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Current brain imaging capabilities lack the resolution required to locate tiny amyloid beta plaques, which form in the brains of Alzheimer’s patients. To overcome this obstacle, scientists from Brookhaven National Laboratory have developed a highly detailed X-ray machine that combines micro-computed tomography with diffraction-enhanced imaging. For their study, the researchers used the technique on mouse models to image the same amyloid beta plaques found in Alzheimer’s patients. The high-resolution imaging capabilities outperformed traditional MRI. In fact, as the researchers noted, “The X-ray images were amazing, but the dose is too high to be used in humans to study Alzheimer’s.”

Being able to take a closer look at the tiny plaques will be able to tell researchers much more than what has been previously known about the disease. In fact, the researchers hope that the technique will provide an inexpensive way to find the miniscule plaques, thereby enabling doctors to identify Alzheimer’s in patients before it progresses and to track the progress of drugs that might be developed for treatment.

“Certain methods can visualize the plaque load, or overall number of plaques, which plays a role in clinical assessment and analysis of drug efficacy. But these methods cannot provide the resolution needed to show us the properties of individual amyloid beta plaques,” says Dean Connor, a former postdoctoral researcher at Brookhaven now working for the University of North Carolina. The new X-ray machine “shows that we can see these plaques in a full brain, which means we can produce images from a live animal and learn how these plaques grow,” says Connor.

News Release: X-ray may detect Alzheimer’s disease early www.emaxhealth.com  June 17, 2009

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How exactly do cancer cells originate? For decades, scientists have debated this question, weighing in on two competing theories. One theory is founded on the idea that all tumor cells are the same and as such, each has the same capacity to divide and form new tumors. The second theory suggests that only a few select cells — cancer stem cells — have the power to form new tumors. Over the past ten years, scientists have successfully isolated a variety of cancer stem cells – including leukemia, brain and breast cancer cells. The belief today is that eventually, scientists will be able to trace back all cancers to their stem cells.

However, it is difficult to find and target stem cells since only a small percentage of the cells in a tumor are stem cells. The cells can lay dormant – and because they are not actively dividing, they can survive chemotherapy and even the newest molecularly targeted treatments being used today. At some point, stem cells renew themselves and begin to differentiate, thereby creating a new tumor — the reason why some people suffer recurrences after years of being cancer free.

Now researchers at UCLA’s Jonsson Comprehensive Cancer Center have developed a unique model that allows them to further investigate the stems cells that many scientists believe to be at the root of all lung cancers. As Raj Batra, an associate professor of medicine and a Jonsson Cancer Center scientist explains, “Lung cancer is not a single disease, but a collection of sub-types with different characteristics. Some lung cancers are invasive and spread quickly throughout the body, while some become drug-resistant.”

Because stem cells possess unique properties, Batra proposed extracting candidate cancer stem cells directly from clinical specimens based on the markers they express and then validating their functionality. To locate the lung cancer stem cells, the team took specimens from patients suffering from malignant pleural effusions. This is a condition in which an abnormal amount of fluid collects between the thin layers of tissue lining the outside of the lung and the wall of the chest cavity. Their goal was to grow cells in a similar environment – in the fluid from the pleural effusions – that facilitates tumor growth within the body.

As noted in the study, which was published in the June issue of PLos One, “We were able to establish cultures in vitro with high efficiency using the novel strategy that utilized an autologous tumor microenvironment.” As Batra explains, “We used not just the tumor cells but also the cells that accompany the tumor cells and the fluid they are living and growing in. This will allow us to develop a more representative model of lung cancer allow us to test, in patient specimens, which markers indicate the presence of lung cancer stem cells. Our ultimate goal is to define lung cancer and the cells that cause it so we can develop more effective therapies.”

News Release: UCLA cancer researchers develop model that may help identify cancer stem cells  www.eurekalert.org   June 15, 2009

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“Countless” attempts have been made to edit human stem cells. Yet according to Linzhao Cheng, Ph.D., an associate professor of gynecology and obstetrics and member of the Johns Hopkins Institute of Cell Engineering, “To date, only about six genes have been successfully targeted or edited in human stem cells. That’s just not efficient enough if we want to move disease research and therapy forward.”

