Gene key to common kidney cancer identified

May 21, 2010 By Leave a Comment

Washington, May 21 (ANI): Scientists have found a key gene that, when turned off, promotes the development of common kidney cancer.

Their findings suggest that a combination of agents now being tested in other cancers may turn the gene back on, providing a much-needed therapy for the difficult-to-treat cancer.

Researchers at Mayo Clinic”s campus in Florida describe a gene called GATA3 that has been silenced in clear cell renal cell carcinoma (ccRCC), the most common kind of kidney cancer, and is a key gene also lost in breast cancer.

GATA3 controls many genes and proteins that regulate cell growth, and one of them, a receptor known as the type III transforming growth factor-ß receptor (TßRIII), is absent in a number of cancers.

According to the study”s senior investigator, John Copland, a cancer biologist at the Mayo Clinic campus at Florida, these findings will surprise many in the cancer field.

“Cancer researchers know that GATA3 is essential for immune T cell development and function. As well, very recent studies show that GATA3 is also critical to breast cancer development, where GATA3 expression is limited to mammary luminal epithelial cells. GATA3 is lost during breast cancer progression and its loss is a strong predictor of poor clinical outcome in luminal breast cancer. GATA3 also plays an important role in renal development and differentiation during embryogenesis, but little is known about the role of GATA3 in the adult human kidney,” he said.

“Now it looks like GATA3 regulates the expression of genes that are critical to cancer control in the kidney, and silencing it appears to be very important to the growth of kidney cancer and probably to others tumors, as well. No one could have guessed that would be the case in kidney cancer. This is a completely novel finding,” he added.

The study has been published in the May 20, 2010 issue of Oncogene. (ANI)

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Worms may harbour human limb regeneration secrets

April 24, 2010 By Leave a Comment

Washington, April 24(ANI): Regeneration of old or damaged human organs and tissues may soon be a reality, as scientists have discovered the gene that enables an extraordinary worm to regenerate its own body parts after amputation.

The team of researchers, led by Dr Aziz Aboobaker, a Research Councils UK Fellow in the School of Biology, found that planarian worms regenerates its body parts, including a head and brain, through a gene called ”Smed-prep”.

These remarkable creatures contain adult stem cells that are constantly dividing and can become all of the missing cell types.

They also have the right set of genes working to make this happen exactly as it should so that when they re-grow body parts they end up in the right place and have the correct size, shape and orientation.

Dr Aboobaker said: “These amazing worms offer us the opportunity to observe tissue regeneration in a very simple animal that can regenerate itself to a remarkable extent and does so as a matter of course.

“We want to be able to understand how adult stem cells can work collectively in any animal to form and replace damaged or missing organs and tissues. Any fundamental advances in understanding from other animals can become relevant to humans surprisingly quickly.

“If we know what is happening when tissues are regenerated under normal circumstances, we can begin to formulate how to replace damaged and diseased organs, tissues and cells in an organised and safe way following an injury caused by trauma or disease.

“This would be desirable for treating Alzheimer’s disease, for example. With this knowledge we can also assess the consequences of what happens when stem cells go wrong during the normal processes of renewal — for example in the blood cell system where rogue stem cells can result in Leukaemia.”

Smed-prep is necessary for the correct differentiation and location of the cells that make up a planarian worm’s head. It is also sufficient for defining where the head should be located on the worm.

The team learnt that although the presence of Smed-prep is vital so that the head and brain are in the right place, the worm stem cells can still be persuaded to form brain cells as a result of the action of other unrelated genes. But even so, without Smed-prep these cells do not organise themselves to form a normal brain.

Daniel Felix, a graduate student who carried out the experimental work said: “The understanding of the molecular basis for tissue remodeling and regeneration is of vital importance for regenerative medicine. Planarians are famous for their immense power of regeneration, being able to regenerate a new head after decapitation.

“With the homeobox gene Smed-prep, we have characterised the first gene necessary for correct anterior fate and patterning during regeneration. It has been a really exciting project and I feel very lucky to have had this study as the centre piece of my thesis work”

The study has been published in the open access journal PLoS Genetics. (ANI)

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‘Liposuction leftovers’ better than skin cells to regenerate tissues

September 8, 2009 By Leave a Comment

Washington, Sep 8 (ANI): Fat that is left after liposuction is a huge bank of versatile cells that could be more quickly and easily coaxed to become induced pluripotent stem (iPS) cells than the often used skin cells, according to a study by researchers at Stanford’s School of Medicine.

Lead researcher Dr. Michael Longaker has even called the readily available liposuction leftovers “liquid gold”.

“We’ve identified a great natural resource,” said Longaker.

Reprogramming adult cells to function like embryonic stem cells is one way the researchers hope to create patient-specific cell lines to regenerate tissue or to study specific diseases in the laboratory.

