Millennium Highlights Updated Survival Data from ADCETRIS® (Brentuximab Vedotin) Pivotal Trial in Patients with …

By adminJune 14, 2012Stem Cell Medical Center

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

Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited (TSE:4502), today announced updated survival data from a pivotal Phase II clinical trial of single-agent brentuximab vedotin in patients with relapsed or refractory Hodgkin lymphoma (HL) after autologous stem cell transplant (ASCT) showing that the median overall survival has not been reached after a 26.5 month median follow-up. The data will be reported during an oral presentation at the 17th European Hematology Association (EHA) Annual Meeting being held June 14-17, 2012 in Amsterdam, Netherlands. Brentuximab vedotin is an antibody-drug conjugate (ADC) directed to CD30, a defining marker of the majority of types of HL.

Heavily pretreated Hodgkin lymphoma patients who relapse following autologous stem cell transplant often have a poor prognosis and there is a high unmet medical need for effective treatment options, said Scott Smith M.D., Ph.D., Loyola University Medical Center. These updated overall survival results from the pivotal trial are encouraging and suggest that brentuximab vedotin may play an important role in the treatment of patients with relapsed or refractory disease.

Long-term Follow-up Results of an Ongoing Pivotal Study of Brentuximab Vedotin in Patients with Relapsed or Refractory Hodgkin Lymphoma

A pivotal trial was conducted in 102 patients with relapsed or refractory HL after ASCT. The primary endpoint was objective response rate (ORR) per independent review. The secondary endpoints were complete remission (CR) rate, duration of response, progression-free survival (PFS), overall survival (OS), and safety and tolerability. At the time of the long-term follow-up analysis, the median observation time from first dose was 26.5months. Data, to be presented by Dr. Smith, include:

Patients received 1.8milligrams per kilogram of brentuximab vedotin every 3 weeks as a 30-minute outpatient intravenous infusion for up to 16cycles. Patients received a median of nine cycles of brentuximab vedotin while on trial. The median age of patients in the pivotal trial was 31 years. Enrolled patients had received a median of 3.5 (range 113) prior cancer-related systemic therapies, excluding ASCT. Seventy-one percent of patients had primary refractory disease, defined in the study protocol as patients who relapsed within three months of attaining CR or failed to achieve a CR, and 42 percent had not responded to their most recent prior therapy.

Details of the oral presentation are as follows:

About Brentuximab Vedotin

Brentuximab vedotin is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

Brentuximab vedotin is not approved for use outside the United States. The marketing authorization application for brentuximab vedotin in relapsed or refractory Hodgkin lymphoma and sALCL, filed by Takeda Global Research & Development Centre (Europe), was accepted for review by the European Medicines Agency for review in June 2011.

Link:
Millennium Highlights Updated Survival Data from ADCETRIS® (Brentuximab Vedotin) Pivotal Trial in Patients with ...

Linux creator, stem cell scientist win big technology prize

By adminJune 13, 2012Stem Cell Medical Center

Agence France-Presse

11:05 pm | Wednesday, June 13th, 2012

Linus Torvalds PHOTO FROM FACEBOOK.COM

HELSINKIUS-Finnish software engineer Linus Torvalds, who created the Linux open source operating system, and Japanese stem cell researcher Shinya Yamanaka on Wednesday won a 1.2-million-euro technology prize in Finland.

Today, millions use computers, smartphones and digital video recorders that run on Linux. Linus Torvaldss achievements have had a great impact on shared software development, networking and the openness of the web, the Millennium Technology Prize organizers said in a statement.

Yamanaka, meanwhile, won for his discovery of a new method to develop induced pluripotent stem cells for medical research, the prize jury said, adding that it was the first time that the award has been split between two scientists.

Using (Yamanakas) method to create stem cells, scientists all over the world are making great strides in research in medical drug testing and biotechnology, it said.

This should one day lead to the successful growth of implant tissues for clinical surgery and combating intractable diseases such as cancer, diabetes and Alzheimers.

Yamanaka himself vowed in the statement to continue to work hard to achieve our goals of developing new drugs and medical treatments to intractable diseases by using iPS cell technology.

Finnish President Sauli Niinistoe presented the prize to the two laureates at a ceremony at the Finnish National Opera in Helsinki Wednesday.

