Cancer Causing Gene Protein Found

Dr. Tak Mak and scientists at The Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital have discovered the role of two "cousins" in the genetic family tree of cancer development.

The findings, published online today in the journal Genes and Development, plant the seed for a critical new branch of scientific inquiry, says Dr. Mak, principal investigator. Dr. Mak, Director of The Campbell Family Institute is also a Professor, University of Toronto, in the Departments of Medical Biophysics and Immunology.

The cousins are proteins related to the gene p53 family – the patriarch known for two decades to be the master gatekeeper that controls all cancer development. When gene p53 is defective, it loses its ability to regulate healthy cells and suppress cancer.

"Until now, we thought these cousins (TAp73 protein isoforms) were not involved in cancer. Our results prove that they are. This is fundamental to understanding every human cancer and furthering the science."

In the lab, Dr. Mak and his team challenged traditional thinking about the role of these proteins. "Before, scientists studied only whether these proteins were present or absent. We decided to study how they interact with each other and discovered that they actually have a split personality. When we turn one 'on' or 'off', the other changes behavior and becomes part of the cancer-causing process. The key is understanding the ratio of the interaction."

"The next step is to understand how the ratio affects cell division that leads to human cancer," says Dr. Mak, whose work was supported by the Canadian Institutes for Health Research.
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Genome analysis reveals new protein associated with breast cancer progression

A novel systems-based approach that combines comprehensive gene expression profiling with genome-wide transcription factor analysis and protein-protein interaction has led researchers to an important genetic marker that can help physicians know which breast cancer patients are at highest risk and will require more aggressive treatment, a research team based at the University of Chicago Medical Center reports in the April 15, 2008, issue of the journal Molecular Systems Biology.

The researchers found that high expression of a protein known as H2A.Z, which is associated with the expression of genes within the nucleus, can help physicians predict which patients are most at risk for disease spread and death. It could also serve as a new target for therapy.

“Elevated H2A.Z expression is significantly associated with metastasis and shorter survival, and it could quickly help doctors make better predictions and treatment choices for their patients,” said study director Kevin White, PhD, professor of human genetics and director of the Institute for Genomics and Systems Biology at the University of Chicago and Argonne National Laboratory. “It could also provide clues to new therapies.”

“But, perhaps more important,” he added, “we think we have developed an integrated approach to genomic analysis that can be applied to a wide range of cancers.”

Instead of a standard whole-genome analysis, looking for genetic variations that correlate with disease risk, White and colleagues integrated multiple genetic technologies to measure the effects of estrogens, which play a crucial role in many breast cancers, on multiple cellular pathways, what they refer to as a “transcriptional regulatory cascade.”

The female hormone estrogen acts by binding to the estrogen receptor, which carries the hormone’s signal to a cell’s nucleus, where it activates many other genes. One of those genes is a known cancer-related gene called c-MYC, which in turn regulates its own cascade of gene targets.

White’s team set out to map out the many sequential genetic events that occur in breast cancer cells after estrogen binding, using a series of innovative technologies. They ultimately found that estrogen-stimulated c-MYC enhanced production of H2A.Z, which altered the positioning and activation of various genes in ways that increased the odds that a cancer would spread to the lymph nodes and ultimately to distant sites, often resulting in the patient’s death.

This is not a simple process. In tumor cells from patients with estrogen-dependent breast cancers, the researchers found estrogen affected 1,615 genetic regions. One of those was the promoter for the gene for c-MYC, which, when activated, could bind another set of overlapping 311 genetic regions.

Both estrogen and c-MYC interact with the gene for H2A.Z, leading to increased production of this protein in breast cancer cells. When the researchers looked at tumor tissue samples collected from 500 patients, they found that elevated levels of H2A.Z were highly correlated with the spread of the cancer to lymph nodes and decreased patient survival. Adding H2A.Z expression to other known risk factors provided “significant prognostic information,” the authors note, “beyond what these factors alone provide.”

“Although it has been implicated in genomic stability and gene transcription, H2A.Z has never been reported to be associated with cancer,” said White. “We would not have found this clinically important factor without taking such a large-scale integrated approach.”

“We suspect this integrated systems approach will lead us to a number of previously unsuspected genes that play a role in disease initiation and progression,” he said. “Many of these could become targets for new treatments.”

