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Stem-cell transplants show limited benefit for double-hit lymphoma patients in remission – Science Daily

By Stem Cell Medical Center

Patients with double hit lymphoma (DHL) who undergo autologous stem-cell transplantation (autoSCT) after achieving remission are not more likely to remain in remission or live longer than patients who do not undergo autoSCT, according to a new analysis from the Perelman School of Medicine and the Abramson Cancer Center of the University of Pennsylvania. The study looked at long term outcomes for patients who achieved remission and, in most cases, found no clear benefit to the transplant, except potentially in patients who received standard front-line chemotherapy, who were less likely to remain in remission than those patients receiving intensive front-line chemotherapy. The findings are published this month in the Journal of Clinical Oncology.

DHL is a form of aggressive B cell non-Hodgkin lymphoma characterized by genetic alterations that drive the lymphoma's growth. This variant is associated with a poor prognosis as compared to other forms of aggressive B cell lymphomas, as patients with this disease survive only an average of two years after diagnosis. Relapses of this disease are almost always fatal, meaning that keeping patients in remission is crucial.

"A major dilemma for oncologists who treat this disease was whether or not to recommend the potentially harmful therapy of autoSCT to patients with this disease a strategy to help keep them in remission," said Daniel J. Landsburg, MD, an assistant professor of Hematology Oncology at Penn and the study's lead author.

Landsburg and his team looked at data on 159 patients from 19 different academic medical centers across the United States. Patients were diagnosed between 2006 and 2015, and all achieved remission following intensive front-line chemotherapy or the standard chemotherapy regimen containing rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP). Of the total patients, 62 underwent an autoSCT, while 97 did not. Landsburg noted that there were no significant differences between the patient groups at baseline.

"Our result is not explained by differences in patients' overall health or disease features," Landsburg said. "The transplant and non-transplant arms of this study were very well-matched."

Overall, 80 percent of the patients were still in remission three years later, and 87 percent were still alive. When researchers broke the patients into two groups, autoSCT and no autoSCT, they found 89 percent of autoSCT patients were still in remission at three years, as were 75 percent of patients who did not receive an autoSCT. Also at three years, 91 percent of autoSCT patients were still alive, compared to 85 percent of non-autoSCT patients. None of these differences were found to be statistically significant.

"Once these patients achieve remission, the data show they are likely to stay in remission," Landsburg said. "In the absence of a large randomized controlled trial, which would be very challenging to carry out in this case, this is the best evidence we have, and it shows there's no clear benefit to these patients undergoing autoSCT."

Landsburg did point to one exception in the data, and that was in patients who underwent RCHOP, the standard front-line chemotherapy regimen. Just 56 percent of them were still in remission at three years, far lower than patients who received the more intensive front-line therapies.

"Even if patients do go into remission with RCHOP, it appears to be less durable, so in these cases, going forward with autoSCT may still make sense," Landsburg said.

Landsburg says the next step will be to study features of patients who don't go into remission in order to understand why their disease is resistant to therapy and if that can be overcome with different treatment strategies. He says it's also important to try to find more effective therapies for DHL patients who relapse.

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Stem-cell transplants show limited benefit for double-hit lymphoma patients in remission - Science Daily

Rosario: Once a migrant worker, he’s revolutionizing brain surgery, cancer fight – TwinCities.com-Pioneer Press

By Stem Cell Clinic

Dr. Qs eyes widen and the hands that once picked grapes and now perform surgeries spring into action. He explains in laymans terms how he and a plastic surgeon teamed up to perform anterior brain tumor removals through an incision on the eyelid.

The way traditional surgery has been done is to remove the scalp forward, and then you do the removal of the bone, and then you take the tumor out, Dr. Alfredo Quiones-Hinojosa explained during a chat Thursday at a hotel in downtown Rochester, Minn.

Now, he explained, the plastic surgeon teammate makes the same incision used for movie stars when their eyelids get droopy. And tumors as large as three centimeters have been excised through this eyebrow-raising technique.

