Category Archives: Cell Medicine

May 25, 2017 by Kristin Samuelson Killer T cells surround a cancer cell. Credit: NIH

A first-of-a-kind neural stem cell therapy that works with a common cold virus to seek out and attack a lethal and aggressive brain cancer is being tested at Northwestern Medicine in a Phase I clinical trial for patients newly diagnosed with malignant glioma.

The novel drug to treat malignant glioma, notorious for recurring after typical bouts of standard cancer treatment, was developed by a Northwestern scientist and has been approved as an investigational drug by the U.S. Food and Drug Administration. This is only the second time the University has supported and filed an investigational new drug as a sponsor.

"We have discovered that combining stem cells with a virus causes the new drug to react like a cancer-seeking missile targeting cancerous cells in the brain" said principal investigator, Dr. Maciej Lesniak, the Michael J. Marchese Professor and chair of neurological surgery at Northwestern University Feinberg School of Medicine and a neuro-oncologist at Northwestern Medicine. "If it works in humans, it could be a powerful weapon against brain cancer and an option that our patients are desperate for."

One reason malignant glioma recurs so often is because a small subpopulation of cancer cells, often deep in the brain tissue, is highly resistant to chemotherapy and radiation.

The pre-clinical work done by Lesniak and his team has shown that the approach being tested at Northwestern Medicine can target this population of therapy resistant cells, further delaying and sometimes even preventing tumor recurrence.

The stem cells used in the research came from a collaboration of researchers from City of Hope.

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"We haven't seen significant progress in the last decade for patients with a brain tumor, and that is why it's crucial to do everything we can to find a better treatment for brain tumors," said Dr. Roger Stupp, a co-investigator who is working alongside Lesniak on this clinical trial. "Combining novel therapy with medical expertise, we are able to get one step closer to eradicating this lethal disease."

Stupp, a world-renowned neuro-oncologist, recently joined Northwestern Medicine as director of neuro-oncology and associate director for strategic initiatives at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University. He is best known for developing temozolomide in combination with radiation as the standard-of-care chemotherapy for patients with glioblastoma.

Lesniak and his team of scientists are starting to test the safety and dosage of the treatment in patients at Northwestern Memorial Hospital. Lesniak began the research more than a decade ago while at the University of Chicago and completed it when he moved to Northwestern in 2015.

This investigational new drug contains neural stem cells to deliver a potent virus responsible for the common cold, oncolyotic adenovirus, which is engineered to kill brain cancer cells. The novel treatment works synergistically with chemotherapy and radiation to enhance the standard cancer treatments effectiveness.

Malignant gliomas are the most aggressive forms of cancer and are predicted to affect nearly 20,000 new patients this year, according to the American Brain Tumor Association. Sometimes called the "grow-and-go" tumors, gliomas can make their own blood supply, which fuels the tumors' rapid growth and helps them hatch satellite tumors. Each tumor sends out tentacles that infiltrate and dig deep into normal brain tissue, making complete removal of cancerous cells impossible. Any cancerous cells in the brain left over from standard of care can cause the tumor to recur.

Lesniak plans to enroll up to 36 newly diagnosed patients with glioma. These patients will be divided into two groups: those with tumors that can be removed and those where the tumors are not removable by surgery.

Next step, Northwestern Memorial will extend this research to the collaborating partners at City of Hope Comprehensive Cancer Center in Duarte, California.

Explore further: Neuroscientists pinpoint key gene controlling tumor growth in brain cancers

Cedars-Sinai investigators have identified a stem cell-regulating gene that affects tumor growth in patients with brain cancer and can strongly influence survival rates of patients. The findings, published in the online edition ...

Northwestern Medicine scientists have found a molecule that stops the growth of an aggressive pediatric brain tumor. The tumor is always fatal and primarily strikes children under 10 years old.

Chicago...Using state-of-the-art gene editing technology, scientists from Ann & Robert H. Lurie Children's Hospital of Chicago have discovered a promising target to treat atypical teratoid/rhabdoid tumor (AT/RT) - a highly ...

Japanese researchers identify process to improve fluorescence detection of cancer stem cells, which are primarily responsible for brain tumor progression and recurrence after treatment

Being diagnosed with a malignant brain tumor is devastating news for patients and their loved ones. Whereas some types of tumor respond well to treatment, others such as glioblastomas - the most common and aggressive brain ...

Marc Symons, PhD, professor in The Feinstein Institute for Medical Research's Karches Center for Oncology Research, is examining if a common medication administered to treat pinworms, could replace the current treatment used ...

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In a new study, scientists at The University of Texas at Dallas have found that some types of cancers have more of a sweet tooth than others.

Swiss scientists from the University of Geneva (UNIGE), Switzerland, and the University of Basel have created artificial viruses that can target cancer. These designer viruses alert the immune system and cause it to send ...

Earlier this week, for the first time, a drug was FDA-approved for cancer based on disease genetics rather than type.

