Archive for the ‘Gene Therapy Research’ Category

BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) announced today that it has submitted a supplemental Biologics License Application (sBLA) to the U.S. Food and Drug Administration (FDA) supporting the use of ADCETRIS (brentuximab vedotin) for retreatment and extended duration beyond 16 cycles of therapy in relapsed Hodgkin lymphoma (HL) and systemic anaplastic large cell lymphoma (sALCL). ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30, a defining marker of HL and sALCL, that was granted accelerated approval by the FDA in August 2011 for relapsed HL and relapsed sALCL.

The sBLA submission includes data demonstrating ADCETRIS activity in managing HL and sALCL when used in the retreatment setting, as well as beyond the 16 cycles described in our current label, while retaining a manageable safety profile, said Clay B. Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. Our goal is to broaden the ADCETRIS U.S. labeling claims to provide both patients and physicians the opportunity to incorporate ADCETRIS into additional HL and sALCL treatment settings. The sBLA submission includes data that support these uses and we look forward to the regulatory outcome.

The sBLA is based on results from a phase II clinical trial with two treatment arms. One arm evaluated retreatment with ADCETRIS in patients who previously responded to treatment with ADCETRIS, then discontinued treatment and subsequently had disease progression or relapse. The other arm allowed treatment extension and evaluated prolonged treatment with ADCETRIS beyond 16 cycles of therapy. The sBLA submission includes updated data sets from this phase II trial. Preliminary data from this trial were previously reported at the 2011 American Society of Hematology (ASH) Annual Meeting and at the 2012 American Society of Clinical Oncology (ASCO) Annual meeting.

At the 2012 ASCO Annual Meeting, retreatment data from the phase II trial were reported from 23 patients, including one patient who was treated twice. Patients had received a median of four prior systemic therapies, including ADCETRIS. Of 23 evaluable patients, 70 percent (16 of 23) achieved an objective response after retreatment with ADCETRIS, including nine complete remissions and seven partial remissions. Median duration of retreatment objective response was 8.8 months. Among retreated HL patients, nine of 16 (56 percent) achieved an objective response. Among retreated sALCL patients, seven of eight (88 percent) achieved an objective response. The most common adverse events were peripheral neuropathy (46 percent), nausea (42 percent), fatigue (38 percent), diarrhea (33 percent) and fever (29 percent).

At the 2011 ASH Annual Meeting, prolonged treatment data were reported from 17 patients with a median duration of treatment of 17.3 months (approximately 24 cycles of every three week dosing). The overall objective response rate with extended treatment was 88 percent, including 76 percent complete remissions and 12 percent partial remissions. ADCETRIS was generally well-tolerated, with the most common adverse events being peripheral neuropathy (71 percent), upper respiratory infection (53 percent) and fatigue (47 percent). Prolonged treatment with ADCETRIS was associated with clinically meaningful durations of response without worsening of toxicity over time.

ADCETRIS is currently not approved for retreatment and extended duration beyond 16 cycles of therapy in relapsed HL and sALCL.

About Lymphoma

Lymphoma is a general term for a group of cancers that originate in the lymphatic system. There are two major categories of lymphoma: Hodgkin lymphoma and non-Hodgkin lymphoma. Hodgkin lymphoma is distinguished from other types of lymphoma by the presence of one characteristic type of cell, known as the Reed-Sternberg cell. The Reed-Sternberg cell generally expresses CD30. Systemic ALCL is an aggressive type of T-cell non-Hodgkin lymphoma that also expresses CD30.

About ADCETRIS

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Seattle Genetics Submits Supplemental BLA to FDA for Retreatment and Extended Duration of Therapy with ADCETRIS® ...

By Carol Davis

PUBLISHED: 19:49 EST, 18 March 2013 | UPDATED: 19:49 EST, 18 March 2013

A new form of gene therapy could help thousands with an inherited eye condition that leads to blindness and possibly treat age-related macular degeneration and glaucoma.

Nick Tuftnell, 36, an IT consultant from Bristol, was the third in the world to have the operation.

'Over the next few years, my peripheral vision became worse,' said Nick Tuftnell

My grandfather was partially sighted, so Ive always known eye disease runs in the family. I remember having to watch out for him when I was younger.