The method reduces, if not eliminates, cranial trauma and retraction of the brain. He has done 60 to 70 such operations in the past five years.

Supremely impressive. The same could be said of Quiones-Hinojosa, who now serves as chair of Neurologic Surgery at the Mayo Clinic complex in Jacksonville, Fla. Colleagues tagged him with that catchy Dr. Q monikeryears ago.

On New Years Day 1987, Quiones-Hinojosa, in pursuit of a dream he felt he could not realize in his native Mexico, scaled an 18-foot barbed wire fence at the U.S.-Mexico border.He was 19.

He began work picking grapes, cotton, cantaloupe, tomatoes and other crops. Twelve years later, he graduated with honors from Harvard Medical School.

Hard work, resiliency, perseverance, never giving up on your dreams are the same principles then that keep me going today as a brain surgeon, scientist, professor, philanthropist and entrepreneur, he said.

As a migrant worker, I worked with my hands and brains, he added. The difference is that the stakes are much higher, because back then I only had my life in my hands. I now have the lives of patients in my hands

The oldest of six children, the 49-year old father of three grew up dirt poor in a small village outside Mexicali in Baja California. The family plunged into further poverty after his father lost his gas station.

Alfredo went to school barefoot at times.

Wanting to help his family, Quiones-Hinojosa was barely 15 when he went to work for an uncle at a migrant farm in Mendota, Calif. He spent the summer months weeding fields and picking cotton and produce. He would return home to Mexico with $1,000, most of which he gave to his parents to make ends meet.

He obtained a teaching license when he was 19 years old. But he had a dream of becoming a doctor a goal inspired by his maternal grandmother, a curandera, Spanish for village healer. He realized America gave him the better shot to achieve it.

Border agents had confiscated his Mexican passport at a checkpoint after learning that he had illegally worked in the U.S. with only a tourist visa.

As he described in his memoir, Becoming Dr. Q: My Journey from Migrant Farm Worker to Brain Surgeon (University of California Press, 2011), Quiones-Hinojosa scaled the fence separating Mexicali from Calexico, Calif. But he was caught by border agents and sent back.

He waited a few hours and climbed over the fence again. A cousin drove him to San Diego, where he bought an airline ticket to Los Angeles with no ID.

It was very different then, he recalled.

Broke and unable to speak a word of English, he slept inside the terminal and ate food travelers had left on tables until another cousin showed up two days later for the ride to the farms in Mendota.

Quiones-Hinojosa worked as a migrant for two years and then landed a job as a welder and cleaner with a railroad company. He nearly lost his life at age 21 when he fell 18 feet into a railroad tanker and was overcome by petroleum fumes. He was pulled up barely conscious and taken to a nearby hospital.

He juggled work and studies at a community college while homeless and living in a small camper trailer with a leaky roof. There were days he woke up drenched.

We are equipping (stem cells body fat), training them, arming them with special tools so we can put them back in humans and fight all kinds of cancer.

At the urging of a friend, Quiones-Hinojosa applied to the University of California at Berkeley. He was accepted. With the help of a scholarship, hemajored in psychology and took several calculus, physics and chemistry classes to boost his grade-point average.

He wrote an honors thesis on neuroscience and was accepted to Harvard Medical School. He married and became a U.S. citizen during his time there. He graduated with honors in 1999 and was the class valedictorian.

He had long resisted the naysayers, the ones who would say Youre not Mexican. You are too smart, or even friends who told him that schools like Harvard were only for the elite, not for Mexican migrant and manual laborers like him. His dream would not let him quit.

Following a residency in San Francisco, Quiones-Hinojosa joined the staff at Johns Hopkins in Baltimore in 2005 as a professor of neurological surgery and oncology. He has served as director of both the brain tumor surgery and pituitary surgery programs at the medical center. And he has authored several textbooks on stem-cell biology and neurosurgical techniques.

