MARLBOROUGH, Mass.--(BUSINESS WIRE)--

Advanced Cell Technology, Inc. (ACT; OTCBB: ACTC), a leader in the field of regenerative medicine, announced today that its chief scientific officer, Robert Lanza, M.D. and Anthony Atala, M.D., W.H. Boyce Professor and Director of the Wake Forest Institute for Regenerative Medicine, have released the second edition of Handbook of Stem Cells (Academic Press/Elsevier), the widely-recognized definitive resource in the field of stem cells. It includes a Forward by Professor Sir Martin Evans, Ph.D., FRS, co-winner of the Nobel Prize for Physiology or Medicine in 2007. Sir Martin is credited with discovering embryonic stem cells and is considered one of the chief architects of the field of stem cell research. The two-volume set also includes contributions from dozens of stem cell pioneers, including James Thomson, Shinya Yamanaka, Doug Melton, Janet Rossant, and Robert Langer (a member of ACTs board of directors), among others, as well as patient advocate Mary Tyler Moore.

Handbook of Stem Cells, Second Edition follows a very successful edition published in 2004. The first edition was the first comprehensive body of work dedicated entirely to the stem cell field. The two-volume set quickly became the most relevant textbook in the stem cell arena. Now, several years later, major advances have occurred, with entirely new classes of stem cells being described. The description of induced pluripotent cells in the last few years brought many more avenues of research and discovery. In 2012, the first paper reporting results of two patients treated with human embryonic stem cells was published by ACT and its collaborators. It might seem that we have waited too long to finally see pluripotent stem cells in the clinic. However, this has been accomplished with incredible speed when it is considered that hESCs were first isolated just 14 years ago. Handbook of Stem Cells integrates this exciting area, combining in two volumes the requisites for a general understanding of both adult and embryonic stem cells. Organized in two volumes, Pluripotent Stem Cells and Adult & Fetal Stem Cells, this work contains contributions from the world's experts in stem cell research to provide a description of the tools, methods, and experimental protocols needed to study and characterize stem cells and progenitor populations as well as a the latest information of what is known about each specific organ system.

The Handbook of Stem Cells, edited by Robert Lanza and colleagues, is an ambitious new text that achieves extraordinary completeness and inclusiveness, wrote Steve Goldman of University of Rochester Medical Center in NATURE CELL BIOLOGY about the first edition. [...] the editors have succeeded in putting together a reference that is broad enough in scope, but sufficiently detailed and rigorous, to be of real interest to both new and seasoned investigators in the field [...] In providing this treatise, which covers the history, biology, methods and applications of stem cells, the editors and authors have succeeded in establishing a conceptual framework and a common language for the field. In so doing, they have ensured that this two-volume set will serve as a benchmark reference in stem cell biology for years to come.

Writing about the first edition in the Times Higher Education Supplement, Ian Wilmut added, These books make an invaluable contribution to the education of researchers and clinicians both of the present day and of the future. They should be available in libraries of all biology and medical schools as well as those of companies and research institutions.

About Advanced Cell Technology, Inc.

Advanced Cell Technology, Inc., is a biotechnology company applying cellular technology in the field of regenerative medicine. For more information, visit http://www.advancedcell.com.

Forward-Looking Statements

Statements in this news release regarding future financial and operating results, future growth in research and development programs, potential applications of our technology, opportunities for the company and any other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Any statements that are not statements of historical fact (including statements containing the words will, believes, plans, anticipates, expects, estimates, and similar expressions) should also be considered to be forward-looking statements. There are a number of important factors that could cause actual results or events to differ materially from those indicated by such forward-looking statements, including: limited operating history, need for future capital, risks inherent in the development and commercialization of potential products, protection of our intellectual property, and economic conditions generally. Additional information on potential factors that could affect our results and other risks and uncertainties are detailed from time to time in the companys periodic reports, including the report on Form 10-K for the year ended December 31, 2011. Forward-looking statements are based on the beliefs, opinions, and expectations of the companys management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. Forward-looking statements are based on the beliefs, opinions, and expectations of the companys management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. There can be no assurance that the Companys clinical trials will be successful.

