Biotech Research

In the move to use induced pluripotent stem cells to both repair and replace damaged bone tissue in patients, recent research by scientist Darja Marolt has helped advance the field in a major way. The investigator with The New York Stem Cell Foundation laboratory has used human embryonic stem cells to successfully grow bone tissue grafts, according to the foundation.

And they're not just a half-hearted first attempt: In mice, the foundation claims, Marolt and her team have proven in a recent study that the new bone growth is strong enough to support major bone tissue regeneration, and also be useful for subsequent studies and therapeutic tests.

The foundation touts the research as the first to use bone cell building material made from human embryonic stem cells to grow bone tissue in enough volume to repair small defects. Mice helped prove the concept. Marolt and others, testing the concept with the trusty rodents, found that the bone tissue they generated supported blood vessel ingrowth and developed in regular bone. And no tumors sprouted up, either, which can be an unfortunate consequence of stem cell research.

So where does embryonic stem cell research connect to the use of induced pluripotent stem cells? Marolt made the initial finding as a post-doctoral fellow at Columbia University. At The New York Stem Cell Foundation, she's pursued the idea using induced pluripotent stem cells instead, which have the same ability of embryonic stem cells to produce nearly any body cell type. But induced pluripotent stem cells come from adult cells in the body and avoid the ethical and political complications that have erupted over the years with embryonic stem cell use. Additionally, induced pluripotent stem cells are thought to be useful in making a more personalized bone graft. After all, if the cells come from the patient's own body, immune rejection and other complications typical to implants become a virtual non-issue.

The key here, however, is human clinical trials. Those are years away, and however promising the trials in mice, researchers must demonstrate similar progress in humans. If they can, the treatment will have a wide range of uses, for everyone from wounded solders to people with birth defects. So in the meanwhile, we await news of the research advancing to human clinical testing.

- read the release

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Let's talk about the p53 protein for a minute. The Star-Ledger describes it as "a kind of intracellular security force" that smacks down cells when they start veering from their designated path. Confronted by cancer, however, p53 mutates and becomes impotent, leading to tumors and the spread of more than 60% of all cancers.

But now scientists at the Cancer Institute of New Jersey and the Institute for Advanced Study have identified a class of compounds--known as thiosemicarbazones--that appears in early testing to correct p53's mutation in mice. Treated with the compounds, tumors either stopped growing so quickly or shrank. The Star-Ledger provides some interesting highlights, and details are published in the journal Cancer Cell.

The p53 protein mutation is "one of the common denominators in all cancers," study co-author Arnold Levine is quoted as saying in the Star-Ledger story. "This may be a correct way to approach it.

As the article points out, addressing the cancer-related p53 mutation could be significant for cancer treatment, as the mutation commonly hits esophageal, lung, breast, pancreatic, and many other cancers. Mice trials are always tricky, because scientists can fail to replicate the same results in people. But the stakes here are high enough to proceed to human trials--even though they would be years away. That's because, as the story notes, success in using the compounds to restore p53's functioning would go a long way to providing a targeted treatment toward fighting a significant group of cancers.

Here's how they got there: The researchers went to a public database to pick existing compounds that could address the mutation and also reboot p53. They found that thiosemicarbazones, compounds tested against cancer for years, beat back human tumor cells implanted in mice, or at least slowed their growth. Of particular note--the treatment didn't harm other cells.

- read the Star-Ledger story
- check out the journal abstract

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The researchers induced growth of extra sensory hair cells. The arrows indicate places where you wouldn't normally see these cells.

How can you help deaf mice regain their ability to hear? It sounds like the first half of a joke, but it's not. Researchers at the Emory University School of Medicine are part of the way toward figuring out a method that could eventually work, using gene therapy that helped promote the growth of new sensory hair cells in the inner ear. But the treatment seemed to benefit pre-pubescent mice far more than adult ones.

Read about the details in the Journal of Neuroscience. But the gist of what they accomplished is this: Bringing the Atoh1 gene into the cochleae of young mice helped promote the growth of those sensory hair cells. (They did this by giving mice an antibiotic that turned on the gene.) Those hair cells, in turn, as the researchers note, both connected with neurons and produced electrical signals just like normal sensory hair cells would. Of course, as is often the case, there is a catch. Prepubescent mice--two weeks old or less--experienced the most benefit. Once they got older, Atoh1 didn't do very much.

