Wednesday, June 24, 2015

Nature Reviews Cancer contents July 2015 Volume 15 Number 7 pp384-448

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Nature Reviews Cancer


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TABLE OF CONTENTS
 
July 2015 Volume 15 Number 7Advertisement
Nature Reviews Cancer cover
Impact Factor 37.912 *
In this issue
Research Highlights
Progress
Reviews
Perspectives

Also this month
 Featured article:
Applications of the CRISPR–Cas9 system in cancer biology
Francisco J. Sánchez-Rivera & Tyler Jacks

 

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RESEARCH HIGHLIGHTS
Top

Metastasis: LOX does some prepping
p384 | doi:10.1038/nrc3976
Cox et al. have shown that metastasis of certain breast cancers to bone can be driven by the enzyme lysyl oxidase (LOX), which induces bone lesions that provide a landing site for circulating tumour cells.
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Multiple myeloma: Mama, I'm coming home
p384 | doi:10.1038/nrc3980
Zhu et al. find that the homing of multiple myeloma cells to the bone marrow is promoted by cyclophilin A-CD147 signalling between bone marrow endothelial cells and myeloma cells.
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RNA splicing: MYC maintains high-fidelity splicing
p385 | doi:10.1038/nrc3977
One way that MYC promotes lymphomagenesis is through maintaining correct pre-mRNA splicing.
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Metastasis: An influential delivery
p386 | doi:10.1038/nrc3974
Two recent studies add to the evidence supporting an important role for extracellular vesicles in promoting metastasis and provide a new technique for analysing these vesicles in vivo.
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Haematological malignancies: Splicing the MDS genome
p393 | doi:10.1038/nrc3975
Three papers now present different aspects of a similar story: altered splicing can lead to myelodysplastic syndrome (MDS) and even to progression to acute myeloid leukaemia (AML).
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PROGRESS
Top
Applications of the CRISPR-Cas9 system in cancer biology
Francisco J. Sánchez-Rivera & Tyler Jacks
p387 | doi:10.1038/nrc3950
The CRISPR–Cas9 (clustered regularly interspaced short palindromic repeats–CRISPR-associated 9) system provides many avenues for improving how we generate models of cancer. This system has numerous uses, including providing a means to understand the importance of genetic alterations as a tumour evolves, and CRISPR–Cas9 may potentially constitute a therapeutic strategy in the future.
Abstract | Full Text | PDF
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REVIEWS
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Forging a signature of in vivo senescence
Norman E. Sharpless & Charles J. Sherr
p397 | doi:10.1038/nrc3960
'Cellular senescence' has been broadened to describe durable states of proliferative arrest induced by disparate stress factors. This Review discusses the limitations of senescence-associated biomarkers and provides suggestions for how to improve the phenotypic description of senescence.
Abstract | Full Text | PDF

The tumour microenvironment after radiotherapy: mechanisms of resistance and recurrence
Holly E. Barker, James T. E. Paget, Aadil A. Khan & Kevin J. Harrington
p409 | doi:10.1038/nrc3958
In this Review, Barker and colleagues describe the mechanisms of radioresistance that are mediated by the tumour stroma and explore how these mechanisms can be targeted to improve radiotherapy responses.
Abstract | Full Text | PDF | Supplementary information

Probing for a deeper understanding of rhabdomyosarcoma: insights from complementary model systems
Venkatesh P. Kashi, Mark E. Hatley & Rene L. Galindo
p426 | doi:10.1038/nrc3961
This Review discusses what we have learned about the biology of rhabdomyosarcoma using various model systems, and how these models might be used to discover new targetable pathogenic mechanisms.
Abstract | Full Text | PDF

 
PERSPECTIVES
Top
OPINION
Metabolic dysregulation in monogenic disorders and cancer — finding method in madness
Ayelet Erez & Ralph J. DeBerardinis
p440 | doi:10.1038/nrc3949
Inborn errors of metabolism are inherited monogenic disorders caused by mutations in genes encoding metabolic enzymes that can result in malignancy. This Opinion article discusses how studying these rare diseases might provide insight into how specific metabolic changes contribute to cancer initiation, development, diagnosis and treatment.
Abstract | Full Text | PDF

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