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World Stem Cell Summit 2010

Thursday, September 24, 2009

Nature Review Cancer contents October 2009 Volume 9 Number 10 pp 683-762

NATURE REVIEWS CANCER

October 2009 Volume 9 Number 10

Visit Nature Reviews Cancer online to browse the journal.

Now available at http://links.ealert.nature.com/ctt?kn=91&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

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Nature Reviews Cancer Impact Factor: 30.762*
* 2008 Journal Citation Report (Thomson Reuters, 2009)
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Focus on p53 - 30 years on

To celebrate the past 30 years of research on p53, Nature Reviews Cancer
presents a Focus issue of specially-commissioned articles that discuss the
many roles of this tumour suppressor.

Click here to access the Focus: http://links.ealert.nature.com/ctt?kn=45&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

A p53 molecular network map is now available from the NCI-Nature Pathway Interaction Database,
and depicts both the mechanisms by which this transcription factor is stabilized and activated
as well as numerous p53 downstream effectors.

View the FREE network map online:
http://links.ealert.nature.com/ctt?kn=93&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0


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This month's Featured article:
p53 and metabolism
Karen H. Vousden and Kevin M. Ryan
p691 | doi:10.1038/nrc2715

http://links.ealert.nature.com/ctt?kn=11&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

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From the editors
p683 | doi:10.1038/nrc2746
http://links.ealert.nature.com/ctt?kn=41&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

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RESEARCH HIGHLIGHTS
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Tumorigenesis: No frills attached
p685 | doi:10.1038/nrc2739
http://links.ealert.nature.com/ctt?kn=48&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

Therapeutics: One and one makes...
p686 | doi:10.1038/nrc2740
http://links.ealert.nature.com/ctt?kn=50&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

Metabolism: Giving antioxidants a bad rap
p686 | doi:10.1038/nrc2742
http://links.ealert.nature.com/ctt?kn=52&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

IN BRIEF
Signalling | Epigenetics | Diabetes | Non-coding RNAs
p687 | doi:10.1038/nrc2744
http://links.ealert.nature.com/ctt?kn=30&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

Senescence: The more the merrier
p688 | doi:10.1038/nrc2737
http://links.ealert.nature.com/ctt?kn=5&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

Chondrosarcoma: p53 and Gli combine forces
p688 | doi:10.1038/nrc2741
http://links.ealert.nature.com/ctt?kn=89&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

Transcription: Reaching a consensus
p689 | doi:10.1038/nrc2743
http://links.ealert.nature.com/ctt?kn=86&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0


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Focus on: p53 - 30 years on
http://links.ealert.nature.com/ctt?kn=26&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0
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REVIEWS
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p53 and metabolism
Karen H. Vousden and Kevin M. Ryan
p691 | doi:10.1038/nrc2715
p53 can regulate numerous aspects of metabolic pathways and thereby influence
the metabolic alterations exhibited by tumour cells. However, the contribution
of p53 is complex and in some cases might promote, rather than inhibit, tumour
progression. So, just what is p53 doing?
Abstract: http://links.ealert.nature.com/ctt?kn=11&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=78&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

When mutants gain new powers: news from the mutant p53 field
Ran Brosh and Varda Rotter
p701 | doi:10.1038/nrc2693
Mutant p53 proteins not only lose their tumour suppressive ability, but
also gain new properties that promote tumorigenesis. What are these properties
and what are the clinical implications?
Abstract: http://links.ealert.nature.com/ctt?kn=33&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=79&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

Tumour suppression by p53: a role for the DNA damage response?
David W. Meek
p714 | doi:10.1038/nrc2716
How important is the DNA damage response in mobilizing the tumour
suppression function of p53? This Review considers how supporting and
conflicting evidence about the role of DNA damage response signalling
in cancer can be reconciled.
Abstract: http://links.ealert.nature.com/ctt?kn=27&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=67&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

The expanding universe of p53 targets
Daniel Menendez, Alberto Inga and Michael A. Resnick
p724 | doi:10.1038/nrc2730
Target response element sequences are a crucial part of the p53 network.
This Review describes how functional response elements can be defined and
discusses the implications of non-canonical p53 response elements, which
greatly expand the universe of p53-regulated genes, on the part that p53
plays as a tumour suppressor.
Abstract: http://links.ealert.nature.com/ctt?kn=28&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=57&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

p53 and E2f: partners in life and death
Shirley Polager and Doron Ginsberg
p738 | doi:10.1038/nrc2718
The Rb-E2f and MDM2-p53 pathways are both defective in most human tumours,
indicating that these pathways function independently in the control of
cell fate. However, extensive crosstalk between these two pathways also
exists. How do they coordinately affect tumour biology?
Abstract: http://links.ealert.nature.com/ctt?kn=16&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=61&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

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Focus on: p53 - 30 years on
http://links.ealert.nature.com/ctt?kn=26&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0
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PERSPECTIVES
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TIMELINE
The first 30 years of p53: growing ever more complex
Arnold J. Levine and Moshe Oren
p749 | doi:10.1038/nrc2723
When p53 was first discovered, it received relatively little attention
from cancer researchers. The road leading to p53's rise to fame, and the
recognition of TP53 as the most frequently altered gene in human cancer,
has been long and winding. This Timeline examines the rich history of
this pivotal tumour suppressor.
Abstract: http://links.ealert.nature.com/ctt?kn=15&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=43&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0

OPINION
p53 ancestry: gazing through an evolutionary lens
Wan-Jin Lu, James F. Amatruda and John M. Abrams
p758 | doi:10.1038/nrc2732
The selective pressures for the retention of primordial p53 genes
predated the appearance of cancer. Therefore, wild-type tumour suppressive
functions were probably co-opted from unrelated primordial activities.
Is it possible to deduce what these early functions might have been?
Abstract: http://links.ealert.nature.com/ctt?kn=6&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=38&m=34068036&r=MTc2Njc4NzkyNgS2&b=2&j=NTgzOTYyNjIS1&mt=1&rt=0


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