When I was a teenager rushing to a cricket match at Lords, I forgot to warn him about a kerb, so he tripped.

But because my vision was fine, I didnt worry about myself too much until I was 17 and wanted my driving licence.

To check I could see properly, and aware of my family history, my ophthalmologist referred me to the specialist my grandad saw at Moorfields Eye Hospital in London.

Although my vision was fine, the specialist confirmed what wed suspected that like my grandad, I had choroideremia.

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Eye condition: Injecting a virus into my eye saved my sight

BOSTON - A unique new cancer treatment uses gene therapy to induce a cancer-fighting immune response whose intensity can then be controlled with a pill. The combination could help tailor treatment to a patients individual response.

The treatment uses the bodys own cells or tumor cells to produce extra copies of a naturally occurring hormone-like molecule called IL-12, which regulates anticancer immune responses. Last week, Ziopharm Oncology announced a clinical study of the treatment for patients with breast cancer. The company is already testing it in patients with melanoma.

Many researchers have explored techniques that rev up the natural response the body uses to detect and attack cancerous cells (see, for example, Engineering Better Immune Cells and Priming the Body to Tackle Cancer). But controlling the killer cells of the immune system can sometimes be a challenge, as researchers found in the 1990s when cancer patients who were given IL-12 in a clinical trial died from toxic side effects.

IL-12 is a very potent [immune system regulator] and can generate a lot of side effects, says Per Basse, a physician-scientist at the University of Pittsburgh School of Medicine, who studies immune cells and their ability to fight cancer. As a clinician, I would like to be able to dial it up and down so that if it all starts to look not so good, you can stop the process, he says.

To avoid the dangerous side of the molecule, Ziopharms system is designed to control IL-12 with a combined genetic and pharmaceutical switch. A virus is injected into the tumor to deliver the gene for IL-12. The gene starts out in off mode, so it doesnt actually produce any IL-12. To activate the gene, a patient has to take a pill that delivers another molecule. The advantage is that any patient who starts to experience nasty side effects from the IL-12 can stop taking the pill. If things go awry, you have an escape valve, says Ziopharms CEO, Jonathan Lewis.

The key to the inducible system is a version of the receptor that controls molting in arthropods (insects, spiders, and crustaceans), modified so that it determines whether the IL-12 gene is on. The gene for that receptor, which is also delivered into the body by a virus, is always on, but its protein product and thus IL-12 expression is activated by the pill. Ziopharm licensed the control system from Intrexon for use in its oncology treatment.

The inducibility is a great idea, but the trick is getting something that you can get into the tumor, says Ralph Weichselbaum, a cancer researcher at the University of Chicago, who has worked on a cancer therapy induced by radiation. Currently, Ziopharm injects the gene-toting virus directly into patients tumors, but Lewis says the plan is to inject it into muscles in the future. Muscle cells are extremely good protein production factories, he says.

But even injecting the virus into a single tumor has an effect on other tumorsboth in lab animals and in humans. In animal studies, the tumor that receives the injection will at first get bigger because immune cells are accumulating in response to the IL-12. Then it will get smaller and go away, says Lewis. Tumors that received no injection will do the same thinggrow, then shrink, and then disappear. We are seeing similar things in people, says Lewis.

Eventually, the system could be used to deliver multiple genetic treatments at once, says Lewis. With one injection you could be able to control three or four [cancer-fighting] proteins in different ways.

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Cancer gene therapy activated by a pill provides personalized treatment

Osmosis | Osmosis Skin Care | Cell Therapy
http://www.skincarebyalana.com/osmosis.html Alana interviews osmosis pur medical skin care cell therapy.

By: Alana Mitchell

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Osmosis | Osmosis Skin Care | Cell Therapy - Video

Osmosis | Osmosis Skin Care | ATP Cell Therapy
Osmosis | Osmosis Skin Care | ATP Cell Therapy. Uploaded by Alana Mitchell on Mar 14 2013. httpwwwskincarebyalanacomosmosishtml Alana interviews osmosis pur medical skin care founder about ATP Cell Therapy.