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Cold virus, stem cells tested to destroy deadly brain cancer - Medical Xpress

May 26, 2017 How Vmem signal strengthens innate immune response: Normal tadpoles have polarized cells, with specific native amounts and distributions of melanocytes (pigment cells) and primitive myeloid cells (part of the innate immune system). Following chemical or genetic treatments that depolarize the cells' Vmem (transmembrane potential, or voltage potential caused by differences in negative and positive ions on opposite sides of a cell's membrane), pathways involving serotonin signaling induce proliferation and redistribution of both melanocytes and primitive myeloid cells, leading to an increase in the efficiency of the immune response when stimulated with a pathogen such as E. coli. Tail amputation induces a strong posterior Vmem depolarization at the site of injury, where melanocytes and primitive myeloid cells are recruited, resulting in a net increase of the latter in the embryo, leading to an enhanced innate immune response. Findings from Tufts University biologists appear in npj Regenerative Medicine on May 26, 2017. Credit: Jean-Francois Pare/Tufts University

Changing the natural electrical signaling that exists in cells outside the nervous system can improve resistance to life-threatening bacterial infections, according to new research from Tufts University biologists. The researchers found that administering drugs, including those already used in humans for other purposes, to make the cell interior more negatively charged strengthens tadpoles' innate immune response to E. coli infection and injury. This reveals a novel aspect of the immune system - regulation by non-neural bioelectricity - and suggests a new approach for clinical applications in human medicine. The study is published online May 26, 2017, in npj Regenerative Medicine, a Nature Research journal.

"All cells, not just nerve cells, naturally generate and receive electrical signals. Being able to regulate such non-neural bioelectricity with the many ion channel and neurotransmitter drugs that are already human-approved gives us an amazing new toolkit to augment the immune system's ability to resist infections," said the paper's corresponding author Michael Levin, Ph.D., Vannevar Bush professor of biology and director of the Allen Discovery Center at Tufts and the Tufts Center for Regenerative and Developmental Biology in the School of Arts and Sciences. Levin is also an associate faculty member of the Wyss Institute of Biologically Inspired Engineering at Harvard University.

All vertebrates, from fish to people, have two kinds of immunity with common features. The adaptive immune system relies on the memory of previous exposure to a specific pathogen and is the basis for current vaccination strategies. The innate immune system is present from the time an egg is fertilized and provides a first line of defense against pathogens through surface barriers, antimicrobial amino acids called peptides, and certain blood cells. The innate immune system also plays a role in tissue repair and regeneration, and the interplay between regeneration and innate immunity is an emerging field of study.

Better understanding of innate immunity can advance efforts to combat new pathogens to which no adaptive memory has developed, address geographic migration of diseases, support immune-deficient patients, and develop more effective treatment of traumatic injuries.

Transmembrane potential (Vmem) - voltage potential caused by differences in negative and positive ions on opposite sides of a cell's membrane - is known to play a critical role in many essential functions in numerous cell types, and the researchers hypothesized that it also could affect innate immunity. In the study, embryonic Xenopus laevis frogs infected with human pathogenic E. coli bacteria were exposed to compounds, including some used in human medicine, to either depolarize (positively charge) or hyperpolarize (negatively charge) their cells. Developing X. laevis frogs are a popular model for regenerative, developmental, cancer and neurobiological studies.

Decreased deaths from pathogenic E. coli

Depolarization with different agents significantly increased the embryos' ability to resist the bacteria. The ratio of embryos that survived infection after receiving ivermectin, a human anti-parasitic, increased on average 32 percent compared with those not receiving the depolarizing compound. Mortality in untreated control embryos was 50 to 70 percent.

To verify that the depolarizing compounds were changing the host cells' electrical charge and not simply harming the bacteria, further experiments were conducted in which tadpole cells were injected with mRNA that encoded (provided the particular genetic language for) specific ion channels that would depolarize the frog cells directly, without affecting the bacteria. This approach validated what was observed with the depolarizing drugs.

In contrast, injecting cells with hyperpolarizing channel-encoding mRNA reduced the ratio of infected embryos that survived by about 20 percent. Similarly, embryo survival was reduced by exposure to chemical compounds that hyperpolarized the embryos or interfered with depolarization.

Experiments also found that the neurotransmitter serotonin is an intermediary between voltage and immune response, a finding consistent with other recent research from the Levin laboratory. The common anti-depressant fluoxetine, which blocks serotonin movement in and out of cell membranes, was shown to negate the beneficial effects of depolarization on embryo survival.

Analysis of the genes whose expression was altered by changing the tadpole cells' bioelectrical state found that the interplay among voltage, neurotransmitter signaling and immune function impacts many of the same genes that are involved in human immune response.

Unexpected finding: Injury boosts immunity

To examine the connection among bioelectrics, immunity and regeneration, the study investigated the effect of tail bud amputation on survival following infection. Surprisingly, removing embryos' tail buds increased their ability to survive E. coli infection. Instead of the added stress of tail regeneration overwhelming the embryo, the injury and the infection induced common defense mechanisms, including recruiting macrophages (a type of white blood cell that is part of the innate immune system), which appeared to increase efficiency in eliminating the bacteria.

"Components of the innate immune system such as macrophages were known to be essential to the process of regeneration, but the new study examines the opposite and equally important side of that relationship - how regeneration impacts the immune system," said Jean-Francois Pare, Ph.D., first author on the paper and a research associate in the Levin laboratory. "The interplay between response to physical injuries and infection has the potential to reveal new ways of treating both infections and severe physical injuries."

Joining Pare and Levin in authorship of the paper was Christopher J. Martyniuk of the Center for Environmental and Human Toxicology and Department of Physiological Sciences, University of Florida Genetics Institute, College of Veterinary Medicine, University of Florida, Gainesville.