Moving disease research forward is precisely what researchers at the Johns Hopkins School of Medicine have done. As reported in Cell Stem Cell, the team of scientists has successfully edited the “genome of human-induced pluripotent stem cells (iPS), making it possible for the future development of patient-specific stem cell therapies.” The researchers modified a gene known to cause a rare blood disease called paroxysmal nocturnal hemoglobinuria (PNH). Their work has – for the first time – brought about a useful system to learn more about the disease. “We’ve been able to improve gene targeting and editing in human embryonic stem cells more than 200 fold,” says Dr. Cheng.

The system they developed involved the use of human embryonic stem cells, which can be expanded without limitation in the laboratory setting. They also were required to create a mutation as found in patients with PNH, an acquired disease that occurs only in adults. As Dr. Cheng explains, “It’s a tough condition to study because we need to study it in blood stem cells and they’re difficult to grow in the lab. So for years we’ve been trying to develop another cell system to better understand and perhaps fix what’s going on in PNH.”

In order to target and remove the function of the one specific gene responsible for causing the disease, the researchers successfully improved upon the standard approach of gene targeting. Their enhancements included the use of custom designed DNA cutting enzymes called molecular scissors, which are made by collaborators at Harvard University and University of Texas Southwestern Medical Center. As the study reports, the scissors were used to make a precise break in the gene that causes PNH. The researchers added the molecular scissors and a fragment of DNA containing a gene that “confers selection of rare targeted clones in both human embryonic stem cells and iPS cells.” (iPS cells are like embryonic stem cells in terms of biological properties, but generated by using adult tissues such as skin.)

Eight iPS cells lines were grown for further study. Closer examination showed that the cells contained the right number of chromosomes. There was also no trace of the molecular scissors found. And the cells had characteristics as cells from PNH patients that lack a group of cell surface molecules. “We are very excited about this accomplishment; it will enable better studies for other blood diseases. But there’s still much to do before we can really use human iPS cells in clinical therapies,” says Dr. Cheng, who says he and his team will continue to improve the techniques and start to apply them to iPS cells from patients.

News Release: Genes edited in human stem cells   www.sciencedaily.com June 19, 2009

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Five years ago, a critical discovery in the understanding of cellular aging was made by researchers from the University of North Carolina (UNC) at Chapel Hill Lineberger Comprehensive Cancer Center. Through their research, they learned that expression of a key tumor suppressor protein — p16INK4a – dramatically increases in most mammalian organs with the aging of cells and tissue.

Now, a new study conducted by the same team of researchers has shown that p16INK4a is also present in human blood and is strongly associated with aging and such behaviors as tobacco use and physical inactivity, both of which are known to accelerate the aging process. Moreover, the researchers have been able to develop a simple blood test capable of detecting p16INK4a, which is present in T-lymphocytes. Their research was based upon two key factors: blood taken from 170 healthy human volunteers and a questionnaire that the participants completed, providing information about past and current health status and behaviours. As the scientists discovered, the expression of p16INK4a increased exponentially with age, and that those increased levels were independently associated with tobacco use, physical inactivity and with biomarkers of human frailty.

“This is a major step toward a practical tool to clinically determine a person’s actual molecular age, as opposed to just their chronological age,” emphasizes UNC Lineberger member Norman Sharpless, M.D., the senior author of the study and associate professor of medicine and genetics at UNC’s School of Medicine. “We found a very weak correlation between the biomarker and obesity as measured by body mass index, despite other data suggesting that caloric restriction slows aging. The data suggest the possibility that reduced exercise may actually be worse with regard to molecular age than a higher BMI,” says Dr. Sharpless, who expressed surprise about the findings.

“Although we don’t know whether this test is a good reflection of cellular age in all types of human tissues, we believe it is a first step toward a better understanding of issues like the suitability of organs for transplantation, how well patients are likely to recover after surgery or the future toxicity of chemotherapy for cancer patients,” he adds. Study findings are being published in the journal Aging Cell.

News Release: Test detects molecular marker of aging in humans   www.eurealert.org June 16, 2009 

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