By: Alana Mitchell

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Osmosis | Osmosis Skin Care | ATP Cell Therapy - Video

Stewart Brand: The dawn of de-extinction. Are you ready?
Throughout humankind #39;s history, we #39;ve driven species after species extinct: the passenger pigeon, the Eastern mountain lion, the dodo .... But now, says Stew...

By: TEDtalksDirector

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Stewart Brand: The dawn of de-extinction. Are you ready? - Video

March 18, 2013, 3 a.m.

There was no doubt in Chontell Johnson's mind. When a genetic test revealed her mother had early onset Alzheimer's, the then-27-year-old decided she would get tested, too.

''If I didn't know, I would spend the rest of my life second-guessing decisions,'' she says.

The results confirmed that within the three billion letters of Johnson's genome, a single mistake means she has a 98 per cent chance of developing the neurological condition that killed her mother at 47.

''It scares the life out of me to think I'll not be able to communicate with people,'' says Johnson, now 33.

When the human genome was first sequenced 13 years ago, it was hailed as a medical revolution, the catalyst for this new era of personalised medicine.

For most of the past decade, however, genetic testing remained an expensive tool for research laboratories only.

But in recent years, the technology to read a person's genome has advanced at a staggering pace. Now a vial of spit or blood and an internet connection is all anybody needs to peer inside their body's blueprint.

But while labs can sequence a person's DNA in a couple of days for less than $1000 - compared with the original human genome project, which took a decade and cost more than $2 billion - interpreting a person's 23,000 or so genes into something meaningful for their future health has proved much more complex.

In a small fraction of diseases, such as cystic fibrosis, Huntington's disease and early onset familial Alzheimer's, genetic mutations are the direct cause. If you have the mutation (or mutations), there is no escaping the disorder.

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Living with a time bomb

Call Girl
When the Griffins find themselves in a financial bind, Lois is forced to find a job of her own. She gets discovered by a "voiceover" talent agent named Randy...

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Call Girl - Video

Fukushima Symposium: Spent Fuel~An After Thought?
HELEN CALDICOTT FOUNDATION FUKUSHIMA SYMPOSIUM: 3-12-13 The Medical and Ecological Consequences of the Fukushima Nuclear Accident. Session Chair: Andrew Kant...

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Fukushima Symposium: Spent Fuel~An After Thought? - Video

DNA 12/03/2013 #1603; #1604; #1606; #1575; #1604; #1581; #1586; #1576; #1575; #1604; #1604; #1607; ...
http://www.facebook.com/FutureTvPrograms http://www.future.com.lb/ http://www.twitter.com/futuretvnews.

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DNA 12/03/2013 كلنا لحزب الله ... - Video

Dr. Wladimir Wertelecki - "Congenital Malformations in Rivne Polossia and Chernobyl Accident" [1/3]
"Congenital Malformations in Rivne Polossia and the Chernobyl Accident" by Dr. Wladimir Wertelecki (Former Chair of the Department of Medical Genetics, Unive...

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Dr. Wladimir Wertelecki - "Congenital Malformations in Rivne Polossia and Chernobyl Accident" [1/3] - Video

Dr. Wladimir Wertelecki - "Congenital Malformations in Rivne Polossia and Chernobyl Accident" [3/3]
"Congenital Malformations in Rivne Polossia and the Chernobyl Accident" by Dr. Wladimir Wertelecki (Former Chair of the Department of Medical Genetics, Unive...

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Dr. Wladimir Wertelecki - "Congenital Malformations in Rivne Polossia and Chernobyl Accident" [3/3] - Video

If your genes revealed you would get a disease, would you want to know?
A massive, groundbreaking new study underway at Kaiser Permanente and the University of California San Francisco may shed light one day on the genetic roots ...

By: PBSNewsHour

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If your genes revealed you would get a disease, would you want to know? - Video

The infamous and ingenious Ho Chi Minh Trail - Cameron Paterson
View full lesson: http://ed.ted.com/lessons/the-infamous-and-ingenious-ho-chi-minh-trail-cameron-paterson The Ho Chi Minh Trail not only connected North and ...