“Thirty to 40 percent of adults in this country are obese. Not only can we start with a lot of cells, we can reprogram them much more efficiently. Fibroblasts, or skin cells, must be grown in the lab for three weeks or more before they can be reprogrammed. But these stem cells from fat are ready to go right away,” said cardiologist Dr. Joseph Wu.

As the cells can also be converted without the need for mouse-derived “feeder cells”, they could be an ideal starting material for human therapies.

The flab, which is left post liposuction, is filled with multipotent cells called adipose, or fat, stem cells.

Unlike highly specialized skin-cell fibroblasts, these cells have a relatively wide portfolio of differentiation options-becoming fat, bone or muscle as needed.

The researchers believe that it is this pre-existing flexibility that gives these cells an edge over the skin cells.

“These cells are not as far along on the differentiation pathway, so they’re easier to back up to an earlier state. They are more embryonic-like than fibroblasts, which take more effort to reprogram,” said first author Dr. Ning Sun.

These reprogrammed iPS cells are usually created by expressing four genes, called Yamanaka factors, normally unexpressed (or expressed at very low levels) in adult cells.

The researchers found that the fat stem cells actually express higher starting levels of two of the four reprogramming genes than do adult skin cells, which indicated that these cells are already primed for change.

After adding all four genes, about 0.01 percent of the skin-cell fibroblasts eventually became iPS cells but about 0.2 percent of the fat stem cells did so-a 20-fold improvement in efficiency.

The new iPS cells passed the standard tests for pluripotency.

“The idea of reprogramming a cell from your body to become anything your body needs is very exciting,” said Longaker

The findings have been published in the Proceedings of the National Academy of Sciences. (ANI)

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Gene key to maintaining embryonic stem cells’ pluripotent state identified

July 10, 2009 By Leave a Comment

London, July 9 (ANI): Scientists at the University of California, San Francisco claim to have identified a gene crucial to maintaining embryonic stem cells’ all-purpose, pluripotent state.

The researchers say that their finding may prove helpful in improving the scientific understanding of how cells acquire their specialized states, and provide a strategy to efficiently reprogram mature cells back into the pluripotent state, an elusive step in stem cell research but one crucial to a range of potential clinical treatments.

They conducted their research on mouse embryo cells, and found that a gene known as Chd1 loosens the packaging that normally protects DNA in the cell nucleus.

The research group say that this step, known as chromatin remodelling, allows the cell’s protein-making machinery to gain access to the DNA, and transform progenitor cells into specialized cells and tissue, such as neurons, muscle and bone.

A number of genes are known to trigger chromatin remodelling, allowing small sections of DNA to become accessible in order to make specific proteins.

The scientists say that Chd1 is the first gene found to regulate a “global” loosening of the DNA in embryonic stem cells. The global condition sets the stage for turning on many different genes to make a broad range of specialized cells.

“Embryonic stem cells are characterized by this open state, but, up to now, we didn’t know the mechanisms that maintain this state, or even if it is necessary for the full stem cell potential,” Nature magazine quoted Alexandre Gaspar-Maia, lead author of the paper, as saying.

“We found that Chd1 is critical for both, and for allowing an efficient reprogramming. Chd1 is important for allowing the normal differentiation process, and it is essential for playing the ‘differentiation tape’ backwards – bringing differentiated cells back to pluripotency,” he added.

The scientists discovered the pivotal role of Chd1 by using the powerful technique of RNA interference (RNAi) to screen this gene, and 40 other candidate genes.

When the researchers silenced the gene by using the technique, embryonic stem cells could not make the full range of specialized cells.

In a laboratory test used to simulate normal cell specialization, the scientists detected no differentiation of cardiac muscle, and also no formation of a tissue known as primitive endoderm, which is essential for the embryo to survive and develop.

The researchers also found Chd1 to be necessary for the reprogramming of specialized cells back to the pluripotent stem cell state.

They are planning to further study chromatin remodelling in more detail to clarify what other molecules work in concert with the Chd1 gene to direct the process, hoping that this would aid efforts to increase the efficiency and safety of reprogramming cells.

According to them, their research may also shed light on how cells transition from one type to another, a process that happens normally during embryonic development and goes astray in cancer.

“We now know that Chd1 is essential, and, so far, appears unique in its global effect, but we expect that there are major players yet to be discovered,” said senior author Ramalho-Santos, UCSF assistant professor of obstetrics, gynecology and reproductive sciences, and pathology.

“If we can understand how Chd1 works, that will also tell us more about how the cells regulate their precise specialization during development, and turn on their pluripotency program during reprogramming,” Ramalho-Santos added.

