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Article Released Sun-9th-November-2008 20:28 GMT
Contact: Ruth Institution: Nature Publishing Group
 A window on breast cancer

Summaries of newsworthy papers including Himalaya rising to a monsoonal tune; Monkey vaccine fights off AIDS; Souped-up T cells; Neuronal contribution to risk of multiple sclerosis; Duplicitous role for classic cancer molecule; Risk variants for intracranial aneurysm; Making polymers with a lazy enzyme and Giving petals their colour

NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE.
For papers that will be published online on 09 November 2008
This press release is copyrighted to the Nature journals mentioned below.

This press release contains:

· Summaries of newsworthy papers:
Methods: A window on breast cancer
Geoscience: Himalaya rising to a monsoonal tune
Nature: Monkey vaccine fights off AIDS
Medicine: Souped-up T cells
Genetics: Neuronal contribution to risk of multiple sclerosis
Nature: Duplicitous role for classic cancer molecule
Genetics: Risk variants for intracranial aneurysm
Chemical Biology: Making polymers with a lazy enzyme
And finally…Cell Biology: Giving petals their colour
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors


PDFs of all the papers mentioned on this release can be found in the relevant journal’s section of http://press.nature.com. Press contacts for the Nature journals are listed at the end of this release.

PICTURES: To obtain artwork from any of the journals, you must first obtain permission from the copyright holder (if named) or author of the research paper in question (if not).

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PLEASE CITE THE SPECIFIC NATURE JOURNAL AND WEBSITE AS THE SOURCE OF THE FOLLOWING ITEMS. IF PUBLISHING ONLINE, PLEASE CARRY A HYPERLINK TO THE APPROPRIATE JOURNAL’S WEBSITE.


[1] Methods: A window on breast cancer
DOI: 10.1038/nmeth.1269

Researchers have developed a technique to track individual breast cancer cells as they metastasize and invade other regions of the body. The approach gives the scientists a literal ‘window on a tumour’.

Cancers are much more amenable to treatment when the cancer cells are confined to a single tumour. Unfortunately many tumours have a propensity to metastasize - a process by which individual cancer cells exit the tumour, enter the bloodstream and travel to other regions of the body.

Online this week in Nature Methods, Jacco van Rheenen and colleagues describe a mammary imaging window they can suture into place on top of a breast cancer tumour in a mouse. Using this window they could image the cells clearly and study metastasis for long periods of time in the living animal. To aid them in tracking tumour cells through the window, the researchers artificially expressed a 'coloured' protein, which could be switched on at will, in the breast cancer cells, before implanting them in the mouse breast to form the tumour. This allowed the investigators to track the cells’ movement over hours and even days.

Using this approach, they observed differences in metastatic behaviour of cells in different parts of the tumour and also monitored the appearance of the coloured cells in other regions of the body. This method will allow detailed long-term investigation of breast cancer biology in a native breast environment and could be extended to diverse studies of cell motility and tissue morphogenesis in the future.

Author contacts:

Jacco van Rheenen (Royal Netherlands Academy of Arts and Sciences and University Medical Centre, Utrecht, Netherlands)
Tel: +31 20 2121 905; E-mail: j.vanrheenen@niob.knaw.nl

Jeffrey E. Segall (Albert Einstein College of Medicine of Yeshiva University, New York, NY, USA)
Tel: +1 718 678 1109; E-mail: segall@aecom.yu.edu

John Condeelis (Albert Einstein College of Medicine of Yeshiva University, New York, NY, USA)
Tel: +1 718 678 1126; E-mail: condeeli@aecom.yu.edu


[2] Geoscience: Himalaya rising to a monsoonal tune
DOI: 10.1038/ngeo351

The onset of the most intense phase of uplift in the Himalaya may have been triggered by a simultaneous strengthening of the Asian monsoons, suggests a study published online in Nature Geoscience.

Deformation and erosion of the Himalaya began around 50 million years ago, causing the mountain range to rise, but these processes accelerated much later. Peter Clift and colleagues integrated various types of data on the onset of intensification of both the Himalayan uplift and the Asian monsoons. Their results suggest that both these processes occurred at more or less at the same time, around 23 million years ago. Their results indicate that the increased erosion caused by the stronger monsoons may have contributed to the uplift of the Himalaya.