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The infamous and ingenious Ho Chi Minh Trail - Cameron Paterson - Video

FIVE POINTS, Calif., March 17, 2013 /PRNewswire/ -- S&W Seed Company (SANW) today announced that it has agreedtopurchase 100% ofSeed Genetics InternationalPty Ltd("SGI"), subject to due diligence and other customary conditions.The combination of S&W with Adelaide, Australia-based SGI will create the world 's largest non-dormant alfalfa seed company. The transaction, which is valued at approximately $16 million, is scheduled to close in early April 2013 and is expected to be immediately accretive to S&W's earnings.

Mark Grewal, president and chief executive officer of S&W Seed Company, commented, "This pact creates a powerhouse that will be unrivaled in its ability to breed and produce non-dormant alfalfa seed all year round.SGI has a tremendous base of contracted growers, very strong customer relationships, andunique genetics.The sales channels that S&W and SGI sell into are highly complementary,with very little overlap in customers. This move considerably strengthens our reach into Argentina and the rest of Latin America."

Grewal added, "I also want to stress the 'people factor.'S&W is gaining a highly competitive team of veteran seedsmen whom we know well and highly respect. We look forward to collaboration with them in all areas. By putting growers first, SGI's breeding program, initiated by Dr. Ross Downes and now continued by David Pengelly, has created grower-focused varieties that produce more seed per acre for the seed farmer than any other varieties in Australia, adding to seed farmer profits and potentially lowering cost of seed for S&W. We have the opportunity to merge David's work with that of S&W's own VP of Genetics and Breeding, Dan Gardner and our emeritus breeder,Bob Sheesley, who himself did pioneering work in salt tolerance and seed yield."

S&W is paying a purchase price ofapproximately $16million, over half of which consists of 865,000 shares S&W Common Stock and will result in SGI's owners becoming significant shareholders of S&W. The remaining considerationconsists of $5million in cash and$3million in the form of athree-yearpromissory note.Based on unaudited information, SGI hadrevenues of approximately AUD $18million for the fiscal year ended June 30, 2012 andhadpre-tax income of$1.6 million. SGI's assets consist primarily of accounts receivable, inventory, a tenured grower base and intellectual property, such as genetics.S&W intends to file audited financial resultsofSGIno later than 74 daysfrom closing,in compliance with SEC guidelines.

SGIcontrols approximately17,000 acres of irrigated alfalfa seed production under contract, and has first call on another 12,000acres of non-irrigated land that is rain dependent and has intermittent production. Australian seed yields per acre, even on irrigated fields, typically are materially lower than S&W's California yields and production costs are also materially lower.In 2013, SGIcontracted for alfalfa seed production with approximately 140contractfarmersin Southern Australia, all for SGI's proprietary varieties.In fiscal 2012, SGI's growers producedapproximately 5.5 million pounds, concluding a growing season that suffered from the impact of highly adverse weather conditions. The 2013 harvest is currently ongoing, but based on initial estimates, SGI managementis estimating that it will have approximately 8million pounds of alfalfa seed available for sale when the harvest concludes in late April 2013. Actual production could vary materially in either direction from estimates, due to unforeseen weather events and other factors.

SGIsells intointernational markets, includingthe Middle East and Africa (MENA), South America, and Southern Europe with the majority of the company's sales concentrated in the April through September time frame.

SGI was founded in 2002, with the goal of commercializing a seed breeding breakthrough by Dr. Ross Downes. Working with alfalfa in the mid 1990's, Dr. Downes had identified a particular trait that resulted in dramatically increased seed yields, even with less than optimum pollinator activity. The intellectual property stemming from Dr. Downes' pioneering work, which has been protected under international law and the Australian Plant Breeders Rights Act, became the cornerstone for over a decade of development by SGI's David Pengelly. SGI has developed well known proprietary varieties, such asSuperSonic, SuperNova, SuperStar, SuperCharge, SuperAurora, SuperSequal and SuperSiriver. Starting in 2002, the varieties developed by SGI quickly attracted a grower base that by 2012 enabled SGIto exceed 60%of Australian alfalfa seed production.SGI'salfalfa seed varieties are bred to resist disease, have tolerance to salt, create persistence in the field, and produce high seed yields in Australian production.The company also has a number of developments within its breeding program pertaining to dormant alfalfa varieties, tropical alfalfa seed varieties, and ease of pollination.