Read the rest here:
Linux creator, stem cell scientist win big technology prize

Fresh, purified fat stem cells grow bone faster, better

By adminJune 12, 2012Stem Cell Medical Center

LOS ANGELES UCLA stem cell scientists who purified a subset of stem cells from fat tissue and used the stem cells to grow bone discovered that the bone formed faster and was of higher quality than bone grown using traditional methods.

The finding may one day eliminate the need for painful bone grafts that use material taken from patients during invasive procedures.

Adipose, or fat, tissue is thought to be an ideal source of mesenchymal stem cells cells capable of developing into bone, cartilage, muscle and other tissues because such cells are plentiful in the tissue and easily obtained through procedures like liposuction, said Dr. Chia Soo, vice chair of research for the UCLA Division of Plastic and Reconstructive Surgery.

Soo and Bruno Pault, the co-senior authors on the project, are members of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Traditionally, cells taken from fat had to be cultured for weeks to isolate the stem cells which could become bone, and their expansion increases the risk of infection and genetic instability. A fresh, non-cultured cell composition called stromal vascular fraction (SVF) also is used to grow bone. However, SVF cells taken from adipose tissue are a highly heterogeneous population that includes cells that aren't capable of becoming bone.

Pault and Soo's team used a cell-sorting machine to isolate and purify human perivascular stem cells (hPSC) from adipose tissue and showed that those cells worked far better than SVF cells in creating bone. They also showed that a growth factor called NELL-1, discovered by Dr. Kang Ting of the UCLA School of Dentistry, enhanced bone formation in their animal model.

"People have shown that culture-derived cells could grow bone, but ours are a fresh cell population, and we didn't have to go through the culture process, which can take weeks," Soo said. "The best bone graft is still your own bone, but that is in limited supply and sometimes not of good quality. What we show here is a faster and better way to create bone that could have clinical applications."

The study was published Monday (June 11) in the early online edition of Stem Cells Translational Medicine, a new peer-reviewed journal that seeks to bridge stem cell research and clinical trials.

In the animal model, Soo and Pault's team put the hPSCs with NELL-1 in a muscle pouch, a place where bone is not normally grown. They then used X-rays to determine that the cells did indeed become bone.

"The purified human hPSCs formed significantly more bone in comparison to the SVF by all parameters," Soo said. "And these cells are plentiful enough that patients with not much excess body fat can donate their own fat tissue."

See the original post:
Fresh, purified fat stem cells grow bone faster, better

Some Stem-Cells May Not Be The Answer For Heart Disease

By adminJune 12, 2012Stem Cell Medical Center

June 12, 2012

The use of stem-cells building-block cells that are harvested from embryos or adults to treat heart disease could rely on faith as much as it does science, after billions of dollars in research has not produced the results that researchers have been looking for.

Questions and concerns on the topic arose during the recent opening of the multi-million-dollar Scottish Center for Regenerative Medicine (SCRM) in Edinburgh, chaired by Sir Ian Wilmut, the renowned scientist whose Dolly the sheep clone in 1996, was a groundbreaking step in stem cell technology.

During the opening ceremonies of the Center, Christine Mummery of the Leiden University Medical Center in the Netherlands discussed how a 2001 claim, based on mice experimentation, indicated that bone-marrow cells could mend heart damaged by coronary disease, caused a mad rush of people to the clinics looking for a cure-all.

With nothing in the way of systematic research in animals, the first patients were being treated within a year, prematurely by Mummerys account. She argued that the paper that launched the mass stampede was completely wrong, and subsequent studies proved that. But despite the findings, the 2001 paper has never been withdrawn.

Norwegian professor Harald Arnesen in 2007 voiced his concerns over those heart trials as well. He concluded that they were not convincing and that one German team had achieved striking results only because the control group had done particularly badly. Arnesen called for a moratorium on this kind of stem-cell therapy, based on that research.

But neither Arnesen, nor Mummery, could deter clinicians. Another trial, the largest to date, began in January 2012 and included 3,000 heart-attack patients recruited from across Europe. The trial was funded by the European Union as well.

The idea behind the trials is straightforward. During a heart attack, a clogged blood vessel starves heart muscle of oxygen. Up to a billion heart muscle cells, called cardiomyocytes, can be damaged, and the body responds by replacing them with relatively inflexible scar tissue, which can lead to fatal heart failure.

What is notably surprising, explained Mummery, is that stem cells come in many different forms: Embryonic stem cells are the building-blocks of the body and have the potential to turn into all 200 cell types found in the human body. Adult stem cells, however, are limited in what they can do. For example, bone marrow stem cells only generate blood cells.