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New Edition of Definitive (Two-Volume) Resource in Stem Cells Released Today

Public release date: 28-Sep-2012 [ | E-mail | Share ]

Contact: Charles Casey charles.casey@ucdmc.ucdavis.edu 916-734-9048 University of California - Davis Health System

(SACRAMENTO, Calif.) UC Davis investigators have found new evidence that a promising type of stem cell now being considered for a variety of disease therapies is very similar to the type of cells that give rise to cancer. The findings suggest that although the cells -- known as induced pluripotent stem cells (iPSCs) -- show substantial promise as a source of replacement cells and tissues to treat injuries, disease and chronic conditions, scientists and physicians must move cautiously with any clinical use because iPSCs could also cause malignant cancer.

The article, "Induced pluripotency and oncogenic transformation are related processes," is now online in the journal, Stem Cells and Development.

"This is the first study that describes the specific molecular pathways that iPSCs and cancer cells share from a direct comparison" said Paul Knoepfler, associate professor of cell biology and human anatomy, and principal investigator of the study. "It means that much more study is required before iPSCs can be used clinically. However, our study adds to a growing knowledge base that not only will help make stem cell therapies safer, but also provide us with new understandings about the cancer-causing process and more effective ways to fight the disease."

Since 2007, cell biologists have been able to induce specialized, differentiated cells (such as those obtained from the skin or muscle of a human adult) to become iPSCs. Like embryonic stem cells, iPSCs are a type of stem cell that is able to become any cell type. This "pluripotent" capability means that iPSCs have the potential of being used in treatments for a variety of human diseases, a fundamentally new type of clinical care known as regenerative medicine.

iPSCs are considered particularly important because their production avoids the controversy that surrounds embryonic stem cells. In addition, iPSCs can be taken from a patient's own skin and induced to produce other needed tissues, thereby evading the possibility of immunologic rejection that arises when transplanting cells from a donor to a recipient. In contrast to therapies based on ES cells, iPSCs would eliminate the need for patients to take immunosuppressive drugs.

Earlier research indicated that both ES cells and iPSCs pose some health risks. Increasing evidence suggests that pluripotency may be related to rapid cellular growth, a characteristic of cancer. iPSCs, as well as embryonic stem cells, are well known by scientists to have the propensity to cause teratomas, an unusual type of benign tumor that consists of many different cell types. The new UC Davis study demonstrates for the first time that iPSCs -- as well as ES cells -- share significant similarities to malignant cancer cells.

The investigators compared iPSCs to a form of malignant cancer known as oncogenic foci that are also produced in laboratories; these cell types are used by medical researchers to create models of cancer, particularly sarcoma. Specifically, the scientists contrasted the different cells' transcriptomes, comprised of the RNA molecules or "transcripts." Unlike DNA analysis, which reflects a cell's entire genetic code whether or not the genes are active, transcriptomes reflect only the genes that are actively expressed at a given time and therefore provide a picture of actual cellular activity.

From this transcriptome analysis, the investigators found that the iPSCs and malignant sarcoma cancer cells are unexpectedly similar in several respects. Genes that were not expressed in iPSCs were also not expressed in the cancer-generating cells, including many that have properties that guide a cell to normally differentiate in certain directions. Both cell types also exhibited evidence of similar metabolic activities, another indication that they are related cell types.

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Researchers find multiple similarities between cancer cells and induced pluripotent stem cells

ScienceDaily (Sep. 28, 2012) UC Davis investigators have found new evidence that a promising type of stem cell now being considered for a variety of disease therapies is very similar to the type of cells that give rise to cancer. The findings suggest that although the cells -- known as induced pluripotent stem cells (iPSCs) -- show substantial promise as a source of replacement cells and tissues to treat injuries, disease and chronic conditions, scientists and physicians must move cautiously with any clinical use because iPSCs could also cause malignant cancer.

The article, "Induced pluripotency and oncogenic transformation are related processes," is now online in the journal, Stem Cells and Development.

"This is the first study that describes the specific molecular pathways that iPSCs and cancer cells share from a direct comparison" said Paul Knoepfler, associate professor of cell biology and human anatomy, and principal investigator of the study. "It means that much more study is required before iPSCs can be used clinically. However, our study adds to a growing knowledge base that not only will help make stem cell therapies safer, but also provide us with new understandings about the cancer-causing process and more effective ways to fight the disease."

Since 2007, cell biologists have been able to induce specialized, differentiated cells (such as those obtained from the skin or muscle of a human adult) to become iPSCs. Like embryonic stem cells, iPSCs are a type of stem cell that is able to become any cell type. This "pluripotent" capability means that iPSCs have the potential of being used in treatments for a variety of human diseases, a fundamentally new type of clinical care known as regenerative medicine.

iPSCs are considered particularly important because their production avoids the controversy that surrounds embryonic stem cells. In addition, iPSCs can be taken from a patient's own skin and induced to produce other needed tissues, thereby evading the possibility of immunologic rejection that arises when transplanting cells from a donor to a recipient. In contrast to therapies based on ES cells, iPSCs would eliminate the need for patients to take immunosuppressive drugs.