There's a lot of promise here, in theory. Some day the method could eventually work in mice (and maybe people), in using gene therapy to grow sensory hair cells that connect to neurons and help restore hearing. But this early study indicates there may be age limitations as to how well the therapy will work. And researchers need to determine if the hair cells' ability to generate electrical signals will function in the context of actual hearing.  Subsequent work by the research team will focus on stimulating sensory hair cell growth in older animals, and then examining how well their hearing recovers once scientists induce Atoh1. They didn't test hearing recovery for the initial trial. For now, sensory hair cell regeneration was enough.

"We have shown that hair cell regeneration is possible in principal," Ping Chen, Emory associate professor of cell biology, said in a statement.

- read the release
- check out the journal abstract

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Merkel cell carcinoma isn't the most common form of cancer. As the National Cancer Institute notes, only 1 person in 227,000 develops it in the United States each year. But the cancer affects older adults, people with weakened immune systems, and patients who are in the sun too much, and it can be very deadly, growing quickly and metastasizing early.

That's what makes a new finding by a husband and wife team of scientists (Patrick Moore and Yuan Chang) at the University of Pittsburgh all the more noteworthy. As Essential Public Radio reports in a story posted online, the pair tested an experimental drug called YM155 in lab mice infested with the rare cancer, and found that the drug beat back tumor growth in lab mice without being toxic. Results of the targeted treatment were so promising, they say, that they're planning human clinical trials later this year.

The treatment connects to how Merkel cell carcinoma starts, with a skin virus that is usually harmless but becomes deadly once it mutates, a phenomenon scientists believe is triggered by factors such as too much sun. The virus then uses its mutated DNA to take over human cells, fortify and multiply, the story explains. To counter this, researchers found, YM155 prevented the Merkel cell virus from taking hold and multiplying in host cells, beating back subsequent tumor growth.

- see the Essential Public Radio story
- read more from the National Cancer Institute

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A dose of antibodies, a bone marrow transplant and treatment with pancreas growth factor helped cure late-stage Type 1 diabetes in mice, researchers have found.

The effort, led by City of Hope National Medical Center endocrinologist Defu Zeng, is detailed in the journal Science Translational Medicine. Bloomberg also reports on the findings with a solid story rounding up some of the crucial fine points.

As always, take these findings with a grain of salt. Results in mice and other animal trials can be enticingly encouraging, with researchers subsequently finding that they can't repeat the same phenomenon in people, or that a treatment is too toxic for humans even though it worked in mice or animals. But a true advance in treating Type 1 diabetes is a long time coming. About 3 million people in the U.S. have Type 1 diabetes, according to data from the Juvenile Diabetes Research Foundation cited by Bloomberg.

Type 1 diabetes erupts when the body's immune system begins to attack and destroy certain pancreatic cells, hampering the body's ability to produce the insulin it needs, the JDRF explains. It also tends to attack children or teenagers first, and patients with the disease can only manage it with insulin injections to replace what the body can't make on its own. And so even though it took place in mice and not people, it's worth noting, as Bloomberg points out, that the researchers were able to cure the disease--particularly in rodents with an advanced form of it.

Scientists pursued their research in three steps. First, they gave mice with advanced Type 1 diabetes antibodies that went after two different immune system cells that attack the pancreatic cells that produce insulin. Second, the researchers then performed a bone marrow transplant on the beleaguered mice to replace the cells killed by the antibodies. This was where the change began to take place. As Bloomberg explains, the bone marrow transplant enabled the mice to begin making immune cells that wouldn't attack the insulin-producing ones. And third, to make the insulin producing-cells grow robustly, researchers essentially "watered" them with pancreas growth factor.

