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World Stem Cell Summit 2010

World Stem Cell Summit 2010

Friday, May 30, 2008

[StemCellInformation] Australian Quadriplegic Thanks Maverick Indian Stem Cell Doctor

Australian Quadriplegic Thanks Maverick Indian Stem Cell Doctor for Ability to Breathe

Tuesday, May 27, 2008

http://www.foxnews.com/images/service_skynews_36.gif

http://www.foxnews.com/images/373219/1_61_052708_quadriplegic.jpg

Perry Cross

  •  

A man who is paralyzed from the neck down says he can now breathe on his own after having controversial embryonic stem cell treatment in India.

Perry Cross is the most high-profile patient to have traveled to India to be injected with the cells - which are banned in his own country Australia and most of the West.

He was left a quadriplegic after being injured playing rugby when just 19 years old and has no movement below his neck.

He has to be connected to a ventilator to breathe and has spent the past 14 years searching for treatment which might help him regain any movement.

During this time, Mr. Cross met Superman actor Christopher Reeve and became the actor's ambassador for stem cell research in Australia.

He has since spoken at the United Nations and is a regular contributor to television and radio debates on the virtues of the research.

He also set up a Foundation to raise money to help find new ways to fight paralysis, which is supported by star Australian cricketer Adam Gilchrist.

"After 14 years of no change at all since my accident, I can now breathe on my own," he told Sky News.

"You know, you put your lottery numbers in every week and I feel by coming here, my lottery numbers have finally come up."

It took a huge leap of faith to travel to India.

The doctor who is administering the stem cells is a controversial figure in her own country and abroad.

Dr. Geeta Shroff is viewed as a bit of a maverick within the medical world because of her fierce determination to do her work under her own terms and in her own way.

She researched her treatment without any grants or financial help and virtually single-handedly developed it over two years, beginning the work in a small lab she set up in her garage.
She now has two hospitals in the capital New Delhi where she treats her own countrymen and women who have terminal conditions or incurable afflictions.

But she also has an increasing number of international patients - mainly from countries like Australia, America and Britain where there are much tighter controls on the use of embryonic stem cell treatment.
Consequently she has fallen out with much of the conventional medical establishment for steadfastly refusing to publish papers outlining her methods, research and technique.
Instead she has applied for a patent on her treatment to stop others from copying and marketing her work.

Dr. Shroff's critics point out that without knowing exactly what she is injecting and without proper clinical trials, it is impossible to say whether there are any long term side-effects and whether the treatment is safe.

She insists that over the five years she has been administering her treatment no patient has shown any adverse reactions.

Under Indian law, she is allowed to treat terminally ill and incurable conditions such as Parkinson's Disease, spinal injury and Alzheimer's.

But this has led her detractors to claim she is offering false hope to desperate people and is essentially using them as guinea pigs.

Perry Cross - along with many of the 500 other patients Dr. Shroff is treating - is unconcerned by the controversy.

"I cannot tell you how restricting my life is in so many ways," he says.

"I can't breathe on my own, I can't bathe on my own. I can't swim or get wet, the list of things I can't do are a mile long. Why wouldn't I try everything?"

His team of carers who look after him 24/7 are astonished at his progress in the last two months since he traveled to India and started receiving injections every day.

Most of them have been with him for many years.

"This is massive," said one, "We have tried so many times over the years to get him off the ventilator but never could. It's amazing."

It has given him hope that with more stem cell treatment he may even be able to develop movement elsewhere in his body.

"Even if I managed to move a finger or one hand, it would be worth it," he says.

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[StemCellInformation] #446 Friday, May 30, 2008 - FDA, THE CANCER SCARE, AND MY SECRET PLAN

#446 Friday, May 30, 2008 - FDA, THE CANCER SCARE, AND MY SECRET PLAN

 

Cancer is prevalent in my family. My mother died young (58) of breast cancer; my older sister died of leukemia, a form of blood cancer (age 23); my younger sister is battling both cancer and leukemia right now.

 

So when I hear that the field of stem cell research may be held up because of the possibility of cancer, how shall I feel?

 

Cautious, definitely. Cancer is a serious risk.

 

But the only way any of us can keep safe from cancer altogether is to live on a different planet.

 

The air we breathe, the water we drink—polluted. The food we take into our bodies—chemicals, pesticides, preservatives, all known carcinogens.

 

Should we stop the research because of that fear?

 

Should we say, no human trials with embryonic stem cells until we can guarantee there are no risks at all?

 

In other words, never?

 

As you know (if you have suffered through this column for any length of time) the FDA is considering allowing human trials for embryonic stem cell therapies.