Based on their findings, the researchers came to the conclusion that embryonic stem cells exist in a dynamic state, poised between the open condition that may assure the cell’s full potential, and the more constrained state that allows only certain kinds of cells to progress.

Chd1, they say, is central to maintaining the open, pluripotent stem cell state. (ANI)

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Scientists create artificial sperm cells from human embryonic stem cells

July 8, 2009 By Leave a Comment

London, July 8 (ANI): Scientists have achieved a major breakthrough in making sperm-like cells from human embryonic stem cells.

Karim Nayernia, of the University of Newcastle Upon Tyne in the UK, has revealed that these cells can swim like sperm do.

He says that his team used the same technique to create sperm-like cells from human embryonic stem cells that he had used in 2006 to produced sperm from mouse embryonic stem cells.

The team labelled embryonic stem cells with a fluorescent marker attached to a particular gene that is expressed during reproductive-cell development, and cultured the cells in a medium that encourages differentiation into sperm cells.

The researchers observed that about three per cent of the resulting cells contained enough DNA for only one set of chromosomes, suggesting that meiosis had occurred.

Some of these cells also formed tails and were motile, they said.

Nayernia and his colleagues have yet to analyse methylation patterns in their sperm-like cells, or conduct a detailed study of the cells’ morphology.

While there work has been hailed by other scientists, the sperm-like cells created by the researchers will still require much more characterization before they can be used as an experimental model for the study of inherited diseases and infertility.

Another hurdle is that, in several countries, it may actually be illegal even if these cells were properly characterised.

Nayernia admits it, but still insists that his team’s work was a “proof-of-principle experiment”.

“We don’t claim that it is fully normal sperm, but they do have some of the right characteristics,” Nature magazine quoted him as saying.

Meanwhile, he and his colleagues have also launched a project to produce sperm cells from induced pluripotent stem cells, which can be generated from adult cells.

The researchers believe that such cells would make it easier to derive sperm cells from many individuals.

“Then we can, for example, see whether environmental factors or genetic factors are affecting fertility, and which step of sperm production has been affected by those factors,” he says. (ANI)

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Indian-origin scientist finds genetic switch that may help treat vascular diseases

July 6, 2009 By Leave a Comment

London, July 6 (ANI): Taking a big leap towards finding a treatment of vascular diseases, a team led by an Indian-origin scientist at the Gladstone Institute of Cardiovascular Disease (GICD) has discovered a key switch that makes stem cells turn into the type of muscle cells that reside in the wall of blood vessels.

Dr. Deepak Srivastava’s study claimed that the same switch could be used in the future to limit growth of vascular muscle cells that cause narrowing of arteries leading to heart attacks and strokes, limit formation of blood vessels that feed cancers, or make new blood vessels for organs that are not getting enough blood flow.

It was found that a tiny RNA molecule, called microRNA-145 (miR-145), not only had all the information necessary to turn a stem cell into a vascular smooth muscle cell (VSMC), but could also affect VSMCs in the adult artery.

VSMCs possess the unique property of dividing on their own when an artery is injured or during atherosclerosis, ultimately causing narrowing of the vessel leading to occlusion.

The researchers found that miR-145 and its sister microRNA, miR-143, work together to stop the pathologic division of VSMCs.

But in the setting of vessel disease, their activity was turned down, which made the VSMCs to divide and clog up the artery.

MicroRNAs are small RNA molecules that do not make protein, but instead affect that amount of protein synthesized by the cell from their target mRNAs-the blueprints for translating the genetic code into proteins.

The researchers found that miR-145 and miR-143 together controlled the synthesis of a network of “master regulators” that control VSMCs, and thereby were able to function as a central “switch” for the behaviour of these important cells.

“The ability of miR-145 to efficiently direct the cell fate of vascular smooth muscle cells from stem cells represents the power of these tiny microRNAs to exert major effects on cells. We hope that we can use this knowledge to control when the body makes or does not make new blood vessels,” Nature magazine quoted Srivastava as saying.

He added: “Our findings in this study offer insights into regulatory mechanisms that govern the differentiation and proliferation of smooth muscle. They have fundamental implications for the treatment of vessel diseases like atherosclerosis and also may be important for cancer.”

The study has been published in the current issue of the journal Nature. (ANI)

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Tumour suppressor gene in flies holds promise to prevent human brain tumours

June 23, 2009 By Leave a Comment

Washington, June 23 (ANI): Researchers at Duke-NUS Graduate Medical School in Singapore have identified a tumour-suppressing protein in the brains of fruit flies, called PP2A (protein phosphatase 2A), which has a counterpart in mammals.

This work attains significance because it holds promise to prevent the formation of brain tumours in humans, say the researchers.