- here's the Bloomberg story
- read the journal abstract

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Japanese researchers at the Jikei University School of Medicine, Jichi Medical University and elsewhere have taken the generation of new organs and transplantation to a whole new level. As the newspaper The Mainichi reports, the scientists grew rat kidneys from cells transplanted from mouse fetuses. They accomplished this through a complex process involving, in part, the creation of genetically modified mice whose cells died after they took a particular medicine. After that, the newly formed kidneys from the mice were taken out and transplanted into rats given antibody suppressants. Over time, the kidneys took on the rats' blood vessels and produced their genetic information, and then subsequent medicine killed off the remaining mouse cells, leaving behind potentially functional kidneys with the rats' genetic details. In time, they hope their accomplishment could help treat liver disease. Story

Inhibiting the protein known as Sun1 helps prolong the lives of mice with the rare genetic condition known as premature aging syndrome, researchers in Singapore, Taiwan and the U.S. have determined. Typical lab mice live about two years, but a mutant mouse with the condition lives about 41 days, according to Taiwan's Central News Agency story covering the research. Researchers inactivated the protein in the mutant mice and then reduced its overall levels, boosting their life span to about 104 days. Those mice also developed some improvement in cardiovascular and bone problems that arise from premature aging syndrome, according to the report. Details are published in the journal Cell. Story

Something honeybees produce (not honey, believe it or not) is showing some serious tumor-fighting properties against prostate cancer, based on early tests on cells in the lab.

The substance is called caffeic acid phenethyl ester, or CAPE, something derived from the resin known as propolis that bees use to patch hive holes. And University of Chicago researchers say they determined that CAPE stopped early-stage prostate cancer from growing by turning off the mechanism tumor cells use to sniff out sustenance for growth. A series of cancer cell lines were used in the study.

Details are published in the journal Cancer Prevention Research. It's worth noting though, that this is an example where a homeopathic remedy may actually have potential as a new drug. For years, the researchers note, propolis has been used as a natural treatment for everything from sore throats to allergies and burns, and yes, cancer. Should the results bare themselves out in subsequent animal and human tests, there are two possible results here. Propolis could gain new clout as a herbal remedy that actually has cancer fighting properties, or it could become the basis for pharmaceutical research using natural elements as a cancer drug. The researchers themselves say the compound could become a valid-co-treatment alongside chemotherapy drugs used to fight tumors.

Right away, the compound joins tarantula venom, poisonous mushrooms, baking soda and other natural substances as possible cancer treatments that have shown promise in early-stage research.

"A typical problem in bringing some of these herbal remedies into the clinic is that nobody knows how they act, nobody knows the mechanism and therefore researchers are typically very hesitant to add them to any pharmaceutical treatment strategy," Richard Jones, a senior author on the paper, said in a statement. "Now we'll actually be able to systemically demonstrate the parts of cell physiology that are affected by these compounds."

- here's the release
- read the journal abstract

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The bird flu secrets are out of the bag. A lab-engineered bird flu strain spread easily among mammals, and the Nature article that reports the findings remains part of a hot debate in science about whether to guard details from research that in the wrong hands could be used to do harm.   

After a U.S. government committee pushed to keep a lid on the research, a University of Wisconsin-led team revealed in a controversial Nature article that a mutated version of H5N1 bird flu passes from one ferret to another without trouble, the Los Angeles Times reported. Spread in the air, the hybrid strain of bird flu included an H5 hemagglutinin gene, which plays a role in binding the virus to airway cells, and genes from the swine flu behind the 2009 pandemic. None of the animals died during the experiment.

This study, led by University of Wisconsin virologist Yoshihiro Kawaoka, underscores how malleable flu strains can be in spreading from one mammalian host to another. His research was one of two flu investigations that a U.S. government group originally set out to limit last year before changing course early this year after deciding that the findings weren't as threatening to the public as once thought, according to an Associated Press article. Bird flu, of course, has been lethal mostly to birds, but a majority of the 602 human cases of H5N1 infections have resulted in death.

Scientists have tinkered with the genetics of bird flu to identify dangerous mutations, the AP reported. The fear has been that a killer strain of the virus could lead to a pandemic, and the recent hold-up from the government committee stemmed from concerns that terrorists or other wicked individuals would use data from the studies to concoct a lethal strain and unleash the virus on the public.

A mutation that emerged in Kawaoka's study has already appeared in the Middle East and Asia, he told the Los Angeles Times. The second study that was delayed from being published because of the government group's concerns is expected to appear in the journal Science in the near future.

- check out the Times' article
- and the AP's report

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Scientists claim plenty of firsts, but this one may be worth watching. We apparently have a first-time success in using human adult stem cells to successfully treat muscular dystrophy, at least in mice.