Studies to extend this research to mammalian systems are now underway at Tufts University and the Wyss Institute. Further research is also needed to determine precisely which cells sense the bioelectric changes and transmit the effect to the innate immune cells involved, how infectious bacteria themselves may respond to changes in the bioelectric microenvironment, and the role of the internal microbiome in these interactions.

Explore further: Drosophila innate immunity: Another piece to the puzzle

More information: Jean-Franois Par et al, Bioelectric regulation of innate immune system function in regenerating and intact Xenopus laevis, npj Regenerative Medicine (2017). DOI: 10.1038/s41536-017-0019-y

Changing the natural electrical signaling that exists in cells outside the nervous system can improve resistance to life-threatening bacterial infections, according to new research from Tufts University biologists. The researchers ...

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Bioelectricity new weapon to fight dangerous infection - Medical Xpress

May 24, 2017 by Collene Ferguson Jeff Biernaskies research identifies a factor essential for dermal stem cells to continuously divide during tissue regeneration. Credit: Riley Brandt, University of Calgary

Stem cell researchers at the University of Calgary have found another piece of the puzzle behind what may contribute to hair loss and prevent wounds from healing normally.

Jeff Biernaskie's research, published recently in the scientific journal npj Regenerative Medicine identifies a key signalling protein called platelet-derived growth factor (PDGF). This protein is critical for driving self-renewal and proliferation of dermal stem cells that live in hair follicles and enable their unique ability to continuously regenerate and produce new hair.

"This is the first study to identify the signals that influence hair follicle dermal stem cell function in your skin," says Biernaskie, an associate professor in comparative biology and experimental medicine at the University of Calgary'sFaculty of Veterinary Medicine, and Calgary Firefighters Burn Treatment Society Chair in Skin Regeneration and Wound Healing. Biernaskie is also a member of the Alberta Children's Hospital Research Institute.

"What we show is that in the absence of PDGF signalling hair follicle dermal stem cells are rapidly diminished because of their inability to generate new stem cells and produce sufficient numbers of mature dermal cells within the hair follicle."

Biernaskie and his team of researchers study dermal stem cells located within hair follicles. They are looking to better understand dermal stem cell function and find ways to use these cells to develop novel therapies for improved wound healing after injury, burns, disease or aging.

This study, co-authored byRaquel Gonzalez and Garrett Moffatt,shows that PDGF is key to maintaining a well-functioning stem cell population in skin. And in normal skin, if you don't have enough of it the stem cell pools start to shrink, meaning eventually the hair will no longer grow and wounds will not heal as well.

"It's an important start in terms of how we might modulate these cells towards developing future therapies that could regenerate new dermal tissue or maintain hair growth" says Biernaskie.

Biernaskie's lab is looking at the potential role of stem cells in wound healing and the potential to stimulate these cells to improve skin regeneration, as opposed to forming scars.

Explore further: Using stem cells to grow new hair

More information: Raquel Gonzlez et al. Platelet-derived growth factor signaling modulates adult hair follicle dermal stem cell maintenance and self-renewal, npj Regenerative Medicine (2017). DOI: 10.1038/s41536-017-0013-4

In a new study from Sanford-Burnham Medical Research Institute (Sanford-Burnham), researchers have used human pluripotent stem cells to generate new hair. The study represents the first step toward the development of a cell-based ...

If the content of many a situation comedy, not to mention late-night TV advertisements, is to be believed, there's an epidemic of balding men, and an intense desire to fix their follicular deficiencies.

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Researchers in the Perelman School of Medicine at the University of Pennsylvania have determined the role of a key growth factor, found in skin cells of limited quantities in humans, which helps hair follicles form and regenerate ...

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(Medical Xpress)A European team of researchers working at Sweden's Karolinska Institutet has found evidence that suggests that humans have an olfactory defense against contagious diseases. In their paper published in Proceedings ...

Stem cell researchers at the University of Calgary have found another piece of the puzzle behind what may contribute to hair loss and prevent wounds from healing normally.

Scientists at the University of Sheffield have developed a new technique to examine human sperm without killing themhelping to improve the diagnosis of fertility problems.

The average human pair of lungs is permeated by a network of about 164 feet of blood vessels (roughly the width of a football field), including microscopic blood capillaries, which facilitate the diffusion of oxygen into ...

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Researchers identify 'signal' crucial to stem cell function in hair follicles - Medical Xpress

Animation of stem cell therapy attacking malignant glioma. (Northwestern Medicine)

CHICAGO - A first-of-a-kind neural stem cell therapy that works with a common cold virus to seek out and attack a lethal and aggressive brain cancer is being tested at Northwestern Medicine in a Phase I clinical trial for patients newly diagnosed with malignant glioma.

The novel drug to treat malignant glioma, notorious for recurring after typical bouts of standard cancer treatment, was developed by a Northwestern scientist and has been approved as an investigational drug by the U.S. Food and Drug Administration. This is only the second time the University has supported and filed an investigational new drug as a sponsor.

We have discovered that combining stem cells with a virus causes the new drug to react like a cancer-seeking missile targeting cancerous cells in the brain said principal investigator, Dr. Maciej Lesniak, the Michael J. Marchese Professor and chair of neurological surgery atNorthwestern University Feinberg School of Medicineand a neuro-oncologist at Northwestern Medicine. If it works in humans, it could be a powerful weapon against brain cancer and an option that our patients are desperate for.

One reason malignant glioma recurs so often is because a small subpopulation of cancer cells, often deep in the brain tissue, is highly resistant to chemotherapy and radiation.