“Our data explicitly show that the fruit-fly protein PP2A (protein phosphatase 2A) suppresses brain tumour formation and controls the balance of self-renewal and differentiation of neural stem cells,” said Dr. Hongyan Wang, senior author of the study.

“Given that mechanisms for stem cell division in flies and mammals are likely to be similar, our study on fly PP2A may provide useful insights for certain types of human brain tumours and possibly in a wide variety of cancers,” said Wang.

The researchers studied flies that had a PP2A mutation and learned that the flies with missing or abnormally expressed PP2A had ten times the amount of stem cell growth in their larval brains.

The flies’ neural stem cells did not become neurons (nerve cells) in the brain, the types of cells needed for normal function. But they effectively grew into a tumour mass.

In an earlier study, the researchers had identified a protein kinase called Polo as a tumour suppressor.

As phosphatases like PP2A usually have the opposite biochemical function to kinase, the scientists predicted that PP2A would stop the tumour suppressor Polo and allow for unchecked cell growth.

“We were very surprised when we found that PP2A also suppressed tumours,” said Wang.

Follow-up experiments showed that PP2A is important for regulating Polo kinase function, and showed that these two critical brain tumour suppressors work in tandem to control neural stem cell divisions.

“Our discovery suggests that PP2A and Polo, both of which are crucial brain tumor-suppressors and cell cycle regulators, can function in the same pathway to regulate stem cell self-renewal and tumor development,” said Wang.

The study has been published online in the journal Development. (ANI)

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Key proteins linked to ovulation identified

May 15, 2009 By Leave a Comment

Washington, May 15 (ANI): Researchers from the National Institutes of Health have identified two proteins that play a vital role in ovulation process.

The discovery, researchers hope, would help in treating infertility resulting from a failure of ovulation. It will also aid in developing new means to prevent pregnancy by preventing the release of the egg.

The proteins, called ERK1 and ERK2, appear to bring about the maturation and release of the egg.

“Ovulation results from a complex interplay of chemical sequences,” said Dr Duane Alexander, director of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)

“The researchers have identified a crucial biochemical intermediary controlling the release of the egg.

“The finding advances our understanding and may one day contribute to new treatments for infertility as well as new ways to prevent pregnancy from occurring,” Alexander added.

ERK1 and ERK2 are a critical nexus between the surge in luteinizing hormone and ovulation, said Dr Louis V. De Paolo chief of the NICHD Reproductive Sciences Branch.

“This is a key chemical pathway that affects not only ovulation, but egg cell maturation and granulosa cell differentiation into luteal cells,” Dr. De Paolo added.

Luteinizing hormone is a hormone produced by the anterior pituitary gland.

Previously, researchers did not know how luteinizing hormone triggered the ovary’s release of the egg and the production of progesterone by the granulosa cells.

In the current study, the researchers discerned that luteinizing hormone appears to signal the release of the ERK 1 and ERK 2 proteins.

“We’re still at the tip of the iceberg. We need to understand it all,” said De Paolo said. (ANI)

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New way to reduce tumour-risk factor in stem cell therapy unveiled

May 7, 2009 By Leave a Comment

Washington, May 7 (ANI): Paving the way for advancement in the field of stem cell therapy, scientists have discovered a method to potentially eliminate the tumour-risk factor in utilizing human embryonic stem cells.

Human embryonic stem cells are theoretically capable of differentiation to all cells of the mature human body, and are hence defined as “pluripotent”.

The above capability, along with the ability to remain undifferentiated indefinitely in culture, make regenerative medicine using human embryonic stem cells a potential tool for the treatment of various diseases, including diabetes, Parkinson’s disease and heart failure.

However, the biggest hurdle in using stem cells is their tendency to grow into a specific kind of tumour, called teratoma, when they are implanted in laboratory experiments into mice.

And scientists have thought that the tumorigenic feature will be manifested upon transplantation to human patients as well.

Thus the development of tumours from embryonic stem cells is especially puzzling, keeping in mind that these cells start out as completely normal cells.

So, researchers at the Stem Cell Unit in the Department of Genetics at the Silberman Institute of Life Sciences at the Hebrew University analysed the genetic basis of tumour formation from human embryonic stem cells, and identified a key gene that is involved in this unique tumorigenicity.

The gene called survivin is expressed in most cancers and in early stage embryos, but it is almost completely absent from mature normal tissues.

The gene is especially highly expressed in undifferentiated human embryonic stem cells and in their derived tumours.

The researchers could neutralise the activity of survivin in the undifferentiated cells as well as in the tumours, and thus managed to initiate programmed cell death (apoptosis) in those cells.

The inhibition of this gene just before or after transplantation of the cells could minimize the chances of tumour formation.