The journal Cell Stem Cell published details of the successful study by scientists at the University of Minnesota's Lillehei Heart Institute.

Here's the gist: This is a milestone in that the scientific team demonstrated that human stem cells (derived from induced pluripotent skin cells) could be used to treat the neuromuscular disease. They did the same successful procedure in the past, using embryonic stem cells. But we all know that embryonic stem cells are highly controversial, and it is not practical to use them on a large scale anyway. What's interesting about this latest preclinical breakthrough is that the University of Minnesota team also figured out an efficient and effective way to use the stem cells, once they had them, to produce human muscle cells.

"Up until now, deriving engraftable skeletal muscle stem cells from human pluripotent stem cells hasn't been possible," principle investigator Rita Perlingeiro said in a statement. "Our results demonstrate that it is indeed possible and sets the stage for the development of a clinically meaningful treatment approach."

To get there, according to the university, the team genetically modified two induced pluripotent skin cells plus an existing embryonic stem cell line using the PAX7 gene. The Pax7 protein is key to regenerating damaged skeletal muscle tissue, the researchers say, and by controlling the gene, they nudge early-stage embryonic and induced pluripotent cells into becoming various muscle forming cells. After figuring out the ideal timing as far as when cells changed, they then had a finished product that could easily be applied toward muscle regrowth. The treatment worked more effectively at improving muscle function than myoblasts, the researchers explained, which are cell cultures coming from biopsies of adult muscle.

- here's the release
- read the journal abstract

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The University of Miami is the latest academic institution to gain a large investment designed to boost its stem cell research work, and also hopefully generate more game-changing results. In this case, the Starr Foundation is giving the university's Leonard M. Miller School of Medicine and its Interdisciplinary Stem Cell Institute (ISCI) a $10 million grant to help boost its pipeline of stem cell discoveries in development as future treatments. Of particular interest: the ISCI's efforts to rebuild damaged hearts.

"We wanted to help further that research as it moved into clinical applications," the Starr Foundation's Chairman Maurice Greenberg said in a statement.

At least 13 clinical trials are under way at the ISCI, looking at the use of stem cells to treat congestive heart failure. But trials are also testing the treatment on skin wounds, burns, pulmonary fibrosis and stroke, according to the university. One, the POSEIDON trial, is looking at the effects of stem cells taken directly from the patient to treat heart failure compared with those used from an unrelated donor. Institute director Joshua Hare is conducting the study and results are expected later this year, the university said.

All of that cash is also set to broaden preclinical and clinical stem cell research. What's more, the investment (plus a steady growth in National Institutes of Health funding), existing technology transfer programs and other efforts to raise money from interested donors will keep the ISCI viable through the end of the decade, Hare said as part of the university's announcement.

Expect more announcements in the coming months about academic institutions either launching or enhancing their stem cell research efforts. Despite years of setbacks, the field is clearly gaining more attention, at least at the academic/research level. But there is pushback, depending on the market and the type of cell being used. Embryonic stem cells, for example, remain controversial and highly political. The University of Michigan, which continues to develop new embryonic stem cell lines, is at risk of losing $7 million in state funding if school officials don't disclose how many embryos they use for research.

- read the release

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Earlier this year, we told you about U.S. government efforts to restrict publication of research involved in building variations of the H5N1 bird flu virus, over fears the viruses could become weapons in a theoretical terrorist attack. But now, as Reuters reports, the journal Nature has published the first of two of the controversial papers involved in the dust-up. Based on tests in ferrets involving a hybrid virus made of a vital H5N1 gene and the pandemic strain of the 2009 H1N1 swine flu virus, study author Yoshihiro Kawaoka of the University of Wisconsin, Madison concludes that the virus could be transmissible to humans and has the potential of becoming a pandemic. Initially, the National Science Advisory Board for Biosecurity recommended Nature redact sensitive information in the paper, and in another by Ron Fouchier of Erasmus Medical College in the Netherlands. The board has since reversed its decision, after meetings involving NIH and WHO flu experts. Kawaoka's paper earned its initial support, the story notes, because it was considered the least controversial. Story

Scientists have successfully transplanted anti-HIV stem cells into mice that served as surrogates for infected patients. Bigger still, however, the process successfully expanded and safeguarded HIV-resistant immune cells, and the cells themselves kept growing even when confronted with the virus.