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Arizona Cancer Center Studying Benefits of Green Tea Extract

The Arizona Cancer Center at The University of Arizona is studying the effects of Polyphenon E, a green tea extract, on prostate cancer prevention. This study will determine whether Polyphenon E affects cancer-related biomarkers in blood and/or prostate tissue in men with prostate cancer.

Tea is one of the world’s most consumed beverages. Polyphenon E is a chemically defined, decaffeinated, catechin-enriched green tea extract. Catechins are plant chemicals that are considered powerful antioxidants and have multiple beneficial biological effects that could lead to cancer prevention.

Prostate cancer is the most common type of cancer found in American men, other than skin cancer. The American Cancer Society estimates that there will be about 186,320 new cases of prostate cancer in the United States in 2008.

Past and ongoing research in numerous experimental studies and in one clinical trial provide evidence that green tea or green tea extracts such as Polyphenon E may have the potential to lower the risk of prostate cancer in the human population. However, rigorous clinical investigations are needed to determine whether green tea extracts such as Polyphenon E are effective at preventing prostate cancer.

The three-year study at the Arizona Cancer Center will recruit men with a recent diagnosis of organ-confined prostate cancer and scheduled to have the prostate removed within three to six weeks from the start of the study.

Eligible participants will take either four Polyphenon E capsules or a matched placebo each morning with food up to the day of their surgery. They will provide blood samples prior to capsule intake and again right before surgery. In addition, they will complete a diary and calendar of the capsules and other medications taken, illnesses and hospitalizations. All qualified participants will be compensated for their role in this study.

Following their surgery, tissue from their prostates will be analyzed to determine whether any of the tea components can be detected.

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Can Robots Cure Cancer

New research released at the Society of Interventional Radiology's (SIR) Annual Scientific Meeting in Washington, D.C. holds promise of a new interventional imaging capability using advanced robotics provided by Siemens Healthcare, to improve the value of chemoembolization in treating cancer.

The research, presented by Dr. John Angle, Associate Professor of Radiology, Chief, Division of Angiography, University of Virginia Health System in Charlottesville, at the "Advanced Imaging Symposium," reveals clinical results from his case study using the Siemens Artis zeego, a multi-axis C-arm that employs robotic technology to enable large-volume syngo DynaCT acquisition for liver chemoembolization.

The Artis zeego is part of the new Artis zee family of interventional imaging systems introduced by Siemens. According to Angle, the combination of the Artis zeego and large-volume syngo(R) DynaCT enables the physician to see the whole abdomen or the entire liver for chemoembolization and biopsies, and provides reliable post-TACE assessment of lipidol uptake.

"The Artis zeego's support for expanded syngo DynaCT anatomical coverage enables the entire liver to be imaged without moving the patient," said Angle. "We have found the system to be reliable, stable and very easy to use. We plan on expanding the scope of cases for which we use the Artis zeego."

The Artis zeego, which recently received FDA 510(k) clearance, offers breakthrough versatility, enhanced image quality and streamlined workflow across an array of clinical environments, from body and neurointerventional radiology suites to operating rooms and hybrid rooms. Additionally, Frost & Sullivan recently selected the Artis zeego as winner of the 2008 Frost & Sullivan Technology Innovation Award at their Excellence in Medical Technologies Awards banquet.

The versatility of the Artis zee family is exemplified by the revolutionary new Artis zeego to extend imaging capabilities through virtually unrestricted C-arm positioning. The ability to support two non-concentric rotations supports advanced cross-sectional imaging, which is not achievable with traditional C-arm systems. The Artis zeego makes it possible for the position of the isocenter to be adjusted according to the procedural needs or the height of the physician, which is particularly beneficial to a physician during lengthy procedures while wearing a heavy lead-shielded apron. The adjustable isocenter also enables off-center rotational angiography for all areas of the body and supports advanced 3D imaging techniques, including cross-sectional imaging through Siemens' first-to-market syngo DynaCT.
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Breast cancer gene carriers’ risk ‘amplified’ by additional genes

Many women with a faulty breast cancer gene could be at greater risk of the disease due to extra ‘risk amplifying’ genes, according to research published in this week in the American Journal of Human Genetics.