But the researchers have warned that a combination of strategies may be needed to address the major safety concerns regarding tumour formation by human embryonic stem cells. (ANI)

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NASA’s electronic nose can detect brain cancer cells

May 3, 2009 By Leave a Comment

Washington, May 1 (ANI): Researchers have found that an electronic nose developed for air quality monitoring on Space Shuttle Endeavour can also be used to detect cancerous brain cells.

The finding can open up new possibilities for neurosurgeons to fight against brain cancer.

Neurosurgeons from the City of Hope Cancer Centre, along with scientists from the Brain Mapping Foundation in West Hollywood and the Jet Propulsion Laboratory (JPL) in Pasadena have found that NASA’s electronic nose can also be used to detect odour differences in normal and cancerous brain cells.

“This pilot study lays the groundwork for future research that may help us to better understand cellular trafficking, contribute to designing better approaches for the detection and differentiation of brain cancer, and understand the pathophysiology of intracranial gliomas,” said Babak Kateb, lead author of the paper, Chairman and Scientific Director of the Brain Mapping Foundation.

The electronic nose, which is to be installed on the International Space Station in order to automatically monitor the station’s air, can detect contaminants within a range of one to approximately 10,000 parts per million.

These experiments will help pave the way for more sophisticated biochemical analysis and experimentation.

The results of the pilot study are set to be published in an IBMISPS-NeuroImage. (ANI)

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Novel genetic regulator involved in head, throat cancers discovered

May 2, 2009 By Leave a Comment

Washington, Apr 29 (ANI): In a major scientific advancement, pharmacy researchers at Oregon State University have discovered a genetic regulator, called CTIP2, which is expressed at higher levels in the most aggressive types of head and neck cancers.

The study might help in the identification of these cancers earlier or even offer a new therapy at some point in the future.

In a recent research, the “transcriptional regulator” CTIP2 was demonstrated to be a master regulator that has important roles in many biological functions, ranging from the proper development of enamel on teeth to skin formation and the possible treatment of eczema or psoriasis.

But, in the latest study, scientists found for the first time that levels of CTIP2 were more than five times higher in the “poorly differentiated” tumour cells that caused the most deadly types of squamous cell carcinomas in the larynx, throat, tongue and other parts of the head.

The researchers even found a high correlation between greater CTIP2 expression and the aggressive nature of the cancer.

They said that head and neck squamous cell cancers are the sixth most common cancers in the world, and a significant cause of mortality. They have been linked to such things as tobacco use and alcohol consumption.

“Serious head and throat cancer is pretty common, and mortality rates from it haven’t improved much in 20 years, despite new types of treatments. With these new findings, we believe it should be possible to create an early screening and diagnostic tool to spot these cancers earlier, tell physicians which ones need the most aggressive treatments and which are most apt to recur,” said Gitali Indra, an assistant professor in the OSU College of Pharmacy.

The scientists hope that the work could lead to new therapeutic approaches.

Also they said that this genetic regulator could be involved in both skin development and these types of cancer makes some sense, as both originate from epithelial cells.

The study speculated that CTIP2 could help regulate the growth of what is believed to be a cancer “stem” or “progenitor” cell, which has a greater potential to generate tumours through the stem cell processes of self-renewal and differentiation into multiple cell types.

Therefore, targeting cancer stem cells holds promise for improvement of survival and quality of life of cancer patients.

The study is published in PLoS ONE a professional journal. (ANI)

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How stem cells could be used to repair damaged heart

April 27, 2009 By Leave a Comment

London, Apr 27 (ANI): In a new study on stem cells, scientists at Gladstone Institute of Cardiovascular Disease have discovered a combination of genes, which can play a vital role in repairing damaged heart.

The research team led by Dr Benoit Bruneau has found that the combination of three genes can turn nonmuscle cells into beating heart cells.

“The heart has very little regenerative capacity after it has been damaged,” said Nature magazine quoted Bruneau as saying.

“With heart disease the leading cause of death in the Western world, this is a significant first step in understanding how we might create new cells to repair a damaged heart,” he added.

In the study conducted using mouse model, Bruneau and postdoctoral fellow Jun K. Takeuchi added different combinations of transcription factors to mouse cells, of which these two appeared key in pushing cells into heart cells, however, they were not enough.

The three proteins, together, direct the differentiation of mouse embryonic cells into beating heart cells.

They are a mix of transcription factors, which bind to DNA and influence gene expression, and a heart-specific chromatin-remodelling protein.

“When we finally identified the key factor that could work with GATA4 and TBX5 to turn cells into beating heart cells, it was somewhat of a surprise to us,” Bruneau added. (ANI)

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BMW CEO says used car values steadying -paper

April 12, 2009 By Leave a Comment

FRANKFURT, April 10 (Reuters) – German carmaker BMW’s (BMWG.DE) chief executive said residual values of used cars have been steadying since the beginning of this year, according to a newspaper interview.