Author contact:
Peter Clift (University of Aberdeen, UK)
Tel: +44 1224 273456; E-mail: p.clift@abdn.ac.uk


[3] Nature: Monkey vaccine fights off AIDS
DOI: 10.1038/nature07469

A study in monkeys, published online in Nature this week, demonstrates that T cells can be commandeered to provide protection against an HIV-like virus. Although this vaccine will never be used in humans, the findings show that in principle a vaccine could be effective in the fight against AIDS.

Dan Barouch and colleagues engineered the virus responsible for the common cold to carry a single protein from simian immunodeficiency virus (SIV), the monkey equivalent of HIV. Unlike other vaccine approaches, the monkeys were given booster shots with a vaccine made from a different strain of cold virus, to spark a robust immune reaction against the SIV protein. When challenged with a lethal dose of SIV, the vaccinated animals were able to fight off the development of AIDS and remain healthy for over a year after infection. The team find that this is due, at least in part, to the powerful immune response generated by the vaccine.

One of the cold virus strains used to prepare the vaccine — adenovirus serotype 5 - has already been shown in human clinical trials to increase susceptibility rather than protect against HIV. For this reason, the vaccine used in this study could never be used in humans. Yet the proof-of-concept suggests that T cells could be used to fight HIV.

Author contact:
Dan Barouch (Beth Israel Deaconess Medical Center, Boston, MA, USA)
Tel: +1 617 735 4485; E-mail: dbarouch@bidmc.harvard.edu


[4] Medicine: Souped-up T cells
DOI: 10.1038/nm.1779

Researchers have engineered killer T cells that are better able to limit the spread of HIV in cell culture. The study published this week in Nature Medicine finds that the enhanced cells can also recognise virus that has mutated to try and escape this response.

T cells are alerted to the presence of HIV by the T-cell receptor (TCR), which recognises fragments of virus proteins displayed as warning flags on the surface of infected cells. Current methods to isolate specific T cells that recognise HIV rely on cloning cells from HIV patients – a slow and painstaking process – and often these cells have TCRs that only weakly detect virus-infected cells. The virus can also mutate to avoid being detected.

James Riley and colleagues used ‘phage display’ technology to isolate a TCR from T cells from an HIV infected patient, which identified a fragment of the virus particularly well. The team then engineered the TCR to be much better at finding the virus. Putting this TCR into T cells created killer cells that were better at restricting the spread of HIV in cell culture. It remains to be seen whether these T cells can control virus infection in animals or patients and therefore become a practical form of therapy.

Author contact:
James Riley (University of Pennsylvania, Philadelphia, PA, USA)
Tel: +1 215 573 6792; E-mail: rileyj@exchange.upenn.edu


[5] Genetics: Neuronal contribution to risk of multiple sclerosis
DOI: 10.1038/ng.251

The first risk variant for multiple sclerosis in a gene expressed specifically in neurons has been identified, according to a study published online this week in Nature Genetics.

Multiple sclerosis is a complex autoimmune disease in which the immune system attacks and destroys the myelin sheath surrounding nerve fibres, resulting in neurodegeneration. Only a very small number of genetic variants have been shown to increase risk, and each is found in genes with functions in the immune system.

Rogier Hintzen and colleagues carried out a genome-wide association study of affected Dutch, Swedish and Canadian individuals, and report a variant in the gene KIF1B to be associated with susceptibility to the disease. KIF1B is enriched in motor neurons, and is a member of a family of proteins involved in transport of cellular components along neuronal axons. This process has been implicated generally in neurodegenerative diseases, and the authors suggest that defective axonal transport may contribute to the pathogenesis of multiple sclerosis as well.

Author contact:
Rogier Hintzen (Erasmus Medical Center, Rotterdam, The Netherlands)
Tel: +31 107 043 780; E-mail: rhintzen@xs4all.nl


[6] & [7] Nature: Duplicitous role for classic cancer molecule

DOI: 10.1038/nature07445
DOI: 10.1038/nature07424

A molecule previously thought to promote cancer may in some circumstances play a part in slowing it down, according to research published online in Nature this week. The findings reveal that the biology of this system is much more complicated than originally thought.

