Tuesday, July 24, 2012

Nature Reviews Cancer contents August 2012 Volume 12 Number 8 pp 503-578

Nature Reviews Cancer


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TABLE OF CONTENTS
 
August 2012 Volume 12 Number 8Advertisement
Nature Reviews Cancer cover
Impact Factor 37.545 *
In this issue
Comment
Research Highlights
Reviews
Perspectives

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Pushing the limits of targeted therapy in chronic myeloid leukaemia
Thomas O'Hare, Matthew S. Zabriskie, Anna M. Eiring & Michael W. Deininger


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Comment: Upper urinary tract urothelial cancers: where it is A:T
Magali Olivier, Monica Hollstein, Heinz Hans Schmeiser, Kurt Straif & Christopher P. Wild
p503 | doi:10.1038/nrc3311
Despite a ban on the use of plants of the Aristolochia genus in herbal medicine, as they contain known carcinogens, renal cancer attributable to the use of this plant seems to be more common than previously thought.

Abstract | Full Text | PDF

RESEARCH HIGHLIGHTS
Top

Tumour microenvironment: The haves and the have nots
p505 | doi:10.1038/nrc3330
Three papers show that hepatocyte growth factor (HGF)–MET signalling is an important determinant of therapeutic responses and can be induced through paracrine, autocrine and endocrine production of HGF.

PDF


Genomics: The great pretenders
p506 | doi:10.1038/nrc3326
Arul Chinnaiyan and colleagues have attempted to map the position of pseudogenes that are expressed throughout the genome.

PDF


Microenvironment: Domino effect
p506 | doi:10.1038/nrc3332
Joan Massagué and colleagues have identified a paracrine signalling network between tumour and stromal cells in breast cancer that seems to drive both metastasis and resistance to chemotherapy.

PDF


Breast cancer: Genes, genes everywhere...
p507 | doi:10.1038/nrc3323
Recently published papers using massively parallel sequencing to look at mutations in breast cancer provide food for thought.

PDF


Tumour microenvironment: Field effect
p508 | doi:10.1038/nrc3324
Knockout of the Notch effector Rbpjk in mesenchymal fibroblasts enhances the formation of squamous cell carcinomas of the skin in mice, and similar changes can be induced by exposure of human skin to ultraviolet A irradiation.

PDF


Therapeutics: Antitumour potential of catalytic DNA
p508 | doi:10.1038/nrc3328
A new study shows that a catalytic DNA molecule might be an effective and safe treatment for some forms of skin cancer.

PDF


Tumour suppressors: At the hypusine of the crime
p509 | doi:10.1038/nrc3325
An in vivo short hairpin RNA screen identifies tumour suppressor genes in commonly deleted regions in lymphoma.

PDF


Chromothripsis: Towards a mechanism
p510 | doi:10.1038/nrc3327
Wigard Kloosterman, Edwin Cuppen and colleagues have evidence that chromothripsis might arise owing to clustered DNA double-strand breaks (DSBs) and nonhomologous repair mechanisms.

PDF


Microenvironment: Suppressing the rejection of pancreatic tumours
p510 | doi:10.1038/nrc3329
Two papers show that KRAS-G12D-transformed pancreatic tumour cells produce GM-CSF, which recruits MDSCs to promote an immunosuppressive microenvironment.

PDF


Mechanotransduction: Catching the X-waves
p510 | doi:10.1038/nrc3331
A paper published in Nature Physics has experimentally and mathematically modelled epithelial cell migration and identified mechanically generated waves that are important for cellular motility.

PDF



IN BRIEF

Therapeutics: First STAT forward | Genomic instability: Divide and conquer | Therapeutics: Therapy targets ribosomal reliance | Tumour evolution: Mutable markers
PDF

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REVIEWS
Top
Pushing the limits of targeted therapy in chronic myeloid leukaemia
Thomas O'Hare, Matthew S. Zabriskie, Anna M. Eiring & Michael W. Deininger
p513 | doi:10.1038/nrc3317
Although chronic myeloid leukaemia (CML) can be treated with tyrosine kinase inhibitors (TKIs) against BCR-ABL1, cure is not achieved in most cases. This Review provides an update on resistance to TKIs, and discusses strategies to target BCR-ABL1-independent resistance, which may be necessary to eliminate CML stem cells and advanced disease.
Abstract | Full Text | PDF

Kinesins and cancer
Oliver Rath & Frank Kozielski
p527 | doi:10.1038/nrc3310
Kinesins — a family of molecular motors that travel unidirectionally along microtubule tracks — have emerged as potential targets for cancer drug development. As discussed in this Review, several compounds that inhibit mitotic kinesins have entered clinical trials and others are being developed, raising the possibility that the range of kinesin-based drug targets may expand in the future.
Abstract | Full Text | PDF | Supplementary information

The rationale for targeting the LOX family in cancer
Holly E. Barker, Thomas R. Cox & Janine T. Erler
p540 | doi:10.1038/nrc3319
The family of lysyl oxidases (LOX) seem to have dichotomous roles in tumour progression: suppressing tumorigenesis and promoting metastasis. This Review discusses the functions of the LOX family and the rationale for targeting them.
Abstract | Full Text | PDF

 
PERSPECTIVES
Top
TIMELINE
The ERBB network: at last, cancer therapy meets systems biology
Yosef Yarden & Gur Pines
p553 | doi:10.1038/nrc3309
This Timeline article focuses on the ERBB network of receptor tyrosine kinases, which exemplifies how a constant dialogue between basic and clinical cancer research can lead to the development of both novel drugs and strategies to overcome acquired resistance.
Abstract | Full Text | PDF

OPINION
NRF2 and cancer: the good, the bad and the importance of context
Michael B. Sporn & Karen T. Liby
p564 | doi:10.1038/nrc3278
NFE2-related factor 2 (NRF2) has apparently contradictory roles in cancer. Activation of NRF2 contributes to the chemopreventive effects of various clinically used drugs against various diseases including cancer. However, NRF2 activity can also accelerate tumorigenesis in mouse models, thus highlighting a potential danger of NRF2 activation. This Opinion article discusses how these opposing roles might be reconciled.
Abstract | Full Text | PDF

OPINION
From cancer genomes to oncogenic drivers, tumour dependencies and therapeutic targets
Cheryl Eifert & R. Scott Powers
p572 | doi:10.1038/nrc3299
How many of the changes identified in human cancer by genome sequencing are meaningful? And how can we exploit these massive data sets to yield new therapeutic targets? This article outlines five approaches that aim to discover oncogenic drivers, tumour dependencies and, ultimately, new cancer therapies from cancer genome data.
Abstract | Full Text | PDF

Corrigendum: Developmental reprogramming of cancer susceptibility
Cheryl Lyn Walker & Shuk-mei Ho
p578 | doi:10.1038/nrc3334
Full Text | PDF
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