Earlier research indicated that both ES cells and iPSCs pose some health risks. Increasing evidence suggests that pluripotency may be related to rapid cellular growth, a characteristic of cancer. iPSCs, as well as embryonic stem cells, are well known by scientists to have the propensity to cause teratomas, an unusual type of benign tumor that consists of many different cell types. The new UC Davis study demonstrates for the first time that iPSCs -- as well as ES cells -- share significant similarities to malignant cancer cells.

The investigators compared iPSCs to a form of malignant cancer known as oncogenic foci that are also produced in laboratories; these cell types are used by medical researchers to create models of cancer, particularly sarcoma. Specifically, the scientists contrasted the different cells' transcriptomes, composed of the RNA molecules or "transcripts." Unlike DNA analysis, which reflects a cell's entire genetic code whether or not the genes are active, transcriptomes reflect only the genes that are actively expressed at a given time and therefore provide a picture of actual cellular activity.

From this transcriptome analysis, the investigators found that the iPSCs and malignant sarcoma cancer cells are unexpectedly similar in several respects. Genes that were not expressed in iPSCs were also not expressed in the cancer-generating cells, including many that have properties that guide a cell to normally differentiate in certain directions. Both cell types also exhibited evidence of similar metabolic activities, another indication that they are related cell types.

"We were surprised how similar iPSCS were to cancer-generating cells," said Knoepfler. "Our findings indicate that the search for therapeutic applications of iPSCs must proceed with considerable caution if we are to do our best to promote patient safety."

Knoepfler noted, for example, that future experimental therapies using iPSCs for human transplants would most often not involve implanting iPSCs directly into a patient. Instead, iPSCs would be used to create differentiated cells -- or tissues -- in the laboratory, which could then be transplanted into a patient. This approach avoids implanting the actual undifferentiated iPSCS, and reduces the risk of tumor development as a side effect. However, Knoepfler noted that even trace amounts of residual iPSCs could cause cancer in patients, a possibility supported by his team's latest research.

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Multiple similarities discovered between cancer cells and induced pluripotent stem cells

ScienceDaily (Sep. 27, 2012) Working with mice, Johns Hopkins researchers have solved a key part of a muscle regeneration mystery plaguing scientists for years, adding strong support to the theory that muscle mass can be built without a complete, fully functional supply of muscle stem cells.

"This is good news for those with muscular dystrophy and other muscle wasting disorders that involve diminished stem cell function," says Se-Jin Lee, M.D., Ph.D., lead author of a report on the research in the August issue of the Proceedings of the National Academy of Sciences, and professor of molecular biology and genetics at the Johns Hopkins University School of Medicine.

Muscle stem cells, known as satellite cells, reside next to muscle fibers and are usually dormant in adult mammals, including humans. After exercise or injury, they are stimulated to divide and fuse, either with themselves or with nearby muscle fibers, to increase or replace muscle mass. In muscle wasting disorders, like muscular dystrophy, muscle degeneration initially activates satellite cells to regenerate lost tissue, but eventually the renewal cycle is exhausted and the balance tips in favor of degeneration, the researchers explain.

Muscle maintenance and growth under healthy, non-injury conditions have been more of a mystery, including the role of myostatin, a protein secreted from muscle cells to stop muscle growth. Blocking myostatin function in normal mice causes them to bulk up by 25 to 50 percent. What is not known is which cells receive and react to the myostatin signal. Current suspects include satellite cells and muscle cells themselves.

In this latest study, researchers used three approaches to figure out whether satellite cells are required for myostatin activity. They first looked at specially bred mice with severe defects in either satellite cell function or number. When they used drugs or genetic engineering to block myostatin function in both types of mice, muscle mass still increased significantly compared to that seen in mice with normal satellite cell function, suggesting that myostatin is able to act, at least partially, without full satellite cell function.

Second, the researchers guessed that if myostatin directly inhibits the growth of satellite cells, their numbers should increase in the absence of myostatin. The researchers marked the satellite cells with a permanent dye and then blocked myostatin activity with a drug. Mouse muscle mass increased significantly as expected, but the satellite cells did not increase in number, nor were they found fusing with muscle fibers at a higher rate. According to Lee, these results strongly suggest that myostatin does not suppress satellite cell proliferation.