 

April 10th was a hearing, and the transcript is available online, at the FDA page. (http://www.fda.gov) The search box is at the upper right corner of the page, type in embryonic, then choose the April 10th hearing transcripts if you want to read the complete word-by-word testimony. Some parts of the hearing were closed, I understand, but you can definitely get the message.

 

The number one topic—voiced on almost every page of the transcript—is the fear of cancer.

 

Over and over and over, statements are made about cancer and teratomas and tumors, as if our field was as dangerous as tobacco, which of course is allowed.

Numerous statements are made about not allowing the trials to go forward until all possible threats of cancer are removed.

 

Is there a risk of cancer?

 

Here are the facts, as plain as I understand them, and always with the proviso that I am neither scientist, nor doctor.

 

If a scientist were to put pure embryonic stem cells into my body, there would almost certainly be a teratoma. A teratoma is a lump, a growth, a tumor—not cancer. A teratoma is harmless of itself, unless it grows in a place where any lump would be dangerous—like the spine. We don't want it, but a teratoma is not cancerous.

 

Also—and this is important— a teratoma comes (if it does) only when undifferentiated embryonic stem cells are put in. To the best of my knowledge, no scientist wants to do this—nobody wants to put undifferentiated cells in. They want to differentiate (change) the cells first.

 

Think of a carpenter's nails, screws, nuts and bolts. These all  begin as hot liquid metal, very dangerous to work with—but we do not use them in that formless shape—at the nail factory, the molten iron is poured into molds, and shaped, and cooled. We only use them when the metal is completely set.

 

Same with stem cells. The embryonic stem cells are differentiated—shaped—into whatever kind of cell is needed. We use them only after differentiation.

 

In the Keirstead/Geron experiments, that means oligodendrocytes, cells to create myelin, cells to insulate damaged nerves in the spine.

 

These are already differentiated.

 

For the past few days I have been struggling with the nearly 300 page FDA report, the transcript of the April 10th hearing on embryonic stem cells and "safety". I put that in quotes because that is not all that is being debated; there is also the unsaid agenda which everybody carries.

 

All of us have a plan. With me, it is to advance the research.

 

With some of the folks in the hearings, it seems to be the opposite—what kind of logical-sounding excuse can they come up with that will delay human trials?

 

It is never easy, guessing the intent of people's minds. Honorable folks can disagree. Very intelligent folks, doctors and scientists, and as always, part of me wants to say, well, these folks are smarter than me, let them alone, don't make a fuss.

 

But everybody on earth is smarter than me in one thing or another—that does not mean I am going to keep silent. Not to mention I am a parent, and this affects my paralyzed son, and millions like him, all around the world, somebody's loved one, afflicted with one incurable condition or another.

 

I don't intend to be on my deathbed (many years from now!) and there is my son in his wheelchair beside me—still in his wheelchair? I am sure he would be polite and not actually say, gee Dad, if only you had stepped up to the plate…

 

No, before I head into the great beyond, I intend to see my son on his feet: walking around, kicking a soccer ball, or kicking an anti-science politician—sorry.   

 

So I will always voice my opinion, no matter how much more qualified the opposition may be.

 

And I will also have a backup plan.

 

So here it is, my secret backup plan.

 

Roman and I will probably go to China.

 

Not now, of course. The research is not ready.  But when it is, I think the Chinese will bring it together first. That's why I'm studying Mandarin every day, one hour, without fail: tapes in the car, books by my bedside, little cards in my wallet.

 

When the time is right, I will borrow on my house again, like I did when Rome was injured, and we will go.

 

I will work with a Chinese spinal cord injury surgeon (some of whom already do 300 traditional spinal cord operations in a year), and a scientist or two, make sure everyone knows exactly what has to be done (always assuming Roman agrees, of course) telling them in two languages exactly the mix of stem cells and neurotrophic agents or whatever has to be administered.    

 

After the operation, I figure it will take six months of rehabilitation, which we will do in China also, because we could not afford it here, even borrowing on the house.

 

Why China? Why not stay in my own land, especially since I honestly believe the research breakthroughs will happen here?

 

There is an American option, of course. I will write about that in the near future.

 

But to go from idea to implantation, the way it looks now, there are too many road blocks in the way.  Naturally, I will be working to remove those obstacles, but… in a few minutes I will pick up my Chinese/English dictionary and start the morning practice.

 

Maybe I am wrong.

 

I hope I am.

 

But when I see cancer fear being systematically spread—even hyped!-- in the FDA report, it feels like they are just going through the motions, after which they fully intend to deny the trials.

 

Right now, as you know, the FDA orally notified Geron that the trials were "on hold", for unspecified reasons.