Quiones-Hinojosa joined the Mayo team eight months ago, where he teaches and also heads a team of scientists working on a potentially promising way fight to fight cancer: stem cells extracted from a persons fat.

We are equipping them, training them, arming them with special tools so we can put them back in humans and fight all kinds of cancer, said Quiones-Hinojosa, who came to Minnesota this past week to make a presentation on the research.

Lab results, in which human cancer cells have been injected into animals and then treated with the fat cells, have been unbelievably positive. We have cured cancer in animals, he said.

He believes it will take another two or three years before the procedure may be done on a human patient at the Mayo Clinic.

Quiones-Hinojosa acknowledges that individuals and groups have pressured him to speak out on the immigration debate.

I always tell people that these are complex issues, he said. I am not an expert on immigration. I know about cancer. I know about brain surgery. I know about cell migration. My responsibility is not so much to talk about immigration but to serve as a role model for all those people who have come to this country with a dream to make this world a better place.

A movie production company headed by Brad Pitt is working on a movie based on his life. The script is scheduled to be completed by this summer. Casting will follow.

I ask Quiones-Hinojosa if he would like Brad Pitt to play him.

No, he chuckled. Hes too good-looking.

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Rosario: Once a migrant worker, he's revolutionizing brain surgery, cancer fight - TwinCities.com-Pioneer Press

Pope Francis: Huntington Sufferers are ‘Respected’ and ‘Loved,’ Condemns Embryonic Stem Cell Research – Gospel Herald

By Embryonic Stem Cells

It is well known that the Catholic Church has opposed the utilization of embryos in scientific research; Pope Francis, in a gallant, gentle, but courageous way, however, reiterated the church's stance in a Vatican meeting Thursday evening.

Surrounded by families coping in various ways with Huntington's disease, Pope Francis urged his fellows in humanity to refrain from any temptation to destroy embryos---no matter how "noble" the cause:

Some branches of research, in fact, utilize human embryos, inevitably causing their destruction. But we know that no ends, even noble in themselves, such as a predicted utility for science, for other human beings or for society, can justify the destruction of human embryos.

The hereditary illness, which involves a gradual degeneration of brain cells, eventually overtaking the mental capacities entirely. The effects are emotional, physical, and psychological. A person's cognitive abilities are eventually dissolved, and sufferers become completely dependent on their caretakers. A medical journal describes it as follows:

"Nerve cells become damaged, causing various parts of the brain to deteriorate. The disease affects movement, behavior and cognition - the affected individuals' abilities to walk, think, reason and talk are gradually eroded to such a point that they eventually become entirely reliant on other people for their care."

Tragically, there is as of now no cure for the disease; current research, however, is making an attempt for a remedy which involves the use of embryonic stem cells. Pope Francis addressed the attitude of Christ in His ministry with the sick, assuring the affected that they are "loved by God" and are not forgotten:

"In many cases the sick and their families have experienced the tragedy of shame, isolation and abandonment. Today, however, we are here because we want to say to ourselves and all the world: HIDDEN NO MORE!

Nonetheless, Francis encourages Christians not to grow weary in doing good. In seeking a means of healing which necessitates the taking of a life only adds to our "throw away culture."

What can be cured, the spiritual leaders insists, is our attitude towards those suffering from the disease:

"The strength and conviction with which we pronounce these words derive precisely from what Jesus himself taught us; Jesus met many sick people; he took on their suffering; he tore down the walls of stigma and of marginalization that prevented so many of them from feeling respected and loved.

The Pope closed with a blessing on the physically unwell, as well as their caretakers:

May the life of each of you both those who are directly affected by Huntingtons disease and those who work hard every day to support the sick in their pain and difficulty be a living witness to the hope that Christ has given us, even through suffering there passes a path of abundant good, which we can travel together.