Vascular endothelial growth factor (VEGF) is a molecule that helps cancer to grow its own blood supply and it has been linked to cancer progression. Randall Johnson and colleagues deleted VEGF production in certain cell types but not others. Unexpectedly, they find that this deletion actually accelerates rather than slows tumour growth in mice. This is in contrast with tumours that lack VEGF altogether, which grow more slowly without a blood supply. The findings reveal the importance of these cell types in regulating the tumour blood vessel network and controlling tumour growth.

In a related paper, David Cheresh and colleagues find that VEGF specifically inhibits the stabilisation of blood vessels as they grow. Together, the research demonstrates the complex role of VEGF in orchestrating blood vessel formation. The implications of this work for therapies that target VEGF are not known, although they have already proven successful in many cases.

Author contact:

Randall Johnson (University of California, La Jolla, CA, USA) Author paper [6]
Tel: +1 858 822 0509; E-mail: rsjohnson@ucsd.edu

David Cheresh (University of California at San Diego, La Jolla, CA, USA) Author paper [7]
Tel: +1 858 822 2232; E-mail: dcheresh@ucsd.edu


[8] Genetics: Risk variants for intracranial aneurysm
DOI: 10.1038/ng.240

Scientists have identified two new genetic risk factors for intracranial aneurysm according to a study published online this week in Nature Genetics.

An intracranial aneurysm is a dilation of a blood vessel in the brain, which can lead to haemorrhage and stroke, the latter being the world’s third leading cause of death. Richard Lifton and colleagues carried out a genome-wide association study of over 2,100 Finnish, Dutch and Japanese individuals who had such an aneurysm, as well as 8,000 controls. They identified three variants associated with increased risk, including variants on chromosomes 2 and 8 that are newly implicated.

The most likely candidate to explain the risk associated with the variant on chromosome 8 is the gene SOX17, which is known to be required for formation and maintenance of endothelial cells, which line blood vessels. SOX17 also has a role in the generation of stem cells that give rise to blood cell and endothelial lineages, and the authors suggest that intracranial aneurysm may result from defective stem cell–mediated vascular development and/or repair.

Author contact:
Richard Lifton (Yale University School of Medicine, New Haven, CT, USA)
Tel: +1 203 737 4420; E-mail: richard.lifton@yale.edu


[9] Chemical Biology: Making polymers with a lazy enzyme
DOI: 10.1038/nchembio.125

Scientists have discovered a new pathway for creating biopolymers, according to a paper to be published online this week in Nature Chemical Biology. In contrast to synthetic polymers, biopolymers – composed of biological building blocks such as amino acids - can be produced inside cells and are more likely to be biodegradable. This report expands our understanding of biological synthesis and provides a method for creating a wider array of biopolymers.

Epsilon-Polylysine is a natural homopolymer – a repeated sequence of the same small building blocks of varying length. It is extremely unusual for a biopolymer to be made without a specific sequence – or, in this case, one preferred length, so the origin of this variability was unknown.

Yoshimitsu Hamano and colleagues show that the different lengths are created by an unusual protein. The biosynthetic enzyme Pls mixes the functions of known enzymes to allow strict control over some parts of the assembly process but variable outcomes in others. The authors further demonstrate that they can take advantage of this enzymatic ‘laziness’ by adding different building blocks to create new polymers, which may prove useful in applications from biodegradable plastics to cellular nanodevices.

Author contact:
Yoshimitsu Hamano (Fukui Prefectural University, Fukui, Japan)
Tel: +81 776 61 6000; Email: hamano@fpu.ac.jp


[10] And finally…Cell Biology: Giving petals their colour
DOI: 10.1038/ncb1805

A protein important for controlling normal petal colouring in petunias is described online this week in Nature Cell Biology. The research, involving manipulation of a key protein in the petals’ cells, could lead to different coloured petals being created in the future.

Flower pigments accumulate in a compartment of petal cells called the vacuole. However, the presence of these pigments alone is not enough to produce the familiar pink and red colours of petunias. For petals to be pink or red, the vacuoles must be acidic, whereas an alkaline environment produces blue coloration. Although scientists have known of factors that control the levels of these pigments, it has not been clear how acidity of the vacuole is controlled.

Francesca Quattrocchio and colleagues identify a protein called PH5, which works as a pump, producing an acidic environment in the vacuole. Mutations in the PH5 gene lead to reduced vacuolar acidity, resulting in blue petunias. The authors also find that the factors controlling the levels of flower pigments also control PH5 expression. This ensures that the pigment and the protein that enables it to work properly are present together.