SGI, like S&W, considers the goodwill of its seed grower base to be of premier importance. SGI's contracts with seedfarmers under long term contracts that typically have initial terms of six years, extendable to ten years. To manage risk for itself and its growers, seed pricing is not fixed by contract, but instead based upon pooled production which is sold over an entire season, with a view to optimizing the prices realized. Due to its Southern Hemisphere location,SGIharvests seed in March through April, which is counter cyclical to S&W's July through October production in the Northern Hemisphere. The combined company will have the competitive advantages of year round production, which extends to all areas of the alfalfa seed business, including sales, inventory management and cash collection cycles.

Mark Harvey,Directorof Seed Genetics International, commented, "First, my thanks to S&W's Chairman, Grover Wickersham, and S&W's CFO, Matt Szot, for their long visits to Australia and their patience in negotiating over the last half year. While this is obviously a big move for us, the directors and management of SGI are trulyexcited about the advantages of a combined S&W/SGI and we want the challenge of continuing to build on what the four partners started."

Mr. Harvey expanded, "For our Australian growers, this means we willbeexpanding production under the umbrella of a public company with a strong balance sheet and financial resources. We also gain access to S&W's proven proprietary genetics. We look forward to collaborating with S&W's well respected breeder, Dan Gardner, who is well known by our own David Pengelly and Ross Downes. When we learned last year that Dan and our tough and respected sales and marketing competitor from IVS, Fred Fabre, had both joined S&W, it piqued ourinterest."

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S&W Seed Company To Acquire Seed Genetics International

Professor Dinggang Li, M.D. - gene therapy, Gendicine
Professor Dinggang Li md gene therapy Gendicine. Uploaded by Danni ElKher on Mar 14 2013. Itroduction of the hospitals of Phoenix Hosiptal Group Beijing Health Palace Hospital and Beijing Yanhua Phoenix Hospital with Professor Dinggang Li md in front Gene therapy also known as Gendicine has been proven to be very useful in the fight against cancer Scandinavian patients wwwkirurgirejserdk. Plu Mb 69.

By: Danni El-Kher

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Patients can turn off an experimental treatment if side effects get too bad.

A unique new cancer treatment uses gene therapy to induce a cancer-fighting immune response whose intensity can then be controlled with a pill. The combination could help tailor treatment to a patients individual response.

The treatment uses the bodys own cells or tumor cells to produce extra copies of a naturally occurring hormone-like molecule called IL-12, which regulates anticancer immune responses. Last week, Ziopharm Oncology announced a clinical study of the treatment for patients with breast cancer. The company is already testing it in patients with melanoma.

Many researchers have explored techniques that rev up the natural response the body uses to detect and attack cancerous cells (see, for example, Engineering Better Immune Cells and Priming the Body to Tackle Cancer). But controlling the killer cells of the immune system can sometimes be a challenge, as researchers found in the 1990s when cancer patients who were given IL-12 in a clinical trial died from toxic side effects.

IL-12 is a very potent [immune system regulator] and can generate a lot of side effects, says Per Basse, a physician-scientist at the University of Pittsburgh School of Medicine, who studies immune cells and their ability to fight cancer. As a clinician, I would like to be able to dial it up and down so that if it all starts to look not so good, you can stop the process, he says.

To avoid the dangerous side of the molecule, Ziopharms system is designed to control IL-12 with a combined genetic and pharmaceutical switch. A virus is injected into the tumor to deliver the gene for IL-12. The gene starts out in off mode, so it doesnt actually produce any IL-12. To activate the gene, a patient has to take a pill that delivers another molecule. The advantage is that any patient who starts to experience nasty side effects from the IL-12 can stop taking the pill. If things go awry, you have an escape valve, says Ziopharms CEO, Jonathan Lewis.

The key to the inducible system is a version of the receptor that controls molting in arthropods (insects, spiders, and crustaceans), modified so that it determines whether the IL-12 gene is on. The gene for that receptor, which is also delivered into the body by a virus, is always on, but its protein product and thus IL-12 expression is activated by the pill. Ziopharm licensed the control system from Intrexon for use in its oncology treatment.