University of California-Davis Health System scientists came up with the process and say they're ready to test it in human clinical trials. To that end, they're applying for a grant to fuel human studies and seeking regulatory approval to proceed. If successful, they say, the system will essentially cure patients infected with HIV, by helping boost their immune system's ability to resist the virus.

"Ideally, it would be a one-time treatment through which stem cells express HIV-resistant genes, which in turn generate an entire HIV-resistant immune system," said Joseph Anderson, a professor and stem cell researcher at UC Davis' Institute for Regenerative Cures. He's also the lead author of a study detailing the finding, which is published in the May issue of the Journal of Virology.

"Ideally" is the key word here. The results in mice are promising enough but the real question will be if the phenomenon can be replicated in humans, which doesn't always happen. There have been plenty of promising discoveries generated by testing on mice that end up screeching to a halt once they didn't repeat in clinical trials involving people. And other researchers are testing similar uses of stem cells to attack and kill HIV. Still, this deserves further watching. A stem cell approach to treating HIV could be far more effective and lasting than the current regimen of antiretroviral drugs that help keep the disease at bay but don't cure it.

The scientists took several steps to reach their milestone, starting first with mice with immune systems that are similar to patients who have HIV. Next, they genetically modified human blood stem cells (food for producing all kinds of immune cells). Then, in a nod to previous work, they came up with several anti-HIV genes and, using standard gene therapy approaches along with viruses to carry the genes, they placed them into the blood cells. Finally, they introduced the cells into the mice and then confronted them with the virus.

What they found: The cells containing HIV-resistant genes were kept safe from infection and survived when confronted with the virus, keeping normal levels of CD4+ T-cells, which are immune cells targeted by HIV and then used to grow the virus. Even more significantly, the resistant cells grew after the HIV challenge, helping further to protect CD4.

- here's the release
- read the journal abstract

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Another potential new Alzheimer's treatment is in the works--a group of compounds that appeared, in the lab, to disrupt the formation of those ominous clumps of amyloid protein many blame for propelling the mental decline in patients with the deadly disease.

Researchers at the University of California, Davis identified the new potential weapon, known as "spin-labeled fluorene compounds," a variation of fluorene compounds initially developed as imaging agents for use with PET scans to detect amyloid protein.

Their work builds on previous efforts, where the researchers found that the fluorenes bind with and destabilize the amyloid beta peptide, which scientists think destroy neurons in the brains of Alzheimer's patients. Their new finding determined that spin-labeled fluorene iterations helped block the amyloid beta formation even better than the non-labeled fluorene variety. An added nitroxide element, used to measure the fluorene activity, also helped protect neurons, the researchers said. (They conducted their tests using electron paramagnetic resonance spectroscopy, for which the nitroxide label enabled easier reading.)

Here is a big early plus: As the researchers explain, fluorene compounds can successfully penetrate the blood-brain barrier. That in itself is a milestone when many potential treatments have failed because they are unable to reach the brain. But this is so early-stage that much more work must be done. Animal tests haven't even begun yet, but researchers plan to start that work soon and will examine the safety and efficacy of spin-labeled fluorene compounds in small animals. Assuming those results are promising, then human trials become the greater challenge, because positive results in animals aren't always repeatable in people. For further study details, read the journal PLoS ONE online.

- read the release
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Nearly two years after a Cleveland Clinic immunologist generated promising results in mice with a potential preventative breast cancer vaccine, local residents and businesses are trying to help him raise enough money so that he can proceed to human clinical trials.

Cleveland's The Plain Dealer newspaper tells a really interesting story about how unconventional sources may raise the needed cash where traditional grant options have failed.

The researcher, Vincent Tuohy, is based at the Cleveland Clinic's Lerner Research Institute, and generated high-profile research in May 2010, according to the story. Nature Medicine published the results and Tuohy talked about them on national TV and in print articles around the world. His research essentially found that one vaccine dose of lactalbumin (found in the breast milk of healthy women and most breast cancers) in mice can stop existing tumors from growing and prevent new ones from forming, according to the story

Tuohy told the newspaper that he had hoped to secure additional grants from sources such as the National Cancer Institute, and new money from Susan G. Komen for the Cure, but those institutions rejected his proposals to proceed. The Department of Defense's Breast Cancer Research Program rejected a smaller grant earlier this year that would continue additional research in mice. Tuohy said the denial was based on "a technicality" because he didn't successful show that the promising data from previous testing in mice was equal scientifically to women "who had lactated during pregnancy, given birth and had breast-fed afterward," according to the article.