The ability to alter the vacuole’s environment by manipulating PH5 may be useful in creating new petunia petal colours — perhaps leading to manipulated variations of the flower in the future.

Author contact:
Francesca Quattrocchio (Vrije Universiteit, Amsterdam, The Netherlands)
Tel: +31 20 598 7201; E-mail: francesca.quattrocchio@falw.vu.nl


***************************************************************************************************************
Items from other Nature journals to be published online at the same time and with the same embargo:

Nature (http://www.nature.com/nature)

[11] Role for perinuclear chromosome tethering in maintenance of genome stability
DOI: 10.1038/nature07460


NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)

[12] The APC/C maintains the spindle assembly checkpoint by targeting Cdc20 for destructionDOI: 10.1038/ncb1799


NATURE GENETICS (http://www.nature.com/naturegenetics)

[13] Gerodermia osteodysplastica is caused by mutations in SCYL1BP1, a Rab-6 interacting golgin
DOI: 10.1038/ng.252

[14] Flowering-time genes modulate meristem determinacy and growth form in Arabidopsis thaliana
DOI: 10.1038/ng.253


NATURE GEOSCIENCE (http://www.nature.com/ngeo)

[15] Increased multidecadal variability of the North Atlantic Oscillation since 1781
DOI: 10.1038/ngeo352


NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)

[16] Noncanonical NF-kappaB activation requires coordinated assembly of a regulatory complex of the adaptors cIAP1, cIAP2, TRAF2 and TRAF3 and the kinase NIK
DOI: 10.1038/ni.1676

[17] Nonredundant and complementary functions of TRAF2 and TRAF3 in a ubiquitination cascade that activates NIK-dependent alternative NF-kappaB signaling
DOI:10.1038/ni.1678

[18] IL-4 inhibits TGF-beta-induced Foxp3+ T cells and, together with TGF-beta, generates Foxp3– effector T cells that produce IL-9 and IL-10
DOI:10.1038/ni.1677


NATURE MATERIALS (http://www.nature.com/naturematerials)

[19] Single-molecule nanocatalysis reveals heterogeneous reaction pathways and catalytic dynamics
DOI: 10.1038/nmat2319

[20] From Mott state to superconductivity in 1T-TaS2
DOI: 10.1038/nmat2318

[21] A metal-free polymeric photocatalyst for hydrogen production from water under visible light
DOI: 10.1038/nmat2317


NATURE METHODS (http://www.nature.com/nmeth)

[22] Micropatterning for quantitative analysis of protein-protein interactions in living cells
DOI: 10.1038/nmeth.1268


NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)

[23] High-throughput solution processing of large-scale graphene
DOI: 10.1038/nnano.2008.329

[24] Power generation with laterally packaged piezoelectric fine wires
DOI: 10.1038/nnano.2008.314

[25] Fast, sensitive and spectrally tuneable colloidal-quantum-dot photodetectors
DOI: 10.1038/nnano.2008.313


Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)

[26] Beta-catenin-mediated Wnt signaling regulates neurogenesis in the ventral telencephalon
DOI: 10.1038/nn.2226

[27] Continuous shifts in the active set of spinal interneurons during changes in locomotor speed
DOI: 10.1038/nn.2225

[28] Sensory-motor mechanisms in human parietal cortex underlie arbitrary visual decisions
DOI: 10.1038/nn.2221


Nature PHYSICS (http://www.nature.com/naturephysics)

[29] Structure from fleeting illumination of faint spinning objects in flight
DOI: 10.1038/nphys1129

[30] Fermi-surface-dependent superconducting gap in C6Ca
DOI: 10.1038/nphys1128


Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)

[31] Structural basis for midbody targeting of spastin by the ESCRT-III protein CHMP1B
DOI: 10.1038/nsmb.1512

[32] Structure of the Shigella T3SS effector IpaH defines a new class of E3 ubiquitin ligases
DOI: 10.1038/nsmb.1511

[33] Structure of a Shigella effector reveals a new class of ubiquitin ligases
DOI: 10.1038/nsmb.1517


************************************************************************************************

GEOGRAPHICAL LISTING OF AUTHORS

The following list of places refers to the whereabouts of authors on the papers numbered in this release. The listing may be for an author's main affiliation, or for a place where they are working temporarily. Please see the PDF of the paper for full details.