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Pope Francis: Huntington Sufferers are 'Respected' and 'Loved,' Condemns Embryonic Stem Cell Research - Gospel Herald

Scientists Are "Tantalisingly Close" to Producing a Limitless Blood Supply From Stem Cells – ScienceAlert

By Embryonic Stem Cells

Two papers published this week have revealed that scientists are "tantalisingly close" to being able to produce large quantities of blood cells from a patient's own stem cells.

This would revolutionise treatments for people who need frequent blood transfusions, as well as those with bone marrow disorders who struggle to find a match with a healthy donor.

"For many years, people have figured out parts of this recipe, but they've never quite gotten there," Mick Bhatia from McMaster University in Canada, who was not involved with either study,told Nature News.

"This is the first time researchers have checked all the boxes and made blood stem cells."

Stem cells are specially programmed cells whose job is to create all the other cells in the body.

There are two different types: embryonic, which are located in an embryo before the cells start to specialise; and adult stem cells, which are used to repair and replace old, worn-out cells.

Since 2006, whenadult mouse cells were converted back into a type of adult stem cell calledinduced pluripotent stem cells (iPS cells) for the first time, the field has been pushing towards producing new blood cells.

The goal is that a patient could have their own cells extracted, converted into iPS cells, and from those, a limitless supply of the patient's blood could be produced - no donor required.

"This step opens up an opportunity to take cells from patients with genetic blood disorders, use gene editing to correct their genetic defect and make functional blood cells," says Rio Sugimurafrom Boston Children's Hospital, one of the researchers behind the recent studies.

"This also gives us the potential to have a limitless supply of blood stem cells and blood by taking cells from universal donors. This could potentially augment the blood supply for patients who need transfusions."

In the first paper, the researchers used both iPS and embryonic stem cells and exposed them to chemical signals that direct stem cells to change into specialised cells, such as hemogenic endothelium (the precursor to blood cells).

Next, the team added transcription factors (genes that code for proteins that 'transcribe' DNA), which was able to force the cells into a blood-forming state.

The researchers discovered that five transcription factors (RUNX1, ERG, LCOR, HOXA5 and HOXA9) were required to force the cells into the correct form.

When they added these new cells to mice, they integrated and formed multiple types of blood cells, including both red blood cells and immune cells.

"We're tantalisingly close to generating bona fide human blood stem cells in a dish," says George Daleyfrom Boston Children's Hospital, head of the research lab for the new paper."This work is the culmination of over 20 years of striving."

The second paper is slightly different although equally important to the field. Instead of using iPS or embryonic cells, a team fromWeill Cornell Medicinein New York managed to use adult stem cells taken from the lung walls of mice.

The team identified four separate transcription factors (Fosb, Gfi1, Runx1, and Spi1), and were able to turn the cells into blood cells without first turning them into iPS cells.

Instead, the extracted cells had the four transcription factors added to their genomes, and kept in a petri dish designed to mimic the environment inside human blood vessels.

The cells morphed into blood cells, and began multiplying. They were also effectively added into mice, which lived with minimal issues, over 1.5 years in the lab.

The head researcher of this project, Shahin Rafii, says the difference between his and Daley's team's techniques is pretty significant.

"Because he bypassed the iPS-cell stage, Rafii compares his approach to a direct aeroplane flight, and Daley's procedure to a flight that takes a detour to the Moon before reaching its final destination," says Amy Maxmen at Nature News.

Although that analogy might make you think Rafii's method is the superior choice, right now, we still don't know which way will be more effective in humans, as the results have only been demonstrated in animal models to work effectively.

But being able to change human cells into proliferating blood cells is a fantastic achievement for both groups, and it's always exciting to see competing science in action.

The studies have both been published in Nature, and you can access Daley's here and Rafii's here.