 

Geron is waiting for a letter from the FDA explaining those reasons.  

 

It is my guess the FDA will deny the trials. The letter will say something like there are too many risks for the trials to go forward at this time, and here are a list of impossible conditions that must be met first, before embryonic stem cell research is allowed a chance.

 

If I am wrong, fine.

 

Some good people tell me, don't worry, be patient, just wait-- the next President will fix things.

 

But what if the FDA establishes guidelines that are impossible to meet, and those guidelines have to be overturned before human trials can take place?

 

It will be very hard for new FDA scientists to overturn safety standards, even misguided ones.

 

If the stem cell trials are blocked by unfair tactics, like setting the safety bar impossibly high, you and I will need to speak up.

 

Start thinking about this. Discuss it with your friends. Think about groups you belong to, media folks you may know.

 

Get ready.

 

Don Reed

www.stemcellbattles.com

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British Journal of Cancer - Table of Contents alert Volume 98 Issue 11

British Journal of Cancer (BJC) publishes full research papers and
short communications under five broad headings: clinical studies,
translational therapeutics, molecular diagnostics, genetics and
genomics, and epidemiology. BJC also commissions a very successful
series of minireviews on highly topical subjects.
Click here to read two free sample issues online:
http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0EN50EF

British Journal of Cancer
27 May 2008, Volume 98, Issue 11
Table of Contents

Editorial

1729 The screening mammography paradox: better when found, perhaps
better not to find
D A Berry

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMR0Ed

_____________________________________________________________________

Reviews

1731 Circulating endothelial cells in oncology: pitfalls and promises
M H Strijbos, J W Gratama, J Kraan, C H Lamers, MA den Bakker & S
Sleijfer
http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMS0Ee

1736 Risks and benefits of bisphosphonates
R E Coleman

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMS0Ee


_____________________________________________________________________

Clinical Studies

1741 Screen-detected vs symptomatic breast cancer: is improved
survival due to stage migration alone?

G C Wishart, D C Greenberg, P D Britton, P Chou, C H Brown, A D
Purushotham & S W Duffy
http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMT0Ef
_____________________________________________________________________

1745 Factors that predict early treatment failure for patients with
locally advanced (T4) breast cancer

E Montagna, V Bagnardi, N Rotmensz, J Rodriguez, P Veronesi, A
Luini, M Intra, E Scarano, A Cardillo,
R Torrisi, G Viale, A Goldhirsch & M Colleoni

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMU0Eg
_____________________________________________________________________

1753 Changes of bone turnover markers and serum PTH after night or
morning administration of zoledronic acid in breast cancer patients
with bone metastases
D Generali, A Dovio, M Tampellini, M Tucci, S Tedoldi, M Torta, S
Bonardi, G Allevi,
S Aguggini, M Milani, A L Harris, A Bottini, L Dogliotti, A
Angeli & A Berruti

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMV0Eh
_____________________________________________________________________

1759 Radiographer gender and breast-screening uptake
P Fitzpatrick, A Winston & T Mooney

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMW0Ei
_____________________________________________________________________

1762 A pharmaco-economic analysis of second-line treatment with
imatinib or sunitinib in patients with advanced gastrointestinal
stromal tumours

I Contreras-Hernández, J F Mould-Quevedo, A Silva, G
Salinas-Escudero, M A Villasís-Keever,
V Granados-García, G Dávila-Loaiza, J A Petersen & J
Garduño-Espinosa

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMX0Ej
_____________________________________________________________________

1769 Enhancing treatment decision-making: pilot study of a treatment
decision aid in stage IV non-small cell lung cancer
N B Leighl, F A Shepherd, D Zawisza, R L Burkes, R Feld, J
Waldron, A Sun,
D Payne, A Bezjak & M H N Tattersall

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMY0Ek
_____________________________________________________________________

1774 A phase Ib trial of docetaxel, carboplatin and erlotinib in
ovarian, fallopian tube and primary peritoneal cancers

P A Vasey, M Gore, R Wilson, G Rustin, H Gabra, J-P Guastalla, E
P Lauraine, J Paul,
K Carty & S Kaye on behalf of the Scottish Gynaecological Cancer
Trials Group
http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMZ0El
_____________________________________________________________________

1781 Inverse association of NSAID use and ovarian cancer in relation
to oral contraceptive use and parity
K J Wernli, P A Newcomb, J M Hampton, A Trentham-Dietz & K M Egan

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMa0Es
_____________________________________________________________________

Translational Therapeutics
_____________________________________________________________________
1784 Characterisation of tumour vasculature in mouse brain by USPIO
contrast-enhanced MRI