So, the 2001 study claiming that bone marrow stem cells could turn into healthy heart muscle was a surprising and exciting claim, although a bold move.

Originally posted here:
Some Stem-Cells May Not Be The Answer For Heart Disease

Clues Found to Way Embryonic Kidney Maintains Its Fleeting Stem Cells

By adminJune 12, 2012Stem Cell Medical Center

Newswise Studying mice and humans, researchers at Washington University School of Medicine in St. Louis and their collaborators in Paris have identified two proteins that are required to maintain a supply of stem cells in the developing kidney.

In the presence of the two proteins, FGF9 and FGF20, mouse kidney stem cells stayed alive outside the body longer than previously reported. Though the cells were maintained only five days (up from about two), the work is a small step toward the future goal of growing kidney stem cells in the lab.

In the developing embryo, these early stem cells give rise to adult cells called nephrons, the blood filtration units of the kidneys.

The results appear online June 11 in Developmental Cell.

When we are born, we get a certain allotment of nephrons, says Raphael Kopan, PhD, the Alan A. and Edith L. Wolff Professor of Developmental Biology. Fortunately, we have a large surplus. We can donate a kidney give away 50 percent of our nephrons and still do fine. But, unlike our skin and gut, our kidneys cant build new nephrons.

The skin and the gut have small pools of stem cells that continually renew these organs throughout life. Scientists call such pools of stem cells and their support system a niche. During early development, the embryonic kidney has a stem cell niche as well. But at some point before birth or shortly after, all stem cells in the kidney differentiate to form nephrons, leaving no self-renewing pool of stem cells.

In other organs, there are cells that specifically form the niche, supporting the stem cells in a protected environment, Kopan says. But in the embryonic kidney, it seems the stem cells form their own niche, making it a bit more fragile. And the signals and conditions that lead the cells to form this niche have been elusive.

Surprisingly, recent clues to the signals that maintain the embryonic kidneys stem cell niche came from studies of the inner ear. David M. Ornitz, MD, PhD, the Alumni Endowed Professor of Developmental Biology, investigates FGF signaling in mice. Earlier this year, Ornitz and his colleagues published a paper in PLoS Biology showing that FGF20 plays an important role in inner ear development.

Mice without FGF20 are profoundly deaf, Ornitz says. While they are otherwise viable and healthy, in some cases we noticed that their kidneys looked small.

Past work from his own lab and others suggested that FGF9, a close chemical cousin of FGF20, might also participate in kidney development. FGF20 and FGF9 are members of a family of proteins known as fibroblast growth factors. In general, members of this family are known to play important and broad roles in embryonic development, tissue maintenance, and wound healing. Mice lacking FGF9 have defects in development of the male urogenital tract and die after birth due to defects in lung development.

Go here to read the rest:
Clues Found to Way Embryonic Kidney Maintains Its Fleeting Stem Cells

A Better Way to Grow Bone: Fresh, Purified Fat Stem Cells Grow Bone Better, Faster

By adminJune 12, 2012Stem Cell Medical Center

Newswise UCLA stem cell scientists purified a subset of stem cells found in fat tissue and made from them bone that was formed faster and was of higher quality than bone grown using traditional methods, a finding that may one day eliminate the need for painful bone grafts that use material taken from the patient during invasive procedures.

Adipose, or fat, tissue is thought to be an ideal source of cells called mesenchymal stem cells - capable of developing into bone, cartilage, muscle and other tissues - because they are plentiful and easily attained through procedures such as liposuction, said Dr. Chia Soo, vice chair for research at UCLA Plastic and Reconstructive Surgery. The co-senior authors on the project, Soo and Bruno Pault, are members of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Traditionally, cells taken from fat had to be cultured for weeks to isolate the stem cells which could become bone, and their expansion increases risk of infection and genetic instability. A fresh, non-cultured cell composition called stromal vascular fraction (SVF) also is used to grow bone. However, SVF cells taken from adipose tissue are a highly heterogeneous population that includes cells that arent capable of becoming bone.

Pault and Soos team used a cell sorting machine to isolate and purify human perivascular stem cells (hPSC) from adipose tissue and showed that those cells worked far better than SVF cells in creating bone. They also showed that a growth factor called NELL-1, discovered by Dr. Kang Ting of the UCLA School of Dentistry, enhanced the bone formation in their animal model.