Cancer Research UK scientists, including lead author Professor Doug Easton at the University of Cambridge, have found that common versions of two genes – FGFR2 and TNRC9 – known to increase breast cancer risk in the general population - also increase the risk in women carrying damaged versions of the BRCA2 gene.

Around one in eighteen women will develop breast cancer by the age of 65. On average, half of women carrying a faulty BRCA2 gene will develop the disease by the age of 70.

This study found that particular combinations of the FGFR2 and TNRC9 genes modify the breast cancer risk in BRCA2 mutation carriers.

Around twenty percent of the BRCA2 mutation carriers have the lowest risk combination of the FGFR2 and TNRC9 genes. The researchers found that their risk is lowered so four in every 10 women in this category are expected to develop breast cancer.

But one per cent of BRCA2 mutation carriers have the highest risk combination of FGFR2 and TNRC9 genes. Seven in every 10 women in this category are predicted to develop the disease.

These findings are the first step in a series of studies hunting for breast cancer susceptibility genes, which aims to better monitor and treat women with a family history of the disease.

Professor Easton, director of Cancer Research UK’s Genetic Epidemiology Unit at the University of Cambridge, said: “This is the first time we have found evidence that common changes in other genes can amplify the risk of breast cancer in women known to have faulty BRCA genes.

“This is the first step in finding a set of genes that modify the risk in BRCA carriers, and may influe nce how we monitor women with a family history of the disease.”

The study brings together results from international research groups looking at a total of more than 10,000 women carrying a BRCA1 or BRCA2 mutation. Dr Lesley Walker, Cancer Research UK’s director of cancer information, said: “It’s important to remember that the prevalence of this combination of gene faults is rare in the general population. But advances like this will add to our ability to identify those most at risk for clinical monitoring, detecting the disease earlier in those who develop it.”
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Researchers develop method to rapidly ID optimal drug cocktails

UCLA researchers have developed a feedback control scheme that can search for the most effective drug combinations to treat a variety of conditions, including cancers and infections. The discovery could play a significant role in facilitating new clinical drug-cocktail trials.

The best known use of drug cocktails has been in the fight against HIV, the virus that causes AIDS. Drug cocktails also have been used to combat several types of cancer. Often, drugs that might not be effective in combating diseases individually do much better in combination.

With the use of the new closed-loop feedback control scheme, an approach guided by a stochastic search algorithm, researchers at the UCLA Henry Samueli School of Engineering and Applied Science and UCLA's Jonsson Comprehensive Cancer Center have devised an invaluable means of identifying potent drug combinations fast and efficiently. Their findings appear in the March 17 online version of the journal Proceedings of the National Academy of Sciences.

It has long been a difficult challenge for clinical researchers to determine the optimal dose of individual drugs used in combination. For example, a researcher testing 10 different concentrations of six drugs in every possible arrangement would be faced with 1 million potential combinations.

"With the development of this optimization method, we've overcome a major roadblock," said study author Chih-Ming Ho, UCLA's Ben Rich-Lockheed Martin Professor and a member of the National Academy of Engineering. "There have always been too many choices and too many combinations to sort through. It was like finding a needle in a haystack."

In one test case, the research team examined how to best prevent a viral infection of host cells. Using the closed-loop optimization scheme, they were able to identify, out of 100,000 possible combinations, the drug cocktails that completely inhibited viral infection after only about a dozen trials. In addition, they found that total inhibition of the virus occurred at much lower drug doses than would be necessary if the drugs were used alone; in fact, the concentrations of the drugs were only about 10 percent of that required when used individually.

"Viruses grow very rapidly and change rapidly as well. Because of that, a virus can become resistant to a particular drug," said Genhong Cheng, a member of the research team at the UCLA Center for Cell Control and UCLA's Jonsson Comprehensive Cancer Center. "This is why it's so important to be able to use a combination of more than one drug. If the virus mutates to become resistant to one drug, it is still sensitive to the other drugs."

Drug combinations can also be used effectively to inhibit infectious diseases because resistance to a single drug is very common, according to Ren Sun, UCLA professor of molecular and medical pharmacology and a member of the research team.

"If we can apply multiple drugs against one infectious agent, it probably will prevent the occurrence of drug resistance," said Sun, who is also a researcher at the Jonsson Cancer Center. "But, of course, when you use multiple drugs, side effects will be strong. With this model, there is a way to optimize the combination to reduce the side effects while maintaining efficacy that will be very beneficial."