“Prices for used cars in the United States and in Great Britain have stabilised. But I would not want to deduce a turnaround from that yet,” Norbert Reithofer told Sueddeutsche Zeitung in an interview to be published on Saturday.

Carmakers including Chrysler and General Motors (GM.N) have halted or cut back their leasing business because falling residual values of cars coming off leases can mean big losses.

BMW absorbed a 1.6 billion euros ($2.13 billion) hit last year after hiking provisions for risky leasing deals, substantially more than peer Daimler’s (DAIGn.DE) 465 million euros impairment charge.

In the global auto industry as a whole, Reithofer said he saw a recovery from 2010 that would strengthen in 2011.

“We are currently seeing a slight improvement, but we do not expect a significant market recovery this year.”

He said he expected that unit sales declines seen across the industry could remain in a double-digit percentage range throughout 2009.

He said BMW could weather the storm of the global economic crisis for a while longer thanks to more than 20 billion euros in equity capital.

“Hypothetically, we could manage one or two years with relatively high losses,” he said.

He also reiterated that he could imagine expanding BMW’s cooperation with Daimler to further parts of the business.

BMW has been pooling component purchases with Daimler’s Mercedes-Benz, but this encompassed less than 100 parts that are not relevant to the brand image.

Reithofer previously said he wanted to expand this cooperation wherever possible without diluting the strong differentiation in brands. ($1=.7530 euros) (Reporting by Maria Sheahan; editing by Mike Nesbit)

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Key gene that protects against leukaemia identified

April 9, 2009 By Leave a Comment

Washington, Apr 9 (ANI): Paving the way for a targeted treatment for leukaemia and other blood cancers, scientists have found a gene called JunB that controls the rapid production and differentiation of the stem cells that produce all blood cell types.

The investigators have also uncovered evidence that could lead to a protocol for bone marrow transplants that could boost the chance of a cure in some patients.

Led by Dr. Emmanuelle Passegue, of the University of California, San Francisco, the research team has shown that the JunB gene is at the centre of a complex network of molecular and environmental signals that regulate the proliferation and differentiation of hematopoietic stem cells.

Hematopoietic stem cells are the multipotent, self-renewing cells that give rise to all blood cell types.

For the study, the researchers studied the behaviour of JunB-deficient HSCs in both the culture dish and when transplanted into mice.

In every case wherein engraftment of the HSCs occurred in the mice, the scientists noted a progressive expansion of the myeloidlineage, which constitutes a type of mature white blood cell that fights infection.

After 6 to 12 months of transplantation, the expansion led to the development of a myeloproliferative disease, which can evolve to leukaemia.

The finding indicated that the proliferating JunB-deficient HSCs causes leukaemia, say the researchers.

JunB curtails both the rate at which HSCs are proliferating and the rate of differentiation toward the myeloid lineage that ultimately results in leukaemia.

When JunB is absent, HSCs lose their ability to respond to signals from the protein receptors Notch and TGF-beta, which reside on the cells’ surface and play critical roles in determining cell fate.

“By uncovering this mechanism, we might one day be able to determine the difference between normal HSCs and leukemic stem cells in gene regulatory networks. This could allow us to develop more targeted therapies. These kinds of therapeutic applications are still down the road, but they can happen very quickly in the blood/leukemia field,” said Passegue.

The study demonstrated that JunB does not affect the cells’ potential for unlimited self-renewal.

The study has been published in the journal Cancer Cell. (ANI)

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Novel stem cell therapy may treat deafness

March 29, 2009 By Leave a Comment

Washington, Mar 29 (ANI): In a breakthrough study, researchers have developed a new stem cell therapy that may help in treating hearing impairment.

Deafness typically involves the loss of sensory receptors, called hair cells, for their “tufts” of hair-like protrusions, and their associated neurons.

Led by Dr. Marcelo N. Rivolta of the University of Sheffield, researchers have has successfully isolated human auditory stem cells from foetal cochleae (the auditory portion of the inner ear) and found that they could be differentiated into sensory hair cells and neurons.

The researchers carefully dissected and cultured cochlear cells from 9-11 week-old human fetuses.

They then expanded the cells and maintained in vitro for up to one year, with continued division for the first 7 to 8 months and up to 30 population doublings, which is similar to other non-embryonic stem cell populations, such as bone marrow.

Gene expression analysis showed that all cell lines expressed otic markers that lead to the development of the inner ear as well as markers expressed by pluripotent embryonic stem cells, from which all tissues and organs develop.

The researchers could formulate conditions that allowed for the progressive differentiation into neurons and hair cells with the same functional electrophysiological characteristics as cells seen in vivo.