G Gambarota, W Leenders, C Maass, P Wesseling, B van der Kogel,
O van Tellingen & A Heerschap
http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMb0Et
_____________________________________________________________________

1790 Knocking down gene expression for growth hormone-releasing
hormone inhibits proliferation of human cancer cell lines
N Barabutis & A V Schally

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMc0Eu
_____________________________________________________________________

1797 Differential effects of ketoconazole on exposure to temsirolimus
following intravenous infusion of temsirolimus
J P Boni, C Leister, J Burns & B Hug
http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMd0Ev
_____________________________________________________________________

1803 Cisplatin alters nitric oxide synthase levels in human ovarian
cancer cells: involvement in p53 regulation and cisplatin resistance
E L Leung, M Fraser, R R Fiscus & B K Tsang
http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMe0Ew
_____________________________________________________________________

1810 SPARC promoter hypermethylation in colorectal cancers can be
reversed by 5-Aza-2'deoxycytidine to increase SPARC expression and
improve therapy response
S Cheetham, M J Tang, F Mesak, H Kennecke, D Owen & I T Tai
http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMf0Ex
_____________________________________________________________________

Molecular Diagnostics

_____________________________________________________________________


1820 MMP-2 geno-phenotype is prognostic for colorectal cancer
survival, whereas MMP-9 is not

A M J Langers, C F M Sier, L J A C Hawinkels, F J G M Kubben, W
van Duijn, J J van der Reijden, C B H W Lamers,
D W Hommes & H W Verspaget
http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMg0Ey
_____________________________________________________________________

1824 Mitotic centromere-associated kinesin is a novel marker for
prognosis and lymph node metastasis in colorectal cancer
K Ishikawa, Y Kamohara, F Tanaka, N Haraguchi, K Mimori, H Inoue
& M Mori

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMh0Ez
_____________________________________________________________________

1830 Prognostic molecular markers with no impact on decision-making:
the paradox of gliomas based on a prospective study
M Wager, P Menei, J Guilhot, P Levillain, S Michalak, B Bataille,
J-L Blanc, F Lapierre,
P Rigoard, S Milin, F Duthe, D Bonneau, C-J Larsen & L
Karayan-Tapon

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMi0E1
_____________________________________________________________________

1839 Mitochondria-dependent signalling pathway are involved in the
early process of radiation-induced bystander effects

S Chen, Y Zhao, W Han, G Zhao, L Zhu, J Wang, L Bao, E Jiang, A
Xu, T K Hei, Z Yu & L Wu

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMj0E2
_____________________________________________________________________

1845 Aberrant CDKN1A transcriptional response associates with abnormal
sensitivity to radiation treatment

C Badie, S Dziwura, C Raffy, T Tsigani, G Alsbeih, J Moody, P
Finnon, E Levine, D Scott & S Bouffler

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMk0E3
_____________________________________________________________________

Epidemiology
_____________________________________________________________________
1852 Diagnostic radiation procedures and risk of prostate cancer
P Myles, S Evans, A Lophatananon, P Dimitropoulou, D Easton, T
Key, R Pocock, D Dearnaley,
M Guy, S Edwards, L O'Brien, B Gehr-Swain, A Hall, R Wilkinson, R
Eeles & K Muir

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMl0E4
_____________________________________________________________________


1857 Opium, tobacco, and alcohol use in relation to oesophageal
squamous cell carcinoma in a high-risk area of Iran
D Nasrollahzadeh, F Kamangar, K Aghcheli, M Sotoudeh, F Islami,
C C Abnet, R Shakeri,
A Pourshams, H A Marjani, M Nouraie, M Khatibian, S Semnani, W
Ye, P Boffetta, S M Dawsey & R Malekzadeh
http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMm0E5
_____________________________________________________________________

1864 Association of physical activity with cancer incidence,
mortality, and survival: a population-based study of men
N Orsini, C S Mantzoros & A Wolk
http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMm0E5
____________________________________________________________________

1870 Incidence of interstitial pneumonitis among breast cancer
patients: a 10-year Danish population-based cohort study
S Christensen, L Pedersen, M Grijota, J B Kornum, A Beiderbeck &
H T Sørensen

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMn0E6
____________________________________________________________________
1876 Lower breast cancer survival in mothers of children with a
malignancy: a national study
H Olsson, S Magnusson & A Bladström

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMn0E6
____________________________________________________________________