The inducibility is a great idea, but the trick is getting something that you can get into the tumor, says Ralph Weichselbaum, a cancer researcher at the University of Chicago, who has worked on a cancer therapy induced by radiation. Currently, Ziopharm injects the gene-toting virus directly into patients tumors, but Lewis says the plan is to inject it into muscles in the future. Muscle cells are extremely good protein production factories, he says.

But even injecting the virus into a single tumor has an effect on other tumorsboth in lab animals and in humans. In animal studies, the tumor that receives the injection will at first get bigger because immune cells are accumulating in response to the IL-12. Then it will get smaller and go away, says Lewis. Tumors that received no injection will do the same thinggrow, then shrink, and then disappear. We are seeing similar things in people, says Lewis.

Eventually, the system could be used to deliver multiple genetic treatments at once, says Lewis. With one injection you could be able to control three or four [cancer-fighting] proteins in different ways.

See the rest here:
A Cancer Gene Therapy Activated by a Pill

Smallpox was eradicated completely in 1980. The only known stocks of the virus that causes smallpox are in carefully guarded laboratories in the U.S. and Russia. Nevertheless, the U.S. government is spending nearly $500 million for about two million doses of smallpox vaccine, according to a recent article in the New York Times.

Does this make sense? Well, yes and no. No one knows for sure whether there are unreported stocks of the virus somewhere, and if there are, whether they might fall into the wrong hands. Apparently the U.S. government thinks that it would be prudent to have a stock of smallpox vaccine on hand, just in case the smallpox virus is used someday in a bioterrorism attack.

Only time will tell whether stockpiling smallpox vaccine will prove to be a $500 million waste of money or a lifesaver. But while you’re considering whether you think it’s a good idea, consider this; if there is an outbreak of smallpox some day, who will be able to get the vaccine? Two million doses wouldn’t cover even a quarter of the population of New York City alone. How much of this vaccine should we be stockpiling?Source:
http://humanbiologyblog.blogspot.com/2013/03/stockpiling-smallpox-vaccine_14.html

Cell Therapy for Myeloma and Lymphoma by Dr Larry Kwak
Dr Larry Kwak, Professor and Chair of the department of Myeloma and Lymphoma at MD Anderson Cancer Center, Houston gave an update on the progress in cell the...

By: TheMedalGroup

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Cell Therapy for Myeloma and Lymphoma by Dr Larry Kwak - Video

Cell Therapy for Allogeneic Stem Cell Transplant by Dr Richard Champlin
Dr Richard Champlin, Professor and Chair of the department of Stem Cell Transplant and Cellular Therapy gave an update on the role of Cell Therapy in improvi...

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Cell Therapy for Allogeneic Stem Cell Transplant by Dr Richard Champlin - Video

STEM CELL Therapy thru Laminine_Part-1(new link)
STEM CELL Therapy thru laminine_part1new link. Uploaded by cabmon0001 on Mar 14 2013. cabmon 0001.

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STEM CELL Therapy thru Laminine_Part-1(new link) - Video

STEM CELL Therapy thru Laminine_Part-2(new link)
STEM CELL Therapy thru laminine_part2new link. Uploaded by cabmon0001 on Mar 14 2013. cabmon 0001.

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Gene breakthrough welcomed by Daisy's Eye Cancer Fund

10:20am Saturday 16th March 2013 in News

AN Oxford-based charity supporting young children suffering eye cancer has welcomed a breakthrough in research.

Abby White, 36, from Iffley, runs Daisys Eye Cancer Fund, which supports families whose children suffer retinoblastoma. Retinoblastoma is a rapidly developing eye cancer affecting about 45 babies a year in the UK under the age of five. Ms White inherited the condition from her father and set up the charity in 2004.

The funds medical director Dr Brenda Gallie, based in Toronto, Canada, has published new findings in Lancet Oncology, which are set to change clinical practice.

She said research revealed that a single gene had been identified as being responsible for a new type of retinoblastoma.

Dr Gallie added: The common type of retinoblastoma can be inherited, so the childs other eye and infant relatives are at risk to develop cancer.

When we remove the eye of a very young baby with a large tumour and discover it is the new oncogene-driven retinoblastoma, there is zero risk for the other eye or infant blood relatives.

Ms White said: Im very pleased with this breakthrough.