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Scientists Are "Tantalisingly Close" to Producing a Limitless Blood Supply From Stem Cells - ScienceAlert

Access Denied: Stem Cell Therapy Shows Some Promise in Refractory Angina, but Patients Can’t Get It – TCTMD

By Uncategorized

NEW ORLEANS, LADespite new data showing that stem cell therapy has the potential to improve exercise time and reduce mortality in patients with refractory angina, researchers said at the Society for Cardiovascular Angiography and Interventions (SCAI) 2017 Scientific Sessions last week that the option is all but dead due to withdrawal of financial support, resulting in patients being denied access to a promising treatment.

Presenting a summation of all the data that have been collected over the last decade on the use of autologous CD34+ cells to treat patients with class III or IV angina despite optimal medical therapy, Thomas Povsic, MD, PhD (Duke Clinical Research Institute, Chapel Hill, NC), said this group of patients is in dire need of new treatment options, and maintained that it is imperative to explore methods to bring this therapy to patients.

He and colleagues conducted a meta-analysis from the only three trials of CD34+ therapy in refractory angina patients: a phase I study (n = 24); ACT-34 CMI and its 24-month extension study (n = 168); and the RENEW study (n = 112). All three were randomized, double-blind, placebo-controlled trials. However, RENEW was terminated early by the sponsor due to financial reasons.

Taken together, the trials showed that among the 187 patients who received the therapy, total exercise time improved by 90.5 seconds at 12 months compared with an improvement of just 39.5 seconds in those who received a placebo.

Additionally, patients who received CD34+ treatment had more than a fourfold lower rate of mortality by 24 months (2.6% vs 11.8%; P = 0.003) and fewer instances of MACE (29.8% vs 40.0%; P = 0.08).

A Cloudy Future

Povsic said the CD34+ trials are extremely expensive to run, resulting in the only sponsor, Baxter Healthcare, divesting itself of all further research in this area.

I personally believe that this therapy has more data associated with it for efficacy and safety than any other cell therapy thats been investigated in the cardiovascular disease space, he observed. The passage of the 21st Century Cures Act may hold some hope for the future, Povsic added, since it allows for a therapy that fulfills a specific medical need to undergo expedited approval.

Its challenging because this patient population has no options, Povsics co-author Timothy Henry, MD (Cedars-Sinai Heart Institute, Los Angeles, CA), said in a press briefing prior to the presentation. This is by far the strongest data for any therapy for refractory angina. Its also the . . . strongest data for cell therapy, and its a shame that its not available to patients.

Henry added that hes hopeful the data from the meta-analysis may be well received by the US Food and Drug Administration.

Povsic noted that although other companies have expressed interest in the therapy, its future is cloudy. Referencing the termination of RENEW for financial reasons, he added that it shows the ramifications that early cessation of a clinical trial can have, because its truly a disservice to the patients that were enrolled in the trial, the investigators that invested time, and the fact that this therapy . . . seemed so close to the finish line, but [now] the path forward is unclear.

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Access Denied: Stem Cell Therapy Shows Some Promise in Refractory Angina, but Patients Can't Get It - TCTMD

Caution urged in using PRP or stem cells to treat young athletes’ injuries – Medical Xpress

By Stem Cell Treatment

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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Caution urged in using PRP or stem cells to treat young athletes' injuries - Medical Xpress

PIO doctor to open application of stem cell research in Nitte … – Times of India

By Stell Cell Research

MANGALURU: UK-based orthopaedic surgeon, Dr Anand A Shetty will start a clinical application of stem cell research in the city along with Nitte University. This will help in curing cancer and other related ailments.

Dr Shetty, who hails from Asode near Koteshwara in Udupi district, was honoured with the 'Outstanding Clinical Excellence' award by the UK's House of Lords this year. Dr Shetty is winner of a host of awards including the prestigious Hunterian Surgical Medal and Hunterian Professorship for 2017 awarded by the Royal College of Surgeons of England for his research on stem cells in particular cartilage repair. Only four Indians have received this award so far.