Third, to further confirm their theory that myostatin acts primarily through muscle cells and not satellite cells, the team engineered mice with muscle cells lacking a protein receptor that binds to myostatin. If satellite cells harbor most of the myostatin receptors, removal of receptors in muscle cells should not alter myostatin activity, and should result in muscles of normal girth. Instead, what the researchers saw was a moderate, but statistically significant, increase in muscle mass. The evidence once again, they said, suggested that muscle cells are themselves important receivers of myostatin signals.

Lee notes that, since the results give no evidence that satellite cells are of primary importance to the myostatin pathway, even patients with low muscle mass due to compromised satellite cell function may be able to rebuild some of their muscle tone through drug therapy that blocks myostatin activity.

"Everybody loses muscle mass as they age, and the most popular explanation is that this occurs as a result of satellite cell loss. If you block the myostatin pathway, can you increase muscle mass, mobility and independence for our aging population?" asks Lee. "Our results in mice suggest that, indeed, this strategy may be a way to get around the satellite cell problem."

Authors on the paper include Se-Jin Lee, Thanh Huynh, Yun-Sil Lee and Suzanne Sebald from The Johns Hopkins University, Sarah Wilcox-Adelman of Boston Biomedical Research Institute, Naoki Iwamori and Martin Matzuk of Baylor College of Medicine, and Christoph Lepper and Chen-Ming Fan from the Carnegie Institution for Science.

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Key part of old mystery in generating muscle mass solved

ScienceDaily (Sep. 27, 2012) A new regulator for heart formation has been discovered by studying how embryonic stem cells adjust the packaging of their DNA. This approach to finding genetic regulators, the scientists say, may have the power to provide insight into the development of any tissue in the body -- liver, brain, blood and so on.

A stem cell has the potential to become any type of cell. Once the choice is made, the cell and other stem cells committed to the same fate divide to form organ tissue.

A University of Washington-led research team was particularly interested in how stem cells turn into heart muscle cells to further research on repairing damaged hearts through tissue regeneration. The leaders of the project were Dr. Charles Murry, a cardiac pathologist and stem cell biologist; Dr. Randall Moon, who studies the control of embryonic development, and Dr. John Stamatoyannopoulos, who explores the operating systems of the human genome.

The paper's lead author is Dr. Sharon Paige, a UW MD-PhD student who completed her Ph.D. in Dr. Murry's lab.

The results are published in the Sept. 28 edition of Cell.

Paige, an aspiring pediatric cardiologist, said, "By identifying regulators of cardiac development, this work has the potential to lead to a better understanding of the causes of congenital heart disease, thereby paving the way for therapeutic advances."

Previously UW researchers had examined the signals that prod cells to grow into various kinds of heart tissue. In this case, the researchers entered a relatively unexplored area. They decided to look at the genetic controls behind the transformation of stem cells into heart tissue.

Because stem cells keep their DNA code under wraps until needed, the scientists examined how this packaging is altered over time to permit reading of portions of the code and thereby produce changes in the cell.

DNA is wound up into a structure called chromatin. "DNA can be packaged as tightly closed, neutral or activated," Murry explained. The tightly closed state, he said, is analogous to setting the brakes on a car.

Like a child who clams up when asked, "What will you be when you grow up?" stem cells are protective of the genes that will determine their future cell type, or what scientists call their cell fate.

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Dynamics of DNA packaging helps regulate formation of heart

The process researchers use to generate induced pluripotent stem cells (iPSCs)-a special type of stem cell that can be made in the lab from any type of adult cell-is time consuming and inefficient. To speed things up, researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) turned to kinase inhibitors.

These chemical compounds block the activity of kinases, enzymes responsible for many aspects of cellular communication, survival, and growth.

As they outline in a paper published September 25 in Nature Communications, the team found several kinase inhibitors that, when added to starter cells, help generate many more iPSCs than the standard method.

This new capability will likely speed up research in many fields, better enabling scientists around the world to study human disease and develop new treatments.

"Generating iPSCs depends on the regulation of communication networks within cells," explained Tariq Rana, Ph.D., program director in Sanford-Burnham's Sanford Children's Health Research Center and senior author of the study.