We havent seen significant progress in the last decade for patients with a brain tumor, and that is why its crucial to do everything we can to find a better treatment for brain tumors.

The pre-clinical work done by Lesniak and his team has shown that the approach being tested at Northwestern Medicine can target this population of therapy resistant cells, further delaying and sometimes even preventing tumor recurrence.

The stem cells used in the research came from a collaboration of researchers from City of Hope.

We havent seen significant progress in the last decade for patients with a brain tumor, and that is why its crucial to do everything we can to find a better treatment for brain tumors, said Dr. Roger Stupp, a co-investigator who is working alongside Lesniak on this clinical trial. Combining novel therapy with medical expertise, we are able to get one step closer to eradicating this lethal disease.

Stupp, a world-renowned neuro-oncologist, recently joined Northwestern Medicine as director of neuro-oncology and associate director for strategic initiatives at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University. He is best known for developing temozolomide in combination with radiation as the standard-of-care chemotherapy for patients with glioblastoma.

Lesniak and his team of scientists are starting to test the safety and dosage of the treatment in patients at Northwestern Memorial Hospital. Lesniak began the research more than a decade ago while at the University of Chicago and completed it when he moved to Northwestern in 2015.

This investigational new drug contains neural stem cells to deliver a potent virus responsible for the common cold, oncolyotic adenovirus, which is engineered to kill brain cancer cells. The novel treatment works synergistically with chemotherapy and radiation to enhance the standard cancer treatments effectiveness.

Malignant gliomas are the most aggressive forms of cancer and are predicted to affect nearly 20,000 new patients this year, according to the American Brain Tumor Association. Sometimes called the grow-and-go tumors, gliomas can make their own blood supply, which fuels the tumors rapid growth and helps them hatch satellite tumors. Each tumor sends out tentacles that infiltrate and dig deep into normal brain tissue, making complete removal of cancerous cells impossible. Any cancerous cells in the brain left over from standard of care can cause the tumor to recur.

Lesniak plans to enroll up to 36 newly diagnosed patients with glioma. These patients will be divided into two groups: those with tumors that can be removed and those where the tumors are not removable by surgery.

Next step, Northwestern Memorial will extend this research to the collaborating partners at City of Hope Comprehensive Cancer Center in Duarte, California.

The study was funded by the National Institutes of Health and the National Institute of Neurological Disorders and Stroke grant U01NS069997.

More here:
New investigational drug acts like a cancer-seeking missile in brain - Northwestern University NewsCenter

Currently, there are only 11 hospitals that are authorized to give stem cell treatments in Indonesia. (Shutterstock/File)

Developments in science and technology have enabled humankind to achieve the unthinkable, including advancements in healthcare. In the next 10 years, patients may not even need medicine to cure certain illnesses as reported by kompas.com.

Principal investigator of Stem Cell and Cancer Institute, Dr. Yuyus Kusnadi, said health scientists are developing stem cell treatments. Stem cells are cells with the ability to renew or regenerate any kind of cells.

Degenerative conditions such as kidney failure and the weakening of heart muscles in the future may be cured by injecting stem cells into the patients body.

Stem cells can be obtained from umbilical cord blood that is kept in a stem cell bank, back bone marrow and fat. However, fat and bone marrow will decline in quality as a person grows older. Stem cells stored in a stem cell bank can be used for future treatments if needed.

Read also: Scientists take first steps to growing human organs in pigs

Health treatments using stem cells exist today although they are not yet developed due to limitations in funding and technology. Yuyus said in Indonesia, those who are allowed stem cell treatment are those who have no option.

For now, stem cell treatment require a doctors approval. Its still subjective, he said.

For those with recommendations for stem cell treatment, the stem cell is obtained from blood or fat. Manipulation in the laboratory is needed to strengthen the stem cell.

Although stem cell treatments are not yet popular these days, Yuyus is optimistic, Lets wait five to ten more years. The current use of medicine only stops symptoms and does not fix the sickness, he said.

Stem cell treatments will not be cheap either, as it will cost patients up to hundreds of millions of rupiah.

Currently, there are only 11 hospitals that are authorized to give stem cell treatments in Indonesia. The hospitals right to provide stem cell treatments is regulated in the Health Ministers Regulation no. 32, 2014 on the Incorporation of Medical Research Service and Education of Tissue and Stem Cell Centers.

Hospitals authorized to provide stem cell treatments in Indonesia include Rumah Sakit Cipto Mangun Kusumo, RS. Sutomo, RS M. Djamil, RS. Persahabatan, RS. Fatmawati, RS. Dharmais, RS. Harapan Kita, RS. Hasan Sadikin, RS. Kariadi, RS. Sardjito and RS. Sanglah. (asw)

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Stem cell treatments ready to replace medicine in 10 years: Expert - Jakarta Post

May 22, 2017 Researchers from Princeton University's Department of Molecular Biology have identified a small RNA molecule that helps maintain the activity of stem cells in both healthy and cancerous breast tissue. Above, the microscopic image shows different cell types in the normal mammary ducts of a mouse. The luminal cells (red) are milk-producing cells and the basal cells (green) have contractile functions, but also are responsible for regenerating the mammary gland, as they contain the majority of mammary gland stem cells. These stem cells, located in the outer layer of the gland, are exposed to microenvironmental factors and interact with various immune cells, including macrophages, in the mammary gland. Credit: Toni Celi-Terrassa and Yibin Kang, Department of Molecular Biology

Researchers from Princeton University's Department of Molecular Biology have identified a small RNA molecule that helps maintain the activity of stem cells in both healthy and cancerous breast tissue. The study, which will be published in the June issue of Nature Cell Biology, suggests that this "microRNA" promotes particularly deadly forms of breast cancer and that inhibiting the effects of this molecule could improve the efficacy of existing breast cancer therapies.