“The results are the first in vitro renewable stem cell system derived from the human auditory organ and have the potential for a variety of applications, such as studying the development of human cochlear neurons and hair cells, as models for drug screening and helping to develop cell-based therapies for deafness,” said the authors.

Although the hair cell-like cells did not show the typical formation of a hair bundle, the authors suggest that future studies will aim to improve the differentiation system.

Now, the researchers are working on using the knowledge from this study to optimise the differentiation of human embryonic stem cells into ear cell types.

“Although considerable information has been obtained about the embryology of the ear using animal models, the lack of a human system has impaired the validation of such information,” noted the authors.

Dr Ralph Holme, director of biomedical research for Royal National Institute for Deaf and Hard of Hearing People, said: “There are currently no treatments to restore permanent hearing loss so this has the potential to make a difference to millions of deaf people.”

The study is published in the April issue of Stem Cells. (ANI)

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Novel test to predict breast cancer metastasis

March 28, 2009 By Leave a Comment

Washington, Mar 28 (ANI): Researchers from NewYork-Presbyterian Hospital/Weill Cornell Medical Center have identified a new marker that may lead to the development of a novel test to predict breast cancer metastasis.

The research team has identified a marker called TMEM, for Tumor Microenvironment of Metastasis, density of which is associated with the development of distant organ metastasis via the bloodstream – the most common cause of death from breast cancer.

“Currently, anyone with a breast cancer diagnosis fears the worst – that the cancer will spread and threaten their lives,” said Dr. Joan G. Jones, professor of clinical pathology and laboratory medicine at Weill Cornell Medical College and director of Anatomic Pathology at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.

“A tissue test for metastatic risk could alleviate those worries, and prevent toxic and costly measures like radiation and chemotherapy,” Jones added.

“If patients can be better classified as either low risk or high risk for metastasis, therapies can be custom tailored to patients, preventing over-treatment or under-treatment of the disease,” said first author Dr. Brian D. Robinson, resident in Anatomic Pathology at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.

During the study, the researchers analysed the tissue samples of 30 patients with invasive ductal carcinoma of the breast who developed systemic, distant-organ metastases.

These samples were compared to matched controls that had only localized disease i.e., invasive ductal carcinoma limited to the breast or with regional lymph node metastasis only.

They found that TMEM density was more than double in the group of patients who developed systemic metastases compared with the patients with only localized breast cancer.

“Traditionally, the likelihood of breast cancer metastasis is estimated based on tumor size, tumor differentiation – how similar or dissimilar the tumor is compared to normal breast tissue – and whether it has spread to the lymph nodes,” said Jones.

“While these are useful measures, TMEM density directly reflects the blood-borne mechanism of metastasis, and therefore may prove to be more specific and directly relevant.”

The findings appear in the journal Clinical Cancer Research. (ANI)

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How stem cells turn into blood cells

March 6, 2009 By Leave a Comment

Washington, Mar 6 (ANI): A research team led by an Indian origin scientist has shed light on how stem cells turn into blood cells.

Stem cells are the building blocks of every organ and tissue in the body. They have a unique ability to become any type of cell in the body including bone, muscle and blood cells.

Dr. Mick Bhatia, director of the McMaster University Stem Cell and Cancer Research Institute claim to have identified a particular cell pathway, known as the noncanonical Wnt that prompts stem cells to specialize and become blood cells.

The pathway appears to organize the stem cells so that they can respond to signals telling them what to turn into.

“By directing cell differentiation, this method provides the most efficient way to produce blood cells that we are aware of to date,” said Bhatia.

“This finding is exciting because it may provide a new way to make blood from human stem cells that could be used to regenerate the blood system in patients, including those with leukemia or those undergoing cancer treatments that indirectly destroy the immune and blood system,” said Dr. Christine Williams, Director of Research Programs at the Canadian Cancer Society Research Institute.

The findings are published in Cell Stem Cell. (ANI)

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Stem cells may stop osteoporosis, promote bone growth

March 5, 2009 By Leave a Comment

Washington, Mar 5 (ANI): A new study has shown that tweaking a certain group of multipotent stem cells-mesenchymal stem cells-with a hormone called interferon (IFN) in our bodies, might stop osteoporosis and promote bone growth.

Scientists from the Research Institute of the McGill University Health Centre say that IFN holds great promise to repair bones affected by osteoporosis.

“We have identified a new pathway, centered on IFN gamma, that controls the bone remodelling process both in-vivo and in-vitro.

More studies are required to describe it more precisely, but we are hopeful that it could lead to a better understanding of the underlying causes of osteoporosis, as well as to innovative treatments,” said Dr. Richard Kremer, the study’s lead author and co-director of the Musculoskeletal Axis of the McGill University Health Centre.

