1038/nrc3397
Based on previous successes and failures, this Review discusses potential future directions for cancer prevention that include the use of genetic, proteomic and other molecular approaches to identify pathways that could be modified during cancer initiation. The use of immunotherapies for cancer prevention is also discussed.
Abstract | Full Text | PDF

The genetic basis of phenotypic heterogeneity in myelodysplastic syndromes
Azra Raza & Naomi Galili
p849 | doi:10.1038/nrc3321
Myelodysplastic syndromes (MDS) are malignant clonal disorders of haematopoietic stem cells and their microenvironment, affecting older individuals. Although emerging insights establish an association between molecular abnormalities (such as specific chromosomal abnormalities) and the phenotypic heterogeneity of MDS, as outlined in this Review the origin and progression of MDS remain enigmatic.
Abstract | Full Text | PDF

Immunogenic cell death and DAMPs in cancer therapy
Dmitri V. Krysko, Abhishek D. Garg, Agnieszka Kaczmarek, Olga Krysko, Patrizia Agostinis & Peter Vandenabeele
p860 | doi:10.1038/nrc3380
In recent years a new concept of immunogenic cell death (ICD) has emerged. In this Review, the authors discuss the role of endoplasmic reticulum (ER) stress and reactive oxygen species (ROS) in regulating the immunogenicity of dying cancer cells and how this might relate to therapeutic intervention.
Abstract | Full Text | PDF | Supplementary information

 
PERSPECTIVES
Top
OPINION
Human tumour viruses and the deregulation of cell polarity in cancer
Lawrence Banks, David Pim & Miranda Thomas
p877 | doi:10.1038/nrc3400
Despite displaying characteristics of tumour suppressors, the core regulators of epithelial cell polarity are rarely mutated in tumours, and it is still unclear whether they directly contribute to cancer development. However, data from human tumour viruses provide compelling evidence of a central role for the perturbation of cell polarity in cancer.
Abstract | Full Text | PDF

Corrigendum: Pushing the limits of targeted therapy in chronic myeloid leukaemia
Thomas O'Hare, Matthew S. Zabriskie, Anna M. Eiring & Michael W. Deininger
p886 | doi:10.1038/nrc3408
Full Text | PDF
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