Stem cells give rise to the different cell types in adult tissues but, in order to maintain these tissues throughout adulthood, stem cells must retain their activity for decades. They do this by "self-renewing," dividing to form additional stem cells, and resisting the effects of environmental signals that would otherwise cause them to prematurely differentiate into other cell types.

Many tumors also contain so-called "cancer stem cells" that can drive tumor formation. Some tumors, such as triple-negative breast cancers, are particularly deadly because they contain large numbers of cancer stem cells that self-renew and resist differentiation.

To identify factors that help non-cancerous mammary gland stem cells (MaSCs) resist differentiation and retain their capacity to self-renew, Yibin Kang, the Warner-Lambert/Parke-Davis Professor of Molecular Biology, and colleagues searched for short RNA molecules called microRNAs that can bind and inhibit protein-coding messenger RNAs to reduce the levels of specific proteins. The researchers identified one microRNA, called miR-199a, that helps MaSCs retain their stem-cell activity by suppressing the production of a protein called LCOR, which binds DNA to regulate gene expression. The team showed that when they boosted miR-199a levels in mouse MaSCs, they suppressed LCOR and increased normal stem cell function. Conversely, when they increased LCOR levels, they could curtail mammary gland stem cell activity.

Kang and colleagues found that miR-199a was also expressed in human and mouse breast cancer stem cells. Just as boosting miR-199a levels helped normal mammary gland stem cells retain their activity, the researchers showed that miR-199a enhanced the ability of cancer stem cells to form tumors. By increasing LCOR levels, in contrast, they could reduce the tumor-forming capacity of the cancer stem cells. In collaboration with researchers led by Zhi-Ming Shao, a professor at Fudan University Shanghai Cancer Center in China, Kang's team found that breast cancer patients whose tumors expressed large amounts of miR-199a showed poor survival rates, whereas tumors with high levels of LCOR had a better prognosis.

Kang and colleagues found that LCOR sensitizes cells to the effects of interferon-signaling molecules released from epithelial and immune cells, particularly macrophages, in the mammary gland. During normal mammary gland development, these cells secrete interferon-alpha to promote cell differentiation and inhibit cell division, the researchers discovered. By suppressing LCOR, miR-199a protects MaSCs from interferon signaling, allowing MaSCs to remain undifferentiated and capable of self-renewal.

The microRNA plays a similar role during tumorigenesis, protecting breast cancer stem cells from the effects of interferons secreted by immune cells present in the tumor. "This is a very nice study linking a normal and malignant mammary gland stem cell program to protection from immune modulators," said Michael Clarke, the Karel H. and Avice N. Beekhuis Professor in Cancer Biology at Stanford School of Medicine, Institute of Stem Cell Biology and Regenerative Medicine, who first discovered breast cancer stem cells but was not involved in this study. "It clearly has therapeutic implications for designing strategies to rationally target the breast cancer stem cells with immune modulators."

Toni Celi -Terrassa, an associate research scholar in the Kang lab and the first author of the study, said, "This study unveils a new property of breast cancer stem cells that give them advantages in their interactions with the immune system, and therefore it represents an excellent opportunity to exploit for improving immunotherapy of cancer."

"Interferons have been widely used for the treatment of multiple cancer types," Kang said. "These treatments might become more effective if the interferon-resistant cancer stem cells can be rendered sensitive by targeting the miR-199a-LCOR pathway."

Explore further: Scientists identify chain reaction that shields breast cancer stem cells from chemotherapy

More information: Toni Celi-Terrassa et al, Normal and cancerous mammary stem cells evade interferon-induced constraint through the miR-199aLCOR axis, Nature Cell Biology (2017). DOI: 10.1038/ncb3533

Working with human breast cancer cells and mice, researchers at Johns Hopkins say they have identified a biochemical pathway that triggers the regrowth of breast cancer stem cells after chemotherapy.

Many cancer patients that receive chemotherapy go into remission at first, but relapse after treatment is discontinued. There is increasing evidence that this is due to the presence of cancer stem cellscells that reproduce ...

In the breast, cancer stem cells and normal stem cells can arise from different cell types but tap into distinct yet related stem cell programs, according to Whitehead Institute researchers. The differences between these ...

Stem cells are different from all other cells in our body because they retain the remarkable genetic plasticity to self-renew indefinitely as well as develop into cell types with more specialized functions. However, this ...

During breast-tissue development, a transcription factor called SLUG plays a role in regulating stem cell function and determines whether breast cells will mature into luminal or basal cells.

A key step in developing effective cancer therapies is identifying differences between normal, healthy cells and cancer cells these differences can then be exploited to specifically kill tumour cells.

The average human pair of lungs is permeated by a network of about 164 feet of blood vessels (roughly the width of a football field), including microscopic blood capillaries, which facilitate the diffusion of oxygen into ...

Researchers from Princeton University's Department of Molecular Biology have identified a small RNA molecule that helps maintain the activity of stem cells in both healthy and cancerous breast tissue. The study, which will ...