"What the search scheme does is it tries to detect trends for optimal output," said Pak Wong, a former UCLA graduate student who participated in the study and is now an assistant professor of mechanical engineering at the University of Arizona. "Basically, the algorithm sees a trend and a direction and drives the trend in that direction. It's like mountain climbing and finding a way to get to the peak. So you keep going, and soon you rapidly find the peak while being guided by a smart search scheme."

In an example used to illustrate the prevention of viral infection of host cells, researchers started with arbitrarily chosen dosages of the drugs. The percentage of non-infected cells under this initial drug-cocktail treatment was fed into the stochastic search algorithm, which essentially helps guide a random search process. The algorithm then suggested the next drug concentrations for producing a higher percentage of non-infected cells. This closed-loop feedback control scheme is carried out continuously until the best combination is found. Randomness is built into the search decision, preventing the trap at local optimum levels and allowing the search process to continue until the optimal drug cocktail is identified.

The model also provides an alternative approach to studying cellular functions. Molecular biologists can identify all the players of a particular regulatory pathway in order to decipher how to block or augment that pathway. Cells are complex systems with many redundant functions, and it is difficult to predict how a cell will respond to multiple stimulations at one time. The model overlooks these details and lets the system determine what works best for itself. If researchers are more interested in how the cellular network functions, this approach can provide an initial bird's-eye view, but it also allows them to home in on the important molecular activities controlled by the best drug combinations.

This search scheme is an extremely effective and versatile tool that can be applied to combat numerous diseases, including cancer, the researchers say, and its multidimensional properties will likely make it useful in a wide variety of additional situations.

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A Protein that Triggers Aggressive Breast Cancer

SATB1 is a nuclear protein well known for its crucial role in regulating gene expression during the differentiation and activation of T cells, making it a key player in the immune system. But SATB1 has now revealed a darker side: it is an essential contributing factor in the most aggressive forms of breast cancer.

SATB1 forms a three-dimensional cage-like structure within the cell nucleus (left) that binds to DNA specific sites within genes, reorganizes chromatin, and recruits enzymes that promote the expression or suppression of genes (right).

Breast cancer cells need SATB1 to become metastatic; metastasis — the stage when cells break away from the original tumor and spread to other parts of the body — is the final step of solid tumor progression and is the most common cause of death in cancer patients.

"In breast tumors, SATB1 reprograms the genome to change the expression of hundreds of genes, promoting tumor growth and metastasis," says Terumi Kohwi-Shigematsu, a scientist in the Life Sciences Division of the Department of Energy's Lawrence Berkeley National Laboratory who, with her colleagues, discovered SATB1 and has since investigated its many functions. She says, "SATB1's role in breast cancer is a new paradigm for the way tumors progress."

Kohwi-Shigematsu, working with Berkeley Lab's Hye-Jung Han and Yoshinori Kohwi, and with Jose Russo of the Fox Chase Cancer Center in Philadelphia, found that when SATB1 is detected in a breast tumor, the cancer is highly likely to progress or recur.

Moreover, by introducing SATB1 into otherwise nonmetastatic breast cancer cells, invasive tumors can be induced in mice; conversely, removing SATB1 from metastatic cells not only abolishes metastasis and tumor growth in mice but also returns cells to their normal appearance in vitro. The researchers have published these and other findings in the March 13, 2008 issue of Nature.

How SATB1 works

Kohwi-Shigematsu and Kohwi originally identified a class of DNA sequences they called base-unpairing regions (BURs), a finding that led Kohwi-Shigematsu's group to the discovery of "special AT-rich sequence binding protein 1" (SATB1). SATB1 binds to BURs in double-stranded DNA by recognizing the BURs' distinctive phosphate-backbone structure. BURs contain unusual sequence contexts that readily unzip to expose DNA's individual strands.

As a nuclear architectural protein, SATB1 forms what Kohwi-Shigematsu calls a "3‑D chickenwire network" inside the nucleus of the cell. SATB1 anchors chromosomes to its cage-like structure by tethering the BURs in the target genes, thus serving as a kind of "glue" for these genes. SATB1 folds and remodels the chromatin — the intertwined DNA and proteins that form chromosomes — into new shapes, bringing even distant parts of the genome together for coordinated control of gene expression and regulation.