AUSTRIA
Linz: 22
Vienna: 22

BELGIUM
Antwerp: 5
Ghent: 14
Leuven: 14

CANADA:
Ottawa: 16
Toronto: 16, 25, 23
Vancouver: 5

CHINA
Beijing: 33
Fuzhou: 21
Hong Kong: 15
Tianjin: 33

CROATIA
Zagreb: 20

FINLAND
Helsinki: 8
Kuopio: 8
Tampere: 8

FRANCE
Paris: 32

GERMANY
Berlin: 13, 21
Bremen: 2
Chemnitz: 13
Cologne: 13
Munich: 13
Munster: 13
Neuherberg:
Potsdam: 21

ITALY
Chieti: 13, 28
Lecce: 1
Perugia: 10
Rome: 13, 28

JAPAN
Chiba: 8
Fukui: 9
Kanagawa: 8
Nara: 9
Sendai: 30
Tokyo: 8, 21
Yokohama: 9

NETHERLANDS
Amsterdam: 10
Groningen: 8
Leiden: 3, 14
Rotterdam: 5, 8
Utrecht: 1, 8

OMAN
Muscat: 13

SWEDEN
Stockholm: 5

SWITZERLAND
Lausanne: 20
Zurich: 13

UNITED KINGDOM
Aberdeen: 2
Abingdon: 4
Cambridge: 8, 12
Cardiff: 4
Liverpool: 13
Manchester: 13
Oxford: 4, 5

UNITED STATES OF AMERICA
Arizona
Scottsdale: 17
Tempe: 2
Arkansas
Jonesboro: 2
California
Irvine: 3
La Jolla: 6, 7
Los Angeles: 13, 16, 23
Menlo Park: 12
Palo Alto: 18
San Diego: 17
Connecticut
New Haven: 8
Georgia
Atlanta: 24
Illinois
Argonne: 32
Maryland
Bethesda: 31
Massachusetts
Boston: 3, 11, 18
Cambridge: 18
Southborough: 3
Woods Hole: 15
Minnesota
Minneapolis: 27
Missouri
St Louis: 28
New York
Bronx: 1
Ithaca: 19, 27
New York: 26
Stony Brook: 27
North Carolina
Chapel Hill:
Ohio
Dayton: 24
Pennsylvania
Philadelphia: 4, 13, 16
Tennessee
Memphis: 17
Wisconsin
Milwaukee: 29


PRESS CONTACTS…

For media inquiries relating to embargo policy for all the Nature Research Journals:

Rachel Twinn (Nature London)
Tel: +44 20 7843 4658; E-mail: r.twinn@nature.com

Katherine Anderson (Nature New York)
Tel: +1 212 726 9231; E-mail: k.anderson@natureny.com

Ruth Francis (Head of Press, Nature, London)
Tel: +44 20 7843 4562; E-mail: r.francis@nature.com

For media inquiries relating to editorial content/policy for the Nature Research Journals, please contact the journals individually:

Nature Cell Biology (London)
Bernd Pulverer
Tel: +44 20 7843 4892; E-mail: cellbio@nature.com

Nature Chemical Biology (Boston)
Andrea Garvey
Tel: +1 617 475 9241, E-mail: chembio@boston.nature.com

Nature Genetics (New York)
Orli Bahcall
Tel: +1 212 726 9311; E-mail: natgen@natureny.com

Nature Geoscience (London)
Heike Langenberg
Tel: +44 20 7843 4042; E-mail: h.langenberg@nature.com

Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: immunology@natureny.com

Nature Materials (London)
Alison Stoddart
Tel: +44 20 7843 4593; E-mail: materials@nature.com

Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: medicine@natureny.com

Nature Methods (New York)
Hugh Ash
Tel: +1 212 726 9627; E-mail: methods@natureny.com

Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email: p.rodgers@nature.com

Nature Neuroscience (New York)
Kalyani Narasimhan
Tel: +1 212 726 9319; E-mail: neurosci@natureny.com

Nature Physics (London)
Alison Wright
Tel: +44 20 7843 4555; E-mail: a.wright@nature.com

Nature Structural & Molecular Biology (New York)
Michelle Montoya
Tel: +1 212 726 9326; E-mail: nsmb@natureny.com


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