He added: “First, we stimulated cultured mesenchymal stem cells to turn into bone cells (osteoblasts) in-vitro. We realised that this differentiation process involved IFN gamma-related genes, but also that these bone cells precursors could both be stimulated by IFN gamma and produced IFN gamma.”

In the next step, the researchers focussed on an animal model where IFN gamma effect is blocked by inactivating its receptor-a model called IFN gamma receptor knock-out.

They later conducted bone density tests, comparable to those used to diagnose people with osteoporosis.

The results revealed that the animals had significantly lower bone mass than their healthy counterparts, and also the mesenchymal stem cells were found to have a decreased ability to make bone.

“These findings confirm that IFN gamma is an integral factor for mesenchymal stem cells’ differentiation into osteoblasts also in-vivo,” said Kremer.

Both in-vitro and in-vivo results proved that IFN gamma was key to the differentiation of mesenchymal cells into bone cells, and to growth process of the bone.

The findings provide hope that IFN gamma itself, or another molecule involved in its pathway, could soon become efficient drug-target for an antidote for osteoporosis.

The study has been published in the journal Stem Cells. (ANI)

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Scientists identify master control gene to suppress cancer

February 24, 2009 By Leave a Comment

Washington, Feb 24 (ANI): Expression of a master control gene called Ato in fruit flies, and ATOH1 in mammals, can suppress cancer, according to scientists at VIB and K. U. Leuven.

The researchers say that these genes, when switched off, may cause cancer in fruit flies, mice, and humans.

They, however, add that it possible to switch the genes on again with drugs.

While all cells in an organism are meant for some specific functions, cancer is a collection of cells without a function, which grow when normal genetic controls of cell division are interrupted.

And as cancer cells are less differentiated than normal cells, the researchers hypothesised that the final steps of differentiation prevent cells from becoming cancerous.

In the new study led by Wouter Bossuyt and Bassem Hassan, the researchers tested the above theory and demonstrated that in the fruit fly, master control genes steering the specialization step inhibit tumour formation.

They demonstrated that loss of one of those genes, Atonal homolog 1 (ATOH1), causes colon cancer in mice.

The gene regulates the last step in the specialization to epithelial cells of the colon, and the researchers have shown that humans with colon cancer frequently have an inactivated ATOH1 gene.

It was possible for researchers to reactivate the gene in human colon cancer cells grown in culture, which in turn caused the tumour cells to stop growing and commit suicide.

The finding indicated that the gene could be switched back on in living patients to target their cancers.

The researchers are currently working towards developing a cancer therapy by incorporating the above findings.

The findings have been reported in two papers in the leading online open access journal PLoS Biology. (ANI)

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Newly discovered brain protein leads to new model for Alzheimer’s disease

February 20, 2009 By Leave a Comment

London, Feb 20 (ANI): While trying to unravel the normal function of a protein implicated in Alzheimer’s disease (AD), scientists have discovered a naturally occurring protein that provides a new therapeutic target for the disease.

The new finding, by scientists in California and France, rules out the current theory that AD is a disease of toxicity stemming from damage caused by sticky plaques that collect in the brain.

However, the Buck Institute for Age Research and the CNRS (Centre Nationale de la Recherche Scientifique) study points to the condition as a disorder involving an imbalance in signalling between neurons.

One of the mysteries of AD has been the normal function of the amyloid precursor protein (APP) that are concentrated at the points where neurons connect.

Although the sticky amyloid plaques are believed to be the biggest characteristic of AD resulting from APP, but there’s not much evidence to prove that APP exists simply to cause Alzheimer’s disease.

In the study, scientists have shown that APP binds to netrin-1, a protein that helps to guide nerves and their connections in the brain, as well as helping nerve cells to survive.

When netrin-1 was given to mice that have a gene for Alzheimer’s disease their symptoms were reversed, and the sticky amyloid was reduced.

The results suggest that the long-held belief that AD is caused by brain cell damage inflicted by the amyloid plaques may be wrong.

Instead, the disease apparently stems from an imbalance between the normal making and breaking of connections in the brain, with netrin-1 supporting the connections and the amyloid breaking the connections – both by binding to APP and activating normal cell programs.

It was found that netrin-1, not only binds to APP keep the nerve cells alive and connected, but it also shut down the production of the amyloid, all of which makes it an interesting potential therapeutic.

“We now believe that APP is part of a ‘plasticity module’ that functions in normal memory and forgetting, and that netrin-1 gives us an important starting point to restore the normal balance, ” Nature quoted Buck Institute Faculty Member Dale Bredesen, MD, who led the California half of the French-Californian collaborative research, as saying.

The study appears online in the Nature publication Cell Death and Differentiation. (ANI)

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