People have shown that culture-derived cells could grow bone, but these are a fresh cell population and we didnt have to go through the culture process, which can take weeks, Soo said. The best bone graft is still your own bone, but that is in limited supply and sometimes not of good quality. What we show here is a faster and better way to create bone that could have clinical applications.

The study appears June 11, 2012 in the early online edition of the peer-reviewed journal Stem Cells Translational Medicine, a new journal that seeks to bridge stem cell research and clinical trials.

In the animal model, Soo and Paults team put the hPSCs with NELL-1 in a muscle pouch, a place where bone is not normally grown. They then used X-rays to determine that the cells did indeed become bone.

The purified human hPSCs formed significantly more bone in comparison to the SVF by all parameters, Soo said. And these cells are plentiful enough that patients with not much excess body fat can donate their own fat tissue.

Soo said if everything goes well, patients may one day have rapid access to high quality bone graft material by which doctors get their fat tissue, purify that into hPSCs and replace their own stem cells with NELL-1 back into the area where bone is required. The hPSC with NELL-1 could grow into bone inside the patient, eliminating the need for painful bone graft harvestings. The goal is for the process to isolate the hPSCs and add the NELL-1 with a matrix or scaffold to aid cell adhesion to take less than an hour, Soo said.

Excitingly, recent studies have already demonstrated the utility of perivascular stem cells for regeneration of disparate tissue types, including skeletal muscle, lung and even myocardium, said Pault, a professor of orthopedic surgery Further studies will extend our findings and apply the robust osteogenic potential of hPSCs to the healing of bone defects.

Excerpt from:
A Better Way to Grow Bone: Fresh, Purified Fat Stem Cells Grow Bone Better, Faster

Scientists Discover A Stem Cell That Causes Heart Disease

By adminJune 9, 2012Stem Cell Medical Center

Editor's Choice Main Category: Heart Disease Also Included In: Stem Cell Research Article Date: 09 Jun 2012 - 2:00 PDT

Current ratings for: 'Scientists Discover A Stem Cell That Causes Heart Disease'

3.95 (19 votes)

4.5 (2 votes)

The research is profound because it contradicts much of the generally accepted theories of what causes arterial hardening, and the concept may also relate to many other diseases could the associated stem cells be pinpointed.

What senior author Song Li, a bioengineering professor at UC Berkeley and a researcher at the Berkeley Stem Cell Center, and his team have uncovered is a dormant stem cell in blood vessel walls, that seems to sit inactive for most of a person's lifetime, before coming to life and causing less functional cells to begin to grow. Li says these new types of cells that start growing in later life, are the root cause of arterial hardening and clogging that are associated with deadly strokes and heart attacks.

Originally, it was thought that the smooth muscle cells in the arteries lining become scarred over time, and this leads to the narrow and brittle arteries that play a major part in causing cardiovascular disease. Not so says Liu: Essentially, what the scientists are saying is that the smooth muscle cells are not to blame. Rather a different kind of stem cell, that Li calls multipotent vascular stem cells, kicks in, and begins growing cells that look much like the smooth muscle cells, but don't function correctly. The cells were not found previously, because there are so few of them, that they were hard to isolate.

Li continues:

It almost sounds like something from Blade Runner, where the replicant humans have been deliberately designed to deteriorate and die at a much faster rate than the natural ones. What purpose would it serve the body under standard evolutionary terms to have cells activating later in life that effectively lead to its demise? With the arteries poorly formed, with wrong cell types, the blood flow becomes slowed and can then stopped completely. This causes strokes or heart attacks, depending on the location of the blockage. Strokes and heart attacks are one of the leading causes of death in the United States.

Creating drugs or other genetic treatments to shut down these stem cells or even deactivate them while a person is still young has the potential in the future to prevent arteriole hardening, reverse the damage already done, and even make this type of cardiovascular disease a thing of the past. Perhaps the futuristic Woody Allen movie "Sleeper" where people smoke tobacco and eat a high fat diet because it's healthier is not so far fetched after all.

Go here to read the rest:
Scientists Discover A Stem Cell That Causes Heart Disease

Mechanism that maintains stem cells readiness identified

By adminJune 1, 2012Stem Cell Medical Center

ScienceDaily (May 31, 2012) An immune-system receptor plays an unexpected but crucially important role in keeping stem cells from differentiating and in helping blood cancer cells grow, researchers at UT Southwestern Medical Center report today in the journal Nature.