A multi-institutional team based at Massachusetts General Hospital (MGH) has discovered how a potential treatment strategy for Huntington disease (HD) produces its effects, verified its action in human cells and identified ...

Some major cell-to-cell communication networks were first studied in worms. Now those worms, Caenorhabditis elegans, are being used to understand the influence of cancer mutations on those networks, report researchers at ...

Anti-aging serums, wrinkle creams and surgeries provide the promise of a youthful appearance that can go only skin-deep.

In a turnabout, a biochemical self-destruct trigger found in many other types of cells appears to guard the lives of brain cells during an infection with West Nile virus.

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Study identifies RNA molecule that shields breast cancer stem cells ... - Medical Xpress

With gene-editing techniques such as CRISPR-Cas9, offending genes could one day be snipped out of hematopoietic stem cells, then be returned to their owners to generate new lines of disease-free blood cells

New research has nudged scientists closer to one of regenerative medicines holy grails: the ability to create customised human stem cells capable of forming blood that would be safe for patients. Advances reported in the journal Nature could not only give scientists a window on what goes wrong in such blood cancers as leukaemia, lymphoma and myeloma, but they could also improve the treatment of those cancers, which affect some 1.2 million Americans. The stem cells that give rise to our blood are a mysterious wellspring of life. In principle, just one of these primitive cells can create much of a human beings immune system, not to mention the complex slurry of cells that courses through a persons arteries, veins and organs. While the use of blood-making stem cells in medicine has been common since the 1950s, it remains pretty crude. After patients with blood cancers have undergone powerful radiation and chemotherapy treatments to kill their cancer cells, they often need a bone-marrow transplant to rebuild their white blood cells, which are destroyed by that treatment. The blood-making stem cells that reside in a donors bone marrow and in umbilical cord blood that is sometimes harvested after a babys birth are called hematopoietic, and they can be life-saving. But even these stem cells can bear the distinctive immune system signatures of the person from whom they were harvested. As a result, they can provoke an attack if the transplant recipients body registers the cells as foreign. This response, called graft-versus-host disease, affects as many as 70 percent of bone-marrow transplant recipients in the months following the treatment, and 40 percent develop a chronic version of the affliction later. It can overwhelm the benefit of a stem cell transplant. And it kills many patients. Rather than hunt for a donor whos a perfect match for a patient in need of a transplant a process that can be lengthy, ethically fraught and ultimately unsuccessful doctors would like to use a patients own cells to engineer the hematopoietic stem cells. The patients mature cells would be reprogrammed to their most primitive form: stem cells capable of becoming virtually any kind of human cell. Then factors in their environment would coax them to become the specific type of stem cells capable of giving rise to blood. Once reintroduced into the patient, the cells would take up residence without prompting rejection and set up a lifelong factory of healthy new blood cells. If the risk of deadly rejection episodes could be eliminated, physicians might also feel more confident treating blood diseases that are painful and difficult but not immediately deadly diseases such as sickle cell disease and immunological disorders with stem cell transplants. The two studies published on Wednesday demonstrate that scientists may soon be capable of pulling off the sequence of operations necessary for such treatments to move ahead. One of two research teams, led by stem cell pioneer Dr George Q. Daley of Harvard Medical School and the Dana Farber Cancer Institute in Boston, started their experiment with human pluripotent stem cells primitive cells capable of becoming virtually any type of mature cell in the body. Some of them were embryonic stem cells and others were induced pluripotent stem cells, or iPS cells, which are made by converting mature cells back to a flexible state. The scientists then programmed those pluripotent stem cells to become endothelial cells, which line the inside of certain blood vessels. Past research had established that those cells are where blood-making stem cells are born. Here, the process needed a nudge. Using suppositions gleaned from experiments with mice, Daley said his team confected a special sauce of proteins that sit on a cells DNA and programme its function. When they incubated the endothelial cells in the sauce, they began producing hematopioetic stem cells in their earliest form. Daleys team then transferred the resulting blood-making stem cells into the bone marrow of mice to see if they would take. In two out of five mice who got the most promising cell types, they did. Not only did the stem cells establish themselves, they continued to renew themselves while giving rise to a wide range of blood cells. A second research team, led by researchers from Weill Cornell Medicines Ansary Stem Cell Institute in New York, achieved a similar result using stem cells from the blood-vessel lining of adult mice. After programming those cells to revert to a more primitive form, the scientists also incubated those stem cells in a concoction of specialised proteins. When the team, led by Raphael Lis and Dr Shahin Rafii, transferred the resulting stem cells back into the tissue lining the blood vessels of the mice from which they came, that graft also took. For at least 40 weeks after the incubated stem cells were returned to their mouse owners, the stem cells continued to regenerate themselves and give rise to many blood-cell types without provoking immune reactions. In addition to making a workhorse treatment for blood cancers safer, the new advances may afford scientists a unique window on the mechanisms by which blood diseases take hold and progress, said Lee Greenberger, chief scientific officer for the Leukemia and Lymphoma Society. From a research point of view you could now actually begin to model diseases, said Greenberger. If you were to take the cell thats defective and make it revert to a stem cell, you could effectively reproduce the disease and watch its progression from the earliest stages. That, in turn, would make it easier to narrow the search for drugs that could disrupt that disease process early. And it would speed the process of discovering which genes are implicated in causing diseases. With gene-editing techniques such as CRISPR-Cas9, those offending genes could one day be snipped out of hematopoietic stem cells, then be returned to their owners to generate new lines of disease-free blood cells. But Daley cautioned that significant hurdles remain before studies like these will transform the treatment of blood diseases. We do know the resulting cells function like blood stem cells, but they still are at some distance, molecularly, from native stem cells, he said. By tinkering with the processes by which pluripotent stem cells mature into blood-producing stem cells, Daley said his team hopes to make these lab-grown cells a better match for the real things. Los Angeles Times/TNS

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May 19, 2017

Physicians, parents and coaches should be cautious when considering treating injured young athletes with platelet rich plasma (PRP), stem cells or other types of regenerative medicine, says a nationally recognized sports medicine clinician and researcher at the University of Miami Miller School of Medicine and UHealth Sports Medicine Institute.