Why would a researcher have such problems raising the cash to proceed? The article posits the idea that competition for cancer research money is just really difficult, with the NCI funding just 12% of the 9,000-plus proposals it received in 2011. The Komen foundation isn't much better, apparently, typically giving money to fewer than 80 of the 1,400 research grant applications it receives annually.

So bit-by-bit, Tuohy has been raising money from the community at large. According to the story, a high school senior presented a $110,000 check from an annual race her family started that raises money for breast cancer research. The Cleveland Clinic itself has raised more than $271,000 for Tuohy's research since 2010, and even folks from across the country who are aware of Tuohy's work are donating money and sending checks. Tuohy is also talking to the Chinese government about developing his vaccine there. It is true that clinical advances in mice and other animal trials aren't always easily replicated in people. But Tuohy and his supporters continue to plow ahead. And the fundraising continues, according to the story, with a need to raise at least $6 million to proceed.

- here's The Plain Dealer story

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University of Sheffield scientists say they've figured out the structure of a significant part of the human obesity receptor, which could lead to development of treatments for both obesity-related diseases and anorexia.

You've probably heard this before: that scientists are "one step closer" to paving the way to developing viable drugs that combat obesity-related health problems. Well, judge for yourself whether that's true or not in this case. In short, using X-ray crystallography, the U.K. researchers say they were able to map the crystal structure of the leptin-binding portion of the obesity receptor.

Leptin is key here of course. Fat produces the hormone, and too much of it can lead to all kinds of problems for overweight and obese folks, including multiple sclerosis, cancer and heart disease, the researchers note. Too little of it (when malnutrition hits, for example) can lead to infertility, immunodeficiency and other problems.

This is what makes successful mapping of the leptin-binding portion of the obesity receptor so important. By having that map in play now, scientists can start designing potential drugs that alter how it works. Some drugs could perhaps slow down or block the receptor to treat obesity-related health problems. Others could stimulate it or speed it up to improve fertility or boost immune response, the researchers explain.

So much of research happens in increments, which are sometimes quite miniscule. But drug developers only need to know clearly what their drug target looks like to start testing compounds that alter how the target works. So the finding is indeed a good--and interesting--first step. Further details are published in the journal Structure.

- read the release
- check out the journal summary

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As University of Michigan researchers continue to resist the Republican state legislators' effort to force it to reveal how many embryos it uses for stem cell research, the fight hasn't stopped scientists from enhancing the school's position in the field.

AnnArbor.com reports that the school placed its second embryonic stem cell line on the National Institutes of Health's stem cell registry (a nationwide resource) following the first one accepted to the registry in February. That's a big deal, the article notes, because the effort helps make the university one to watch as far as stem cell research goes, and also lets NIH-backed researchers use the same line for their own efforts. Academia is all about collaboration, after all. And the particular line, according to the story, is thought to be very useful in developing a cure for Charcot-Marie-Tooth disease, a neurological disorder that causes early degeneration of muscles in legs, hand and feet. And more disease-specific embryonic stem cell lines are awaiting NIH approval.

But the action is likely to be seen as defiant by Republican lawmakers, the article explains, who say they will hold back up to $7 million in performance funding from the university if officials there don't fully reveal how many embryos they use for research. Michigan state lawmakers passed a law as part of the 2011 budget that requires state universities to reveal the embryo number, as well as other details about human embryonic research. School officials have said they don't have exact numbers and continue to resist those demands.

Specifically, University of Michigan president Mary Sue Coleman has said that her institution doesn't collect data according to the state law, but does so "according to the strict regulations of the federal government," according to the article. She added that the demand to count the number of embryos used according to the new state law is "trivializing the complexity" of stem cell research. The fight will be one to watch: Will academia ultimately triumph over political winds, or will politics shape future research funding at the state's university system?