"Cancer cells grow rapidly in part because they fail to differentiate into mature cells. Drugs that induce differentiation can be used to treat cancers," said Dr. Chengcheng "Alec" Zhang, assistant professor in UT Southwestern's departments of physiology and developmental biology. "Our research identified a protein receptor on cancer cells that inhibits differentiation, and knowing the identity of this protein should facilitate the development of new drugs to treat cancers."

The family of proteins investigated in the study could help open a new field of biology integrating immunology with stem cell and cancer research, he added.

"The receptor we identified turned out to be a protein called a classical immune inhibitory receptor, which is known to maintain stemness of normal adult stem cells and to be important in the development of leukemia," he said.

Stemness refers to the blood stem cells' potential to develop into a range of different kinds of cells as needed, for instance to replenish red blood cells lost to bleeding or to produce more white blood cells to fight off infection. Once stem cells differentiate into adult cells, they cannot go back to being stem cells. Current thinking is that the body has a finite number of stem cells and it is best to avoid depleting them, Dr. Zhang explained.

Prior to this study, no high-affinity receptors had been identified for the family of seven proteins called the human angiopoetic-like proteins. These seven proteins are known to be involved in inflammation, supporting the activity of stem cells, breaking down fats in the blood, and growing new blood vessels to nourish tumors. Because the receptor to which these proteins bind had not been identified, the angiopoetic-like proteins were referred to as "orphans," he said.

The researchers found that the human immune-inhibitory receptor LILRB2 and a corresponding receptor on the surface of mouse cells bind to several of the angiopoetic-like proteins. Further studies, Dr. Zhang said, showed that two of the seven family members bind particularly well to the LILRB2 receptor and that binding exerts an inhibitory effect on the cell, similar to a car's brakes.

In the case of stem cells, inhibition keeps them in their stem state. They retain their potential to mature into all kinds of blood cells as needed but they don't use up their energy differentiating into mature cells. That inhibition helps stem cells maintain their potential to create new stem cells because in addition to differentiation, self-renewal is the cells' other major activity, Dr. Zhang said. He stressed that the inhibition doesn't cause them to create new stem cells but does preserve their potential to do so.

In future research, the scientists hope to find subtle differences between stem cells and leukemia cells that will identify treatments to block the receptors' action only in leukemia.

Other UT Southwestern researchers involved in the study from the departments of physiology and developmental biology include postdoctoral researchers Dr. ChangHao Cui, Dr. Xiaoli Chen, Dr. Chaozheng Zhang, Dr. HoangDinh Huynh, and Dr. Xunlei Kang; senior research associates Robert Silvany and Jiyuan Li; and graduate student Xuan Wan. Researchers from the department of immunology include former technician Alberto Puig Cant and Dr. E. Sally Ward, professor of immunology.

Here is the original post:
Mechanism that maintains stem cells readiness identified

UT Southwestern Researchers Identify Mechanism That Maintains Stem-Cell Readiness, Helps Leukemia Cells Growth

By adminJune 1, 2012Stem Cell Medical Center

Newswise DALLAS May 31, 2012 An immune-system receptor plays an unexpected but crucially important role in keeping stem cells from differentiating and in helping blood cancer cells grow, researchers at UT Southwestern Medical Center report today in the journal Nature.

Cancer cells grow rapidly in part because they fail to differentiate into mature cells. Drugs that induce differentiation can be used to treat cancers, said Dr. Chengcheng Alec Zhang, assistant professor in UT Southwesterns departments of physiology and developmental biology. Our research identified a protein receptor on cancer cells that inhibits differentiation, and knowing the identity of this protein should facilitate the development of new drugs to treat cancers.

The family of proteins investigated in the study could help open a new field of biology integrating immunology with stem cell and cancer research, he added.

The receptor we identified turned out to be a protein called a classical immune inhibitory receptor, which is known to maintain stemness of normal adult stem cells and to be important in the development of leukemia, he said.

Stemness refers to the blood stem cells potential to develop into a range of different kinds of cells as needed, for instance to replenish red blood cells lost to bleeding or to produce more white blood cells to fight off infection. Once stem cells differentiate into adult cells, they cannot go back to being stem cells. Current thinking is that the body has a finite number of stem cells and it is best to avoid depleting them, Dr. Zhang explained.