"While regenerative medicine appears to have promise in many areas of medicine, little is known about the safety or effectiveness of these treatments for bone, cartilage, ligament or muscle tissue injuries in children and adolescents," said Thomas Best, M.D., Ph.D., professor of orthopedics, family medicine, biomedical engineering and kinesiology, and team physician for University of Miami athletics and the Miami Marlins. "Everyone wants a young athlete to get back to sports as quickly as possible, but it is important to look first at treatments that have been shown to be effective, before considering unproven options."

Best was the lead author of a new collaborative study, "Not Missing the Future: A Call to Action for Investigating the Role of Regenerative Medicine Therapies in Pediatric/Adolescent Sports Injuries," published May 15 in the American College of Sports Medicine's Current Sports Medicine Reports.

"Evidence from laboratory and veterinary research suggests that mesenchymal stem cells (MSC) may provide an alternative treatment option for conditions that affect muscle, tendons, ligaments, and cartilage," said the authors. "This evidence, however, is based largely on studies in adults and it remains unknown whether these results will be duplicated in our younger populations."

Young athletes are vulnerable to a wide range of injuries, including overuse of arm, shoulder and leg muscles, ligaments and joints in sports like baseball, tennis, soccer and golf, said Best, who is past president of the American College of Sports Medicine (ACSM). "Unregulated clinics may sound attractive to parents and youngsters seeking aggressive regenerative therapy," Best said. "But far more scientific research is necessary to determine if those treatments are helpful in overcoming sports injuries and, more importantly, without serious short- or long-term side effects."

The new ACSM study grew from an August 2016 meeting of sport medicine clinicians, researchers, and a bioethicist who felt that a call to action was urgently needed to understand the current evidence, risks and rewards, and future directions of research and clinical practice for regenerative medicine therapies in youth sports. The meeting was supported by the National Youth Sports Health and Safety Institute, a partnership between the American College of Sports Medicine and SanfordHealth, a Midwest HMO.

The collaborative study included a seven-point call to action:

1. Exercise caution in treating youth with cell-based therapies as research continues.

2. Improve regulatory oversight of these emerging therapies.

3. Expand governmental and private research funding.

4. Create a system of patient registries to gather treatment and outcomes data.

5. Develop a multiyear policy and outreach agenda to increase public awareness.

6. Build a multidisciplinary consortium to gather data and promote systematic regulation.

7. Develop and pursue a clear collective impact agenda to address the "hype" surrounding regenerative medicine.

Reflecting on the evidence, the study's authors wrote, "Despite the media attention and perceived benefits of these therapies, there are still limited data as to efficacy and long-term safety. The involvement of clinicians, scientists and ethicists is essential in ourquest for the truth."

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May 19, 2017 West Nile virus-infected brain neurons. Credit: Brian Daniels

In a turnabout, a biochemical self-destruct trigger found in many other types of cells appears to guard the lives of brain cells during an infection with West Nile virus.

UW Medicine scientists led research showing that this chemical pathway doesn't have to sacrifice brain cells to destroy the viruses and recruit the body's defenses against infection.

The same chemical pathway can preserve the brain's nerve cells, or neurons, by using an alternative approach to summon protection.

The self-destruct trigger, a protein called RIPK3 (pronounced rip-3), is better known for activating a certain type of cell death during infection or damaging events in other parts of the body. The death of infected cells in this manner is a protective mechanism that helps the body eliminate the infection.

During a West Nile virus infection, however, the activation of RIPK3 in brain cells doesn't cause them to die. That's because its signaling within the central nervous system is not the same as in cell types elsewhere in the body. Its brain-specific role implies that there are central nervous system functions for RIPK3 not observed in other tissues.

"There is something special about neurons, perhaps because they are non-renewable and too important to undergo cell death," said Andrew Oberst, assistant professor of immunology at the University of Washington School of Medicine. He is the senior author of a recent Cell paper on how brain cells ward off West Nile virus.

"RIPK3 acts as part of the milieu of signals that support anti-viral inflammation in the brain," said the lead author of the paper, Brian Daniels, a UW Medicine postdoctoral fellow in immunology.

RIPK3 responds to the presence of West Nile virus in the brain by placing an order for chemokines, the researchers observed.

Daniels explained that these chemicals underlie a successful ousting of West Nile virus. Chemokines attract an influx of infection-fighting white blood cells.

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These efforts contribute to the clearance of the virus from the brain, but not by directly stopping replacement virus from reproducing within brain cells. Instead, the brain tissue undergoes a kind of inflammation that restricts the West Nile virus infection.

In a different cell type, such as a fibroblast, the entry of a West Nile virus would result in the cell initiating its own demise.