Letter to the Editor

____________________________________________________________________

1879 Japanese mobile phone study
B Hocking

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMn0E6
____________________________________________________________________
Corrigendum
____________________________________________________________________
1880 The E3 ubiquitin ligase EDD is an adverse prognostic factor for
serous epithelial ovarian cancer and modulates cisplatin resistance in
vitro
P M O'Brien, M J Davies, J P Scurry, A N Smith, C A Barton, M J
Henderson, D N Saunders,
B S Gloss, K I Patterson, J L Clancy, V A Heinzelmann-Schwarz, R
Murali, R A Scolyer,
Y Zeng, E D Williams, L Scurr, A DeFazio, Di Quinn, C K W Watts,
N F Hacker, S M Henshall & R L Sutherland

http://ealerts.nature.com/cgi-bin24/DM/y/elAf0Xztnp0Hhi0BwMo0E7
____________________________________________________________________


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Signaling Update contents for 30 May 2008

*********************************************************************
Signaling Gateway - 30 May 2008
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0M40Eg
*********************************************************************

Signaling Update is a one-stop online resource designed to keep you
in touch with the latest and most exciting research in cell
signaling. New content is uploaded every Friday.

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

In Signaling Update this week:

------------------------
Featured Article
------------------------
ANGIOGENESIS: PI3K SUBUNITS BRANCH OUT

The catalytic subunits of class IA phosphoinositide 3-kinases (PI3K)
are activated by distinct signals and have discrete roles in
angiogenesis and vascular remodeling.

Original research paper: Nature 453, 662-666 (2008)

http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0vP0Ep

-------------------------
Signaling Survey
-------------------------
SIGNALING GATEWAY SURVEY: WHAT DO YOU THINK?
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0Bvd80ED

The Signaling Gateway team invites you to complete a brief online
survey on the usability of the site for the chance to win a FREE iPod
Touch or two-year subscription to Nature. Your feedback will help
ensure that we continue to present content and information that meet
your needs. To complete the survey and enter the prize draw, please
click here.

-------------------
Selected Updates
-------------------
MECHANISMS OF DISEASE: STRESS AND DISEASE CONNECT AT mTORC1
Loss of tuberous sclerosis complex (Tsc) genes causes constitutive
activation of mTOR, leading to endoplasmic reticulum (ER) stress and
dysregulation of insulin receptor signaling.
Original research paper: Mol. Cell 29, 541-551 (2008)
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0BwKR0EF

SIGNALLING: AN ONCOGENE BECOMES RESTLESS
The abundance of the protein REST (repressor-element-1 silencing
transcription factor) is regulated by a cell cycle-dependent
ubiquitin pathway.
Original research paper: Nature 452, 365-369 (2008)
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0BwKS0EG

CELL FATE: THE PATH TO NEUROGENESIS
In mice, oxidative conditions increase the interaction between the
histone deacetylase Sirt1 and the transcription factor Hes1, which
represses expression of the pro-neuronal-fate transcription factor
Mash1 and promotes differentiation of neural progenitor cells.
Original research paper: Nature Cell Biol. 10, 385-394 (2008)
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0BwKT0EH

More Updates:
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0vO0Eo

------------------------
Research Library
------------------------
p53 REGULATES GLUCOSE METABOLISM THROUGH AN IKK-NF-kappaB PATHWAY
AND INHIBITS CELL TRANSFORMATION
Nature Cell Biology 10, 611-618 (2008)
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0BwKU0EI

SPHEROID-BASED ENGINEERING OF A HUMAN VASCULATURE IN MICE
Nature Methods 5, 439-445 (2008)
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0BwKV0EJ

IDENTIFICATION OF RIP1 KINASE AS A SPECIFIC CELLULAR TARGET OF
NECROSTATINS
Nature Chemical Biology 4, 313-321 (2008)
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0BwKW0EK


------------------------
Signaling News
------------------------
MARINE MICROBIOLOGY: ORIGINS OF DEATH
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0Bv3j0EE

Programmed cell death is usually seen as the unique prerogative of
plants and animals. However, plankton and photosynthetic cyanobacteria
undergo a process strikingly similar to apoptosis. Plankton diatoms
that contain high levels of nitric oxide grow slowly and are highly
sensitive to stress, and activate as many as six metacaspases during
their cell-death program.

More News
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0Crw0EX

-------------------------
Gateway Updates
-------------------------
NCI-NATURE PATHWAY INTERACTION DATABASE - MAY UPDATE
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0BGyx0Ep

The Pathway Interaction Database is a free, high-quality resource of
signaling pathways in human cells for biologists and bioinformaticians
to explore, visualize and mine signaling events.