Prior to this study, no high-affinity receptors had been identified for the family of seven proteins called the human angiopoetic-like proteins. These seven proteins are known to be involved in inflammation, supporting the activity of stem cells, breaking down fats in the blood, and growing new blood vessels to nourish tumors. Because the receptor to which these proteins bind had not been identified, the angiopoetic-like proteins were referred to as orphans, he said.

The researchers found that the human immune-inhibitory receptor LILRB2 and a corresponding receptor on the surface of mouse cells bind to several of the angiopoetic-like proteins. Further studies, Dr. Zhang said, showed that two of the seven family members bind particularly well to the LILRB2 receptor and that binding exerts an inhibitory effect on the cell, similar to a cars brakes.

In the case of stem cells, inhibition keeps them in their stem state. They retain their potential to mature into all kinds of blood cells as needed but they dont use up their energy differentiating into mature cells. That inhibition helps stem cells maintain their potential to create new stem cells because in addition to differentiation, self-renewal is the cells other major activity, Dr. Zhang said. He stressed that the inhibition doesnt cause them to create new stem cells but does preserve their potential to do so.

In future research, the scientists hope to find subtle differences between stem cells and leukemia cells that will identify treatments to block the receptors action only in leukemia.

Other UT Southwestern researchers involved in the study from the departments of physiology and developmental biology include postdoctoral researchers Dr. ChangHao Cui, Dr. Xiaoli Chen, Dr. Chaozheng Zhang, Dr. HoangDinh Huynh, and Dr. Xunlei Kang; senior research associates Robert Silvany and Jiyuan Li; and graduate student Xuan Wan. Researchers from the department of immunology include former technician Alberto Puig Cant and Dr. E. Sally Ward, professor of immunology.

More:
UT Southwestern Researchers Identify Mechanism That Maintains Stem-Cell Readiness, Helps Leukemia Cells Growth

Researchers identify mechanism that maintains stem cells readiness

By adminJune 1, 2012Stem Cell Medical Center

An immune-system receptor plays an unexpected but crucially important role in keeping stem cells from differentiating and in helping blood cancer cells grow, researchers at UT Southwestern Medical Center report today in the journal Nature.

"Cancer cells grow rapidly in part because they fail to differentiate into mature cells. Drugs that induce differentiation can be used to treat cancers," said Dr. Chengcheng "Alec" Zhang, assistant professor in UT Southwestern's departments of physiology and developmental biology. "Our research identified a protein receptor on cancer cells that induces differentiation, and knowing the identity of this protein should facilitate the development of new drugs to treat cancers."

The family of proteins investigated in the study could help open a new field of biology integrating immunology with stem cell and cancer research, he added.

"The receptor we identified turned out to be a protein called a classical immune inhibitory receptor, which is known to maintain stemness of normal adult stem cells and to be important in the development of leukemia," he said.

Stemness refers to the blood stem cells' potential to develop into a range of different kinds of cells as needed, for instance to replenish red blood cells lost to bleeding or to produce more white blood cells to fight off infection. Once stem cells differentiate into adult cells, they cannot go back to being stem cells. Current thinking is that the body has a finite number of stem cells and it is best to avoid depleting them, Dr. Zhang explained.

Prior to this study, no high-affinity receptors had been identified for the family of seven proteins called the human angiopoetic-like proteins. These seven proteins are known to be involved in inflammation, supporting the activity of stem cells, breaking down fats in the blood, and growing new blood vessels to nourish tumors. Because the receptor to which these proteins bind had not been identified, the angiopoetic-like proteins were referred to as "orphans," he said.

The researchers found that the human immune-inhibitory receptor LILRB2 and a corresponding receptor on the surface of mouse cells bind to several of the angiopoetic-like proteins. Further studies, Dr. Zhang said, showed that two of the seven family members bind particularly well to the LILRB2 receptor and that binding exerts an inhibitory effect on the cell, similar to a car's brakes.

In the case of stem cells, inhibition keeps them in their stem state. They retain their potential to mature into all kinds of blood cells as needed but they don't use up their energy differentiating into mature cells. That inhibition helps stem cells maintain their potential to create new stem cells because in addition to differentiation, self-renewal is the cells' other major activity, Dr. Zhang said. He stressed that the inhibition doesn't cause them to create new stem cells but does preserve their potential to do so.

In future research, the scientists hope to find subtle differences between stem cells and leukemia cells that will identify treatments to block the receptors' action only in leukemia.

Journal reference: Nature

Continued here:
Researchers identify mechanism that maintains stem cells readiness