SATB1 also globally regulates histone status in the chromatin by recruiting histone-modifying enzymes to the target-gene loci. Histones are the proteins around which DNA in chromatin is wound like thread on a spool; histone status renders DNA sequences accessible or inaccessible for transcription.

Early on, SATB1's ability to regulate gene expression was identified as critical to T-cell development. Although Kohwi-Shigematsu and her colleagues have found several other cell types that use SATB1 to reshape chromatin and regulate gene expression in a similar way, SATB1 is not expressed in all cells. SATB1 seems particularly important in cells which must change their function — as do many progenitor cells, including the thymocytes that turn into T cells. And as cancerous cells must do to turn into metastatic cells.

"Hye-Jung Han of our group started by looking at two dozen breast-cell lines, including normal human epithelial cells" — epithelial cells are the kind that form the linings of hollow glands in the breast — "and both nonmetastatic and metastatic breast cancer cells," Kohwi-Shigematsu says. "Only the metastatic cells expressed SATB1, with the most aggressive breast cancer cells showing the highest levels of the protein."

The researchers examined over 2,000 human primary breast cancer tissue samples for which clinical follow-up studies were available. The highest levels of SATB1 were in samples from patients whose survival times had been shortest; patients whose tumor samples had no SATB1 expression generally had longer survival times.

The analysis showed that a high level of SATB1 expression by itself is an excellent indicator of poor prognosis — independent of whether breast cancer cells have already metastasized to the lymph nodes at the time of diagnosis.

SATB1 takes command

The reason why SATB1 is a good prognostic marker is because SATB1 drives breast cancer cells to become invasive, as revealed by both in vitro and in vivo studies.

The researchers performed in vitro studies of highly metastatic cell lines, reducing SATB1 expression through the use of shRNAs, "short-hairpin-interfering" RNAs, that dramatically reduced the invasive capacity of these cells and also reduced their capacity for unattached growth — a necessity if metastasizing cancer cells are to travel through the blood and lymph vessels.

With increasing stages of breast cancer, initially nonmalignant cells making up the acini in the breast become increasingly disorganized and finally metastasize (top). Breast cells cultured in a three-dimensional matrix form acinar structures, but the expression of SATB1 in these cells causes increasing disorganization. When SATB1 expression is reduced in these metastatic cells, they return to normal appearance (bottom).

Other in vitro studies used normal breast epithelial cells, the kind that form the hollow oriented structures called acini, the milk-secreting glands of the breast. Normal cells form similar, well-organized acinar structures in vitro, whereas in highly metastatic epithelial cell lines these structures are disorganized and lack polarity. When SATB1 expression is reduced in the metastatic cell lines, they too form the kind of polarized, uniform acinar structures found in normal mammary epithelial cells.

These in vitro results were confirmed in vivo, in mice. Nine weeks after human aggressive breast cancer cells were injected into the tails of test mice, these cells developed into metastatic nodules (tumors) on the lungs. But when SATB1 expression was reduced or removed from the injected cancer cells, the mice developed fewer or even no nodules, depending on the remaining levels of SATB1. Once SATB1 is greatly reduced, these cells no longer form tumors when injected directly into breast fat pads.

In vivo studies also established that cancer cells which do not normally express SATB1, and do not normally metastasize, can become aggressive if they are modified to express SATB1. Once SATB1 is expressed, they form large tumors when injected into breast fat pads; they then invade the blood circulatory system and form metastatic tumors in lungs.

The tests of human breast cancer cell lines in mice allowed the researchers to establish that, for these cells, SATB1 is necessary and sufficient for tumor growth and metastatic activity.

"SATB1 is a key player in the metastasis of breast cancer cells, controlling expression of over a thousand genes," says Kohwi-Shigematsu. "It increases the expression of genes that promote tumor growth and reduces the expression of tumor suppressors. Among the regulated genes are numerous growth-factor genes and genes affecting cell adhesion, cell signaling, cell-cycle regulation, and other functions."

Among the important genes regulated by SATB1, the researcher identified many that are already known to play a role in aggressive breast cancers, including the epidermal growth factor gene ERBB2, otherwise known as HER2.

"What we have found is a new model of altered gene regulation during the progression of tumors, which depends on SATB1's reprogramming of the gene expression profile," Kohwi-Shigematsu says. "What results is a new and aggressive cancer phenotype that promotes both tumor growth and metastasis."