This month's update features:
Cardiovascular signaling mediated by endothelins,

http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0Buvs0ET

BMP receptor signaling

http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0Buvt0EU

and a

Bioinformatics primer on GenMAPP
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0BsEP0E2
http://ealerts.nature.com/cgi-bin24/DM/y/elEX0Xztnp0H2W0BwKX0EL

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Professorship positions
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Location: Vienna, Austria
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Molecular Microbiology. The cell signaling candidate should focus on
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Oncogene Table of Contents alert Volume 27 Issue 24

ONCOGENE

May 2008 Volume 27 Number 24, pp 3361 - 3500

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Celebrating over 20 years of excellence in cancer research

Oncogene is published weekly and covers the structure and function of
oncogenes.

Visit the website at:
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What is Oncogene Reviews?

Oncogene Reviews - an in-depth look into hot topics in cancer
research.

Each year Oncogene publishes a series of review issues that take a
closer look into the most current research and advances that are
impacting the study of cancer. Visit
http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0Hi30Ex to read the latest
articles from Oncogene Reviews!

----------------------
ORIGINAL ARTICLES
----------------------
A PARP-1//JNK1 cascade participates in the synergistic apoptotic
effect of TNF[alpha] and all-trans retinoic acid in APL cells
J Mathieu, M Flexor, M Lanotte and F Besancon
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEH0Eb
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEI0Ec

Chaperone-dependent stabilization and degradation of p53 mutants
P Muller, R Hrstka, D Coomber, D P Lane and B Vojtesek
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEJ0Ed
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEK0Ee

SIRT1 negatively regulates HDAC1-dependent transcriptional repression
by the RBP1 family of proteins
O Binda, C Nassif and P E Branton
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEL0Ef
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEM0Eg

Caspase-2 is required for cell death induced by cytoskeletal
disruption
L H Ho, S H Read, L Dorstyn, L Lambrusco and S Kumar
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEN0Eh
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEO0Ei

Hepatitis B virus X protein induces the expression of MTA1 and HDAC1,
which enhances hypoxia signaling in hepatocellular carcinoma cells
Y-G Yoo, T-Y Na, H-W Seo, J K Seong, C K Park, Y K Shin and M-O Lee
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEP0Ej
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEQ0Ek

A new fusion gene NUP98-IQCG identified in an acute
T-lymphoid//myeloid leukemia with a t(3;11)(q29q13;p15)del(3)(q29)
translocation
Q Pan, Y-J Zhu, B-W Gu, X Cai, X-T Bai, H-Y Yun, J Zhu, B Chen, L
Weng, Z Chen, Y-Q Xue and S-J Chen
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwER0El
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwES0Em

N-myc augments death and attenuates protective effects of Bcl-2 in
trophically stressed neuroblastoma cells
A Ushmorov, M D Hogarty, X Liu, H Knausz, K M Debatin and C Beltinger
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwET0En
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEU0Eo

Mechanisms of enhancement of TRAIL tumoricidal activity against human
cancer cells of different origin by dipyridamole
A E Goda, T Yoshida, M Horinaka, T Yasuda, T Shiraishi, M Wakada and T
Sakai
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEV0Ep
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEW0Eq

TGF[beta]-mediated apoptosis of Burkitt's lymphoma BL41 cells is
associated with the relocation of mitochondrial BimEL
C Clybouw, B E L Mchichi, A Hadji, A Portier, M T Auffredou, D
Arnoult, G Leca and A Vazquez
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEX0Er
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEY0Es

HBV X protein targets hBubR1, which induces dysregulation of the
mitotic checkpoint
S Kim, S-Y Park, H Yong, J K Famulski, S Chae, J-H Lee, C-M Kang, H
Saya, G K Chan and H Cho
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEZ0Et
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEa0E1

Overexpression//enhanced kinase activity of BCR//ABL and altered
expression of Notch1 induced acute leukemia in p210BCR//ABL transgenic
mice
T Mizuno, N Yamasaki, K Miyazaki, T Tazaki, R Koller, H Oda, Z-i
Honda, M Ochi, L Wolff and H Honda
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEb0E2
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEc0E3

Cdc7 kinase mediates Claspin phosphorylation in DNA replication
checkpoint
J M Kim, N Kakusho, M Yamada, Y Kanoh, N Takemoto and H Masai
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEd0E4
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEe0E5

----------------------
SHORT COMMUNICATIONS
----------------------
Suppression of PPN//MG61 attenuates Wnt//[beta]-catenin signaling
pathway and induces apoptosis in human lung cancer
Z Chen, J Li, Q S Li, J Q Fan, X M Dong, J P Xu, X M Wang, G W Yang, P
Yan, G Z Wen, Y T Zhang, R G Niu, P H Nan, J He and H M Zhou
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEf0E6
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEg0E7