Children are diagnosed earliest when parents notice the eye has a white, instead of black, pupil in flash photos or dim light.

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Gene breakthrough welcomed by Daisy's Eye Cancer Fund

Mar. 14, 2013 For deer mice living in the Nebraska Sandhills, color can be the difference between life and death.

When the dark-coated mice first colonized the region, they stood out starkly against the light-colored, sandy soil, making them easy prey for predators. Over the next 8,000 years, however, the mice evolved a system of camouflage, with lighter coats, changes in the stripe on their tails, and changes in body pigment that allowed them to blend into their habitat.

Now Harvard researchers are using their example to answer one of the fundamental questions about evolution. Is it a process marked by large leaps -- single mutations that result in dramatic changes in an organism -- or is it the result of many smaller changes that accumulate over time?

As described in a March 15 paper in the journal Science, a team of researchers, including former Harvard postdoctoral fellow Catherine Linnen, now an assistant professor at the University of Kentucky, and led by Hopi Hoekstra, Harvard professor of organismic and evolutionary biology and molecular and cellular biology, were able to show that the changes in mouse coat color were the result not of a single mutation but of at least nine mutations within a single gene.

"The findings demonstrate how the cumulative effect of natural selection, acting on many small genetic changes, can produce rapid and dramatic change," said Linnen, the first author of the paper. "This helps us to understand, from a genetic perspective, the uncanny fit between so many organisms and their environments. By acting on many small changes, rather than a handful of large ones, natural selection can produce very finely honed adaptations."

Surprisingly, Hoekstra said, that honing occurred in a single gene.

The role of this gene, called agouti, in camouflage was first discovered by Linnen, Hoekstra, and colleagues in 2009, and it is responsible for changes in pigmentation in the coats of many animals. Every domesticated black cat, for example, has a DNA deletion in the gene.

What surprised Hoekstra and her team, however, wasn't that the gene was involved, but that each of the nine mutations were tied to a unique change in the animal's coats, that all the new mutations led to more camouflaging color, and that the mutations occurred in a relatively short, 8,000-year timeframe.

"Essentially, it seems as though these mutations -- each of which makes the mouse a little lighter and more camouflaged -- have accumulated over time," Hoekstra said.

Focusing on these mutations, researchers then examined the DNA of natural populations of the mice to determine whether the mutations are actually beneficial.

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One gene , many mutations: Key that controls coat color in mice evolved nine times

Johnathan Blair / National Geographic

A museum worker inspects a replica of a woolly mammoth, a species that went extinct 3,000 to 10,000 years ago. In March 2012, scientists in Russia and South Korea announced a partnership to try to clone the mammoth and generate a living specimen.

By Alan Boyle, Science Editor, NBC News

If scientists can use genetic engineering to bring back the woolly mammoth, should they do it? How about the passenger pigeon? Or the western black rhino? Do we humans have a responsibility to restore at least some of the species that our ancestors wiped out? And if we bring them back, will they really be the same?

Such questions are the focus of TEDxDeExtinction, a public forum that's being presented on Friday from 8 a.m. to 5 p.m. ET at National Geographic's Washington headquarters. You can watch the whole thing online via LivestreamTEDx and National Geographic's De-Extinction website, which also has loads of articles and resources on the issue. The event has been organized by Revive & Restore, a nonprofit clearinghouse for worldwide de-extinction work that's under the aegis of the Long Now Foundation in San Francisco.

"De-extinction"? What's that?

"It's using new technologies like cloning and genome sequencing to reconstruct a species that went extinct," science writer Carl Zimmer explained. Zimmer's talk at Friday's TEDx event will help set the scene for the de-extinction debate, and he's also written a cover story on the topic for National Geographic's April issue.

National Geographic

National Geographic's cover story for the April issue focuses on the prospects of reviving ancient species.

De-extinction has been in the works for more than a decade, basically ever since Dolly the Sheep demonstrated in 1996 that mammals could be cloned from cells in a lab dish. Spanish and French scientists worked for years on an effort to bring the Pyrenean ibex back from extinction, by cloning cells that had been preserved from the last known animal of the species. They succeeded only in producing a deformed kid that died 10 minutes after birth.

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Should we revive extinct species? Watch experts debate de-extinction