Their findings, the researchers noted, suggest that additional care might need to be taken in developing and testing drugs against RIPK3 to treat neurodegenerative disorders, brain damage from stroke or injury, and autoimmune diseases of the nervous system such as multiple sclerosis. Too much interference with RIPK3 in the brain could make it prone to certain viral infections.

Yueh-Ming Loo is a UW research assistant professor of immunology and another key scientist on the study. Like Oberst, she is from the UW Center for Innate Immunity and Immune Disease. She's interested in why certain pathogens like West Nile virus gravitate toward and invade the central nervous system in some people and animals, but not in others.

Not everyone infected with the West Nile virus develops neurological disease. Some don't even realize they were exposed.

How the body controls brain infections when they do occur, especially with the blood-brain barrier restricting access, is also still poorly understood.

Loo explained that the efforts to subdue the virus in the brain can be a delicate balance. An inappropriately zealous immune response to the pathogen can inadvertently cause long-term neurological problems.

The UW Medicine researchers conducted part of their studies in mice to learn more about the role of RIPK3 in fighting brain infections. They found that mice that were genetically deficient in RIPK3 were highly susceptible to having West Nile virus overtake the brain. These mice displayed a fatal defect in their ability to produce a chemokine-generated neuroinflammation.

The mouse studies and related lab work, the researchers noted, provide evidence that RIPK3 coordinates the infiltration of disease-fighting cells into the central nervous system during West Nile virus infection.

Central nervous system infections are a "profound and growing burden to global public health," the researchers noted in discussing the significance of this scientific question.

Explore further: Researchers moving towards ending threat of West Nile virus

More information: Brian P. Daniels et al, RIPK3 Restricts Viral Pathogenesis via Cell Death-Independent Neuroinflammation, Cell (2017). DOI: 10.1016/j.cell.2017.03.011

Journal reference: Cell

Provided by: University of Washington

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May 17, 2017 This illustration shows the bone-tissue engineering technique developed by Cedars-Sinai investigators. 'Endogenous MSCs' refers to stem cells from a patient's bone. The 'BMP gene' is a gene that promotes bone repair. Credit: Gazit Group/Cedars-Sinai

A Cedars-Sinai-led team of investigators has successfully repaired severe limb fractures in laboratory animals with an innovative technique that cues bone to regrow its own tissue. If found to be safe and effective in humans, the pioneering method of combining ultrasound, stem cell and gene therapies could eventually replace grafting as a way to mend severely broken bones.

"We are just at the beginning of a revolution in orthopedics," said Dan Gazit, PhD, DMD, co-director of the Skeletal Regeneration and Stem Cell Therapy Program in the Department of Surgery and the Cedars-Sinai Board of Governors Regenerative Medicine Institute. "We're combining an engineering approach with a biological approach to advance regenerative engineering, which we believe is the future of medicine."

Gazit was the principal investigator and co-senior author of the research study, published in the journal Science Translational Medicine.

More than 2 million bone grafts, frequently necessitated by severe injuries involving traffic accidents, war or tumor removal, are performed worldwide each year. Such injuries can create gaps between the edges of a fracture that are too large for the bone to bridge on its own. The grafts require implanting pieces from either the patient's or a donor's bone into the gap.

"Unfortunately, bone grafts carry disadvantages," said Gazit, a professor of surgery at Cedars-Sinai. "There are huge unmet needs in skeleton repair."

One problem is that enough healthy bone is not always available for repairs. Surgeries to remove a bone piece, typically from the pelvis, and implant it can lead to prolonged pain and expensive, lengthy hospitalizations. Further, grafts from donors may not integrate or grow properly, causing the repair to fail.

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The new technique developed by the Cedars-Sinai-led team could provide a much-needed alternative to bone grafts.

In their experiment, the investigators constructed a matrix of collagen, a protein the body uses to build bones, and implanted it in the gap between the two sides of a fractured leg bone in laboratory animals. This matrix recruited the fractured leg's own stem cells into the gap over a period of two weeks. To initiate the bone repair process, the team delivered a bone-inducing gene directly into the stem cells, using an ultrasound pulse and microbubbles that facilitated the entry of the gene into the cells.

Eight weeks after the surgery, the bone gap was closed and the leg fracture was healed in all the laboratory animals that received the treatment. Tests showed that the bone grown in the gap was as strong as that produced by surgical bone grafts, said Gadi Pelled, PhD, DMD, assistant professor of surgery at Cedars-Sinai and the study's co-senior author.

"This study is the first to demonstrate that ultrasound-mediated gene delivery to an animal's own stem cells can effectively be used to treat nonhealing bone fractures," Pelled said. "It addresses a major orthopedic unmet need and offers new possibilities for clinical translation."

The study involved six departments at Cedars-Sinai, plus investigators from Hebrew University in Jerusalem; the University of Rochester in Rochester, New York; and the University of California, Davis.

"Our project demonstrates how scientists from diverse disciplines can combine forces to find solutions to today's medical challenges and help develop treatments for the patients of tomorrow," said Bruce Gewertz, MD, surgeon-in-chief and chair of the Department of Surgery at Cedars-Sinai.

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More information: DOI: 10.1126/scitranslmed.aal3128 "In situ bone tissue engineering via ultrasound-mediated gene delivery to endogenous progenitor cells in mini-pigs," Science Translational Medicine (2017). http://stm.sciencemag.org/lookup/doi/10.1126/scitranslmed.aal3128

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Injured bones reconstructed by gene and stem cell therapies - Medical Xpress