PU.1 binding to the p53 family of tumor suppressors impairs their
transcriptional activity
M P Tschan, V A Reddy, A Ress, G Arvidsson, M F Fey and B E Torbett
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEh0E8
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEi0EA

The Src-like adaptor protein regulates PDGF-induced actin dorsal
ruffles in a c-Cbl-dependent manner
A Sirvent, C Leroy, A Boureux, V Simon and S Roche
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEj0EB
Article: http://ealerts.nature.com/cgi-bin24/DM/y/elCp0Xztnp0Hjk0BwEk0EC


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[StemCells] Stopping Cancer AND turning mature to SC

May 15, 2008

Adult Cells Steal Trick from Cancer to Become Stem Cell-Like
A route used by tumor cells to spread could be exploited to make stem
cells for regenerative medicine and cancer therapies
By Nikhil Swaminathan

In a boon to cancer treatment and regenerative medicine, scientists
have discovered that a trick used by tumor cells that allows them to
migrate around the body can cause normal, adult cells to revert into
stem cell–like cells.

Large quantities of these reverted cells could be used to treat
anything from spinal cord injury to liver damage without the risk of
tissue rejection, said Robert Weinberg, a biologist at the
Massachusetts Institute of Technology's Whitehead Institute for
Biomedical Research and co-author of a study appearing in Cell.
Learning more about how cancer cells move around the body is also
providing scientists with new insights that could thwart the spread
of the disease.

The key to the process is a better understanding of developmental
changes in the body's two primary cell types: epithelial cells (those
that constitute the skin and most internal organs) and mesenchymal
cells (which make up connective tissue). The key difference between
the two cell categories is that epithelial cells adhere very tightly
to one another, making sheetlike layers, whereas mesenchymal cells
are only loosely bound and can migrate within the body. In the
developing embryo, an initial group of epithelial cells undergoes a
shift called an "epithelial to mesenchymal transition" (EMT) to form
bones, blood and cartilage as well as the heart.

Likewise, some cancerous cells can perform a temporary EMT
transformation to the mobile mesenchymal form. The conversion
improves the cells' tumor-forming ability, cutting the number of
tumor cells required to form a carcinoma from one million to just
10,000, the researchers say.

"More than 80 percent of cancer in humans occurs in epithelial
cells," says study co-author Sendurai Mani, an assistant professor of
molecular pathology at the University of Texas' M.D. Anderson Cancer
Center in Houston and a former postdoc in Weinberg's lab. Previous
work in Weinberg's lab had shown that after a tumor forms in one part
of the body, some of the cancer cells undergo EMT, Mani explains. The
now-mesenchymal cells can then travel to a remote site, where they
eventually convert back to their epithelial state and clump together
into a secondary tumor.

Working with human breast tissue, the new study's authors attempted
to induce EMT in normal cells; they figured they would just get
fibroblasts, a type of connective tissue that is important in wound
healing. When they looked closely, however, they noted that the
transformed cells had surface proteins that were common to stem
cells. Cultured in the lab, the changed cells showed an ability to
differentiate into (or become) two discrete cells found in breast
tissue. And the transformed cells proved to be very similar to actual
stem cells from both mice and humans.

"What we're doing is inducing dedifferentiation," Mani says. He noted
that it's not yet clear how far these cells can go down the path to
immaturity—and, with it, the ability to become any tissue in the
body. "We found, surprisingly, that EMT and stem cells could be
linked; we show that, yes, they are very closely linked."

Mani says that the scientists may next pursue two paths: The team can
determine how to stop cancer cells from undergoing this
transformation in the first place. Second—a path they are already
pursuing—they can gauge these transformed adult cells' worth as stem
cell surrogates for regenerative medicine.

As far as the promise of regenerative therapies, the team will
attempt to determine just how stem cell–like these cells are by
inducing EMT in epithelial cells from the mammaries of mice to see if
they can grow a breast in the lab. If they succeed, they can be
reasonably confident that epithelial cells can be taken from a
patient and used to regenerate damaged tissue in that same person.

http://www.sciam.com/article.cfm?id=adult-cells-steal-trick-f

__._,_.___
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StemCells subscribers may also be interested in these sites:

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The CNS Healing Group
http://groups.yahoo.com/group/CNS_Healing
____________________________________________
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[StemCells] Slowing ALS - Marrow SCs

Media Release | May 26, 2008
Vancouver Researchers Pioneer Safe Pathway to Slow ALS Using Stem
Cells
A unique pilot study has established a safe pathway for using bone-
marrow stem cells to slow down and potentially treat Amyotrophic
Lateral Sclerosis (ALS), a fatal neurodegenerative disease without
cure.