- read the AnnArbor.com story

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This just in: News about another non-stem cell-related tissue regeneration therapy. Scientists at Duke University used microRNAs to convert fibroblasts, or scar tissue, into heart muscle cells in a mouse, boosting the heart's ability to do its job. Such research, also pursued at the University of California, San Francisco, is potentially a significant breakthrough in regenerative medicine, which has relied on embryonic stem cells for much of the work in the field thus far. As a Fox News story on the research explains, these cells are the most flexible because they can become any type of cell. But microRNAs do the job more easily than stem cell transplants and avoid the ethical concerns that embryonic stem cells create, the article notes. Details are published in the journal Circulation Research. Story

Cancer is bad enough. But anxiety could make the disease even worse as it progresses, Stanford University School of Medicine researchers believe. The key to minimizing the damage, however, may be simply keeping calm, cool and collected. And Valium could potentially help (more on that in a bit).

The finding, published April 25 in PLoS One online, builds on previous research that shows chronic stress can heighten the risk of getting cancer and other diseases. But the key here is "anxiety"--the scientists say their study is the first of its kind to directly connect high levels of anxiety to a more severe onslaught of accelerated, aggressive cancer.

Hairless, anxiety-prone mice were crucial tools toward making the discovery. First, they needed to determine what constitutes an overload of stress. They theorized that anxious mice would likely avoid danger, so they placed a number of hairless mice on a raised, cross shaped track that had both an open walkway and one concealed by walls. They also tested the rodents in a large box that was half dark and half filled with light. Scientists sifted out the anxious mice by pulling the ones out that avoided the dark part of the box and the enclosed walkway, like when people decide to avoid a dark alley in case of crime.

Once they had their anxious, hairless mice, the scientists exposed them to ultraviolet rays similar to what humans may face with too much sun exposure (10-minute blasts of radiation, three times per week for about 10 weeks). It turns out that the anxious mice developed more tumors than the calm ones and came down with invasive types of cancer, while the calm ones did not (all developed skin cancer). What's more, the nervous mice developed greater amounts of regulatory T cells, which suppress the immune system, and the anxious rodents also secreted much higher levels of corticosterone, a hormone that kicks in during stress and disease.

Yes, a finding like this in anxious, hairless mice isn't necessarily going to happen in humans. But the researchers say they will plow ahead to hopefully test the theory in human trials. More immediately, they will test to see if reducing the negative effects caused by anxiety and stress will boost how well a cancer treatment works. A regular dose of Valium over a short period of another anxiety medication might do the trick, said first author Firdaus Dhabhar, who is also a stress expert and immunologist at the Stanford Cancer Institute and Stanford Institute for Immunity, Transplantation and Infection.

"The goal," he said in a statement, "is to ameliorate or eliminate the effects of anxiety and chronic stress, at least at the time of cancer diagnosis and during treatment."

- here's the release
- read the Live Science story

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TopBP1: Remember that somewhat unwieldy name. It refers to a protein researchers at St. Jude Children's Research Hospital believe prevents DNA damage early in the formation of a brain. What's more, they think it could suppress tumor development.

The effort, led by Peter McKinnon, the paper's senior author and a member of St. Jude's Department of Genetics, tracked what happens when TopBP1 was selectively shut down in mice, at different stages of the development of their brains. They found the loss of the protein hurt the brain the worst when removed in early progenitor cells, which subdivide and develop cells that control cortex functions such as memory, vision and movement. If clinicians waited a few days before disabling the TopBP1 protein, the brain and nervous system development-related progenitor cells developed less drastic defects.

Subsequently, they found that low-dose radiation was more likely to lead to cell "suicide" in the earlier progenitor cells, with the DNA strand more sensitive to breaks. In short, they determined that TopBP1's mission in the body is to monitor DNA damage, and then step in when that damage takes place during cell replication. This refutes an earlier belief that TopBP1 was responsible for DNA replication and cell growth and development.

This is in early stages. And we all know the risks of it not being replicated in future trials. But McKinnon and the others plan to explore their finding further with additional studies.

"When we selectively knocked out TopBP1 in mice, the amount of DNA damage we saw suggests that TopBP1 is likely to be a tumor suppressor," McKinnon said in a statement. "We are exploring that question now." Further details are in the journal Nature Neuroscience.

- here's the release
- read the journal abstract

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