The discovery of SATB1's key part in aggressive breast cancer has profound implications for prognosis and for possible new treatments for cancer's most malignant forms. At the same time, the discovery opens a wide field of fundamental scientific inquiry, beginning with the most basic questions. What determines the particular sets of genes affected by SATB1 in specific tissues? What other factors may work together with SATB1?

"An important question is what turns on SATB1 during breast cancer progression," says Kohwi-Shigematsu. "That's just the beginning of the things we really want to know."

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Human skin cells into embryonic stem cells

UCLA stem cell scientists have reprogrammed human skin cells into cells with the same unlimited properties as embryonic stem cells, without using embryos or eggs.

Led by scientists Kathrin Plath and William Lowry, UCLA researchers used genetic alteration to turn back the clock on human skin cells and create cells that are nearly identical to human embryonic stem cells, which have the ability to become every cell type found in the human body. Four regulator genes were used to create the cells, which are called induced pluripotent stem cells, or iPS cells.

The UCLA study confirms the work of researchers Shinya Yamanaka at Kyoto University and James Thomson at the University of Wisconsin, first reported in late November 2007. The UCLA research appears today in an early online edition of the journal Proceedings of the National Academy of the Sciences.

The implications for disease treatment could be significant. Reprogramming adult stem cells into embryonic stem cells could generate a potentially limitless source of immune-compatible cells for tissue engineering and transplantation medicine. A patient's skin cells, for example, could be reprogrammed into embryonic stem cells, and those stem cells could be prodded into becoming various cells types — beta islet cells to treat diabetes, hematopoetic cells to create a new blood supply for a leukemia patient or motor neuron cells to treat Parkinson's disease.

"Our reprogrammed human skin cells were virtually indistinguishable from human embryonic stem cells," said lead author Plath, an assistant professor of biological chemistry and a researcher with UCLA's Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research. "Our findings are an important step towards manipulating differentiated human cells to generate an unlimited supply of patient-specific pluripotent stem cells. We are very excited about the potential implications."

The UCLA work was completed at about the same time the Yamanaka and Thomson reports were published. Taken together, the studies demonstrate that human iPS cells can be easily created by different laboratories and are likely to mark a milestone in stem cell-based regenerative medicine, Plath said.

These new techniques to develop stem cells could potentially replace a controversial cell-reprogramming method known as somatic cell nuclear transfer (SCNT), which is sometimes referred to as therapeutic cloning. To date, therapeutic cloning has not been successful in humans. However, top stem cell scientists worldwide stress that further research comparing these reprogrammed iPS cells with stem cells derived from embryos — considered the gold standard — is necessary. Additionally, many technical problems, such as the use of viruses to deliver the four genes for reprogramming, need to be overcome to produce safe iPS cells that can be used in the clinic.

"Reprogramming normal human cells into cells with identical properties to those in embryonic stem cells without SCNT may have important therapeutic ramifications and provide us with another valuable method to develop human stem cell lines," said first author Lowry, an assistant professor of molecular, cell and developmental biology and a Broad Stem Cell Center researcher. "It is important to remember that our research does not eliminate the need for embryo-based human embryonic stem cell research but rather provides another avenue of worthwhile investigation."

The four genes used in combination to reprogram the skin cells regulate expression of downstream genes and either activate or silence their expression. The reprogrammed cells were not just functionally identical to human embryonic stem cells — they also had an identical biological structure, expressed the same genes and could be coaxed into giving rise to the same types of cells.

The UCLA research team included four young scientists recruited to UCLA's new stem cell center following the passage of California's Proposition 71 in 2004, which created $3 billion in funding for embryonic stem cell research. The scientists were drawn to UCLA in part because of California's stem cell research-friendly atmosphere and the funding opportunities created by the initiative. In addition to Plath and Lowry, the team included Amander Clarke, assistant professor of molecular, cell and developmental biology, and April Pyle, assistant professor of microbiology, immunology and molecular genetics.

The creation of the human iPS cells is an extension of Plath's work on mouse stem cell reprogramming. Plath headed one of three research teams that were able to successfully reprogram mouse skin cells into mouse embryonic stem cells. That work appeared in the inaugural June 2007 issue of the journal Cell Stem Cell.

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