A knee surgeon and director of stem cell research at Canterbury Christ Church University, Dr Shetty's main interest lies in stem cell research, cartilage transplant, accelerated bone healing, and robotics in minimally invasive surgery.

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PIO doctor to open application of stem cell research in Nitte ... - Times of India

Cancer therapy may work in unexpected way, study finds – Science Daily

By Stem Cell Medical Center

Antibodies to the proteins PD-1 and PD-L1 have been shown to fight cancer by unleashing the body's T cells, a type of immune cell. Now, researchers at the Stanford University School of Medicine have shown that the therapy also fights cancer in a completely different way, by prompting immune cells called macrophages to engulf and devour cancer cells.

The finding may have important implications for improving and expanding the use of this cancer treatment, the researchers said.

A study describing the work, which was done in mice, published online May 17 in Nature. The senior author is Irving Weissman, MD, professor of pathology and of developmental biology. The lead author is graduate student Sydney Gordon.

PD-1 is a cell receptor that plays an important role in protecting the body from an overactive immune system. T cells, which are immune cells that learn to detect and destroy damaged or diseased cells, can at times mistakenly attack healthy cells, producing autoimmune disorders like lupus or multiple sclerosis. PD-1 is what's called an "immune checkpoint," a protein receptor that tamps down highly active T cells so that they are less likely to attack healthy tissue.

How cancer hijacks PD-1

About 10 years ago, researchers discovered that cancer cells learn to use this immune safeguard for their own purposes. Tumor cells crank up the production of PD-L1 proteins, which are detected by the PD-1 receptor, inhibiting T cells from attacking the tumors. In effect, the proteins are a "don't kill me" signal to the immune system, the Stanford researchers said. Cancer patients are now being treated with antibodies that block the PD-1 receptor or latch onto its binding partner, PD-L1, to turn off this "don't kill me" signal and enable the T cells' attack.

"Using antibodies to PD-1 or PD-L1 is one of the major advances in cancer immunotherapy," said Weissman, who is also the Virginia and D.K. Ludwig Professor for Clinical Investigation in Cancer Research, director of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and director of the Ludwig Center for Cancer Stem Cell Research and Medicine at Stanford. "While most investigators accept the idea that anti-PD-1 and PD-L1 antibodies work by taking the brakes off of the T-cell attack on cancer cells, we have shown that there is a second mechanism that is also involved."

What Weissman and his colleagues discovered is that PD-1 activation also inhibits the anti-cancer activity of other immune cells called macrophages. "Macrophages that infiltrate tumors are induced to create the PD-1 receptor on their surface, and when PD-1 or PD-L1 is blocked with antibodies, it prompts those macrophage cells to attack the cancer," Gordon said.

Similar to anti-CD47 antibody

This mechanism is similar to that of another antibody studied in the Weissman lab: the antibody that blocks the protein CD47. Weissman and his colleagues showed that using anti-CD47 antibodies prompted macrophages to destroy cancer cells. The approach is now the subject of small clinical trials in human patients.

As it stands, it's unclear to what degree macrophages are responsible for the therapeutic success of the anti-PD-1 and anti-PD-L1 antibodies.

The practical implications of the discovery could be important, the researchers said. "This could lead to novel therapies that are aimed at promoting either the T-cell component of the attack on cancer or promoting the macrophage component," Gordon said.

Another implication is that antibodies to PD-1 or PD-L1 may be more potent and broadly effective than previously thought. "In order for T cells to attack cancer when you take the brakes off with antibodies, you need to start with a population of T cells that have learned to recognize specific cancer cells in the first place," Weissman said. "Macrophage cells are part of the innate immune system, which means they should be able to recognize every kind of cancer in every patient."

Story Source:

Materials provided by Stanford University Medical Center. Original written by Christopher Vaughan. Note: Content may be edited for style and length.

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Cancer therapy may work in unexpected way, study finds - Science Daily

Brain fights West Nile Virus in unexpected way – Medical Xpress

By Uncategorized

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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