"So, when you start manipulating which genes are turned on or off in cells to create pluripotent stem cells, you are probably activating a large number of kinases. Since many of these active kinases are likely inhibiting the conversion to iPSCs, it made sense to us that adding inhibitors might lower the barrier."

According to Tony Hunter, Ph.D., professor in the Molecular and Cell Biology Laboratory at the Salk Institute for Biological Studies and director of the Salk Institute Cancer Center, "The identification of small molecules that improve the efficiency of generating iPSCs is an important step forward in being able to use these cells therapeutically.

"Tariq Rana's exciting new work has uncovered a class of protein kinase inhibitors that override the normal barriers to efficient iPSC formation, and these inhibitors should prove useful in generating iPSCs from new sources for experimental and ultimately therapeutic purposes." Hunter, a kinase expert, was not involved in this study.

The promise of iPSCs At the moment, the only treatment option available to many heart failure patients is a heart transplant. Looking for a better alternative, many researchers are coaxing stem cells into new heart muscle.

In Alzheimer's disease, researchers are also interested in stem cells, using them to reproduce a person's own malfunctioning brain cells in a dish, where they can be used to test therapeutic drugs.

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Making it easier to make stem cells

---Implications for treating muscular dystrophy and other muscle wasting diseases

Newswise Working with mice, Johns Hopkins researchers have solved a key part of a muscle regeneration mystery plaguing scientists for years, adding strong support to the theory that muscle mass can be built without a complete, fully functional supply of muscle stem cells.

This is good news for those with muscular dystrophy and other muscle wasting disorders that involve diminished stem cell function, says Se-Jin Lee, M.D., Ph.D., lead author of a report on the research in the August issue of the Proceedings of the National Academy of Sciences, and professor of molecular biology and genetics at the Johns Hopkins University School of Medicine.

Muscle stem cells, known as satellite cells, reside next to muscle fibers and are usually dormant in adult mammals, including humans. After exercise or injury, they are stimulated to divide and fuse, either with themselves or with nearby muscle fibers, to increase or replace muscle mass. In muscle wasting disorders, like muscular dystrophy, muscle degeneration initially activates satellite cells to regenerate lost tissue, but eventually the renewal cycle is exhausted and the balance tips in favor of degeneration, the researchers explain.

Muscle maintenance and growth under healthy, non-injury conditions have been more of a mystery, including the role of myostatin, a protein secreted from muscle cells to stop muscle growth. Blocking myostatin function in normal mice causes them to bulk up by 25 to 50 percent. What is not known is which cells receive and react to the myostatin signal. Current suspects include satellite cells and muscle cells themselves.

In this latest study, researchers used three approaches to figure out whether satellite cells are required for myostatin activity. They first looked at specially bred mice with severe defects in either satellite cell function or number. When they used drugs or genetic engineering to block myostatin function in both types of mice, muscle mass still increased significantly compared to that seen in mice with normal satellite cell function, suggesting that myostatin is able to act, at least partially, without full satellite cell function.

Second, the researchers guessed that if myostatin directly inhibits the growth of satellite cells, their numbers should increase in the absence of myostatin. The researchers marked the satellite cells with a permanent dye and then blocked myostatin activity with a drug. Mouse muscle mass increased significantly as expected, but the satellite cells did not increase in number, nor were they found fusing with muscle fibers at a higher rate. According to Lee, these results strongly suggest that myostatin does not suppress satellite cell proliferation.

Third, to further confirm their theory that myostatin acts primarily through muscle cells and not satellite cells, the team engineered mice with muscle cells lacking a protein receptor that binds to myostatin. If satellite cells harbor most of the myostatin receptors, removal of receptors in muscle cells should not alter myostatin activity, and should result in muscles of normal girth. Instead, what the researchers saw was a moderate, but statistically significant, increase in muscle mass. The evidence once again, they said, suggested that muscle cells are themselves important receivers of myostatin signals.

Lee notes that, since the results give no evidence that satellite cells are of primary importance to the myostatin pathway, even patients with low muscle mass due to compromised satellite cell function may be able to rebuild some of their muscle tone through drug therapy that blocks myostatin activity.

Everybody loses muscle mass as they age, and the most popular explanation is that this occurs as a result of satellite cell loss. If you block the myostatin pathway, can you increase muscle mass, mobility and independence for our aging population? asks Lee. Our results in mice suggest that, indeed, this strategy may be a way to get around the satellite cell problem.

Originally posted here:
Hopkins Researchers Solve Key Part of Old Mystery in Generating Muscle Mass