The study, published in the journal, Muscle & Nerve and led by Dr.
Neil Cashman, professor of neurology at The University of British
Columbia and director of the ALS program at Vancouver Coastal Health
and VCH Research Institute, tested the use of a growth factor
stimulant in ALS patients and found that bone-marrow stem cells
became activated with no adverse effects to patients.

"Our idea was to use a growth factor stimulant to increase the number
of circulating stem cells from within the body's bone marrow where
they would have the potential to travel to the site of injury and
begin repair, slowing down the progression of ALS," says Cashman, who
also holds the Canada Research Chair in Neurodegeneration and Protein
Misfolding Diseases at UBC and is a member of the Brain Research
Centre at UBC Hospital.

"This pathway, if one day successful, may provide a new therapy that
will avoid the ethical debate surrounding embryonic stem cells," says
Cashman.

Growth factors are proteins that can stimulate cell division. They
occur naturally in the human body and can also be developed in a
laboratory. Stem cells serve as a "repair system" in the human body
and have the potential to develop and divide into many different cell
types.

"The project was complex because growth factors have the potential to
activate the wrong cells in the brain and spinal cord, which could be
harmful to ALS patients" says Cashman.

The researchers identified Granulocyte Colony Stimulating Factor (G-
CSF) as the safest possible growth factor to use. They then conducted
the pilot trial to establish safety and measure stem cell
mobilization.

"We were able to measure a prominent effect on stem cell mobilization
and found no adverse effects in the patients," said Cashman. "There
have been many misgivings in using stem cell stimulators in ALS
patients but now we know we can safely do this. This is an important
first step in providing a new treatment for ALS."

The research team is now developing a larger scale multicentre trial
to look at therapeutic effect. This trial is at least one year away
from beginning.

ALS is a progressive and ultimately fatal neurodegenerative disease
that produces weakness, atrophy – partial or complete wasting away of
a part of the body, and spasticity – continuous contracting of
certain muscles. It results from progressive degeneration of motor
neurons in the brain, brainstem, and spinal cord. There is no cure
for ALS and to date the only registered pharmacological treatment is
riluzole, which slows the progression of the disease on average by 10-
15 per cent. New effective therapies are greatly needed to slow or
halt this disease.

The Webster Foundation in Montreal through the VGH & UBC Hospital
Foundation in Vancouver, as well as the Temerty Family Foundation in
Toronto provided funding for this study. The co-authors include Dr.
Andy Eisen (senior author), professor Emeritus, Neurology, University
of British Columbia and former director Vancouver Coastal Health ALS
program; and Dr. Charles Krieger, associate professor of
kinesiology, Simon Fraser University, professor, neurology, clinical
associate professor, Neurology, University of British Columbia, and
clinician researcher VCH ALS program.

VCHRI is the research body of Vancouver Coastal Health Authority. In
academic partnership with UBC, the institute advances health research
and innovation across B.C., Canada, and beyond. www.vchri.ca

The Faculty of Medicine at UBC provides innovative programs in the
health and life sciences, teaching students at the undergraduate,
graduate and postgraduate levels, and generates more than $200
million in research funding each year.

The Brain Research Centre at UBC Hospital is a multidisciplinary
centre dedicated to improving understanding and finding new
treatments for brain diseases. The centre is a partnership of the
University of British Columbia and Vancouver Coastal Health Research
Institute.

- 30 -
Contact
Catherine Loiacono
UBC Public Affairs
Tel: 604.822.2644
Cell: 604.209.3048
E-mail: catherine.loiacono@ubc.ca

Lisa Carver
VCHRI Communications
Tel: 604.875.4111, loc. 61777
Cell: 604.319.7533
E-mail: lisa.carver@vch.ca




Last reviewed 29-May-2008
http://www.publicaffairs.ubc.ca/media/releases/2008/mr-08-061.html

__._,_.___
____________________________________________
«¤»¥«¤»§«¤»¥«¤»§«¤»¥«¤»«¤»¥«¤»§«¤»¥«¤»§«¤»¥«
¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯¯
StemCells subscribers may also be interested in these sites:

Children's Neurobiological Solutions
http://www.CNSfoundation.org/

Cord Blood Registry
http://www.CordBlood.com/at.cgi?a=150123

The CNS Healing Group
http://groups.yahoo.com/group/CNS_Healing
____________________________________________
«¤»¥«¤»§«¤»¥«¤»§«¤»¥«¤»«¤»¥«¤»§«¤»¥«¤»§«¤»¥«
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