Facebook Live – Ask the Stem Cell Team about Patient Advocacy

How often do you get to ask an expert a question about something that matters deeply to you and get an answer right away? Not very often I’m guessing. That’s why CIRM’s Facebook Live “Ask the Stem Cell Team About Patient Advocacy” gives you a chance to do just that this Thursday, March 14th from noon till 1pm PST.

We have three amazing individuals who will share their experiences, their expertise and advice as Patient Advocates, and answer your questions about how to be an effective advocate for your cause.

The three are:

Gigi McMillan became a Patient Advocate when her 5-year-old son was diagnosed with a brain tumor. That led her to helping develop support systems for families going through the same ordeal, to help researchers develop appropriate consent processes and to campaign for the rights of children and their families in research.

Adrienne Shapiro comes from a family with a long history of Sickle Cell Disease (SCD) and has fought to help people with SCD have access to compassionate care. She is the co-founder of Axis Advocacy, an organization dedicated to raising awareness about SCD and support for those with it. In addition she is now on the FDA’s Patient Engagement Collaborative, a new group helping the FDA ensure the voice of the patient is heard at the highest levels.

David Higgins is a CIRM Board member and a Patient Advocate for Parkinson’s Disease. David has a family history of the disease and in 2011 was diagnosed with Parkinson’s. As a scientist and advocate he has championed research into the disease and worked to raise greater awareness about the needs of people with Parkinson’s.

Also, make sure to “like” our FaceBook page before the event to receive a notification when we’ve gone live for this and future events. If you miss the broadcast, not to worry. We’ll be posting it on our Facebook video page, our website, and YouTube channel shortly afterwards.

We want to answer your most pressing questions, so please email them directly to us beforehand at info@cirm.ca.gov.

And, of course, feel free to share this information with anyone you think might be interested.

Targeted treatment for pediatric brain tumors shows promising results

Image of medulloblastoma

Imagine sitting in the doctor’s office and being told the heartbreaking news that your child has been diagnosed with a malignant brain tumor. As one might expect, the doctor states that the most effective treatment option is typically a combination of chemotherapy and radiation. However, the doctor reveals that there are additional risks to take into account that apply to children. Since children’s tiny bodies are still growing and developing, chemotherapy and radiation can cause long-term side effects such as intellectual disabilities. As a parent, it is painful enough to have to watch a child go through chemotherapy and radiation without adding permanent damage into the fold.

Sadly, this scenario is not unique. Medulloblastoma is the most prevalent form of a pediatric brain tumor with more than 350 children diagnosed with cancer each year. There are four distinct subtypes of medulloblastoma, with the deadliest being known as Group 3.

Researchers at Sanford Burnham Prebys Medical Discovery Institute (SBP) are trying to minimize the collateral damage by finding personalized treatments that reduce side effects while remaining effective. Scientists at SBP are working with an inhibitor known as LSD1 that specifically targets Group 3 medulloblastoma in a mouse model. The study, published in Nature Communications, showed that the drug dramatically decreased the size of tumors grown under the mouse’s skin by shrinking the cancer by more than 80 percent. This suggested that it could also be effective against patients’ tumors if it could be delivered to the brain. The LSD1 inhibitor has shown promise in clinical trials, where it has been tested for treating other types of cancer.

According to Robert Wechsler-Reya, Ph.D., senior author of the paper and director of the Tumor Initiation and Maintenance Program at SBP: “Our lab is working to understand the genetic pathways that drive medulloblastoma so we can find better ways to intervene and treat tumors. This study shows that a personalized treatment based upon a patient’s specific tumor type might be within our reach.”

Dr. Wechsler-Reya’s work on medulloblastoma was, in part, funded by the CIRM (LA1-01747) in the form of a Research Leadership Award for $5,226,049.

Novel approach to slowing deadly brain cancer stem cells may lead to new treatments

Glioblastoma, a form of brain cancer, is one of the most dreaded cancer diagnoses. Standard radiation and chemotherapy treatments for glioblastoma almost always prove ineffective because of the cancer’s ability to grow back. With their unlimited potential to self-renew, cancer stem cells within the brain tumor are thought to be responsible for its aggressive reoccurrence. Not surprisingly, researchers looking to develop more effective therapies are focused on trying to better understand the biology of these cancer stem cells in order to exploit their vulnerabilities.

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MRI image of high grade glioma brain tumor (white mass on left). Image: Wikipedia

This week, the Dartmouth-Hitchcock Medical Center reports that a research team led by Damian A. Almiron Bonnin has identified a cell signal that the brain cancer stem cells rely on to resist standard treatments and to regrow. They also showed that drugs which interrupt this signal reduced tumor growth in animal studies.

Because if its aggressive growth, the cells within the glioblastoma eventually become starved for oxygen or, in scientific lingo, they become hypoxic. The presence of hypoxia in brain tumors is actually predictive of a poor prognosis in affected patients. A protein called hypoxia-inducible factor (HIF) becomes activated in these low oxygen conditions and helps the cancer stem cells to survive and continue to grow. The research team found that HIF carries out this function by triggering a cascade of cell activity that leads to the secretion of a protein called VEGF out into the microenvironment of the tumor. As secreted VEGF spreads through the tumor, it stimulates new blood vessel growth which is key to the tumor’s survival by nourishing the tumor with oxygen and nutrients.

Adding drugs that block a cell’s ability to release proteins, led to a reduction in glioblastoma tumor growth both in petri dishes and in animal studies. With these results, published in Oncogene, Dr. Almiron Bonnin’s team is performing the necessary preclinical studies that could lead to testing this novel strategy in patients. He summed this effort in a press release:

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Damian Almiron Bonnin

“Being able to target the cancer stem cells within these tumors, like we did here, could potentially improve response to current chemotherapies and prevent recurrences, which would translate into an increase in patient survival rates.”

 

Taking a new approach to fighting a deadly brain cancer

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Christine Brown, Ph.D., City of Hope researcher

CIRM’s 2017 Annual Report will be going live online very soon. In anticipation of that we are highlighting some of the key elements from the report here on the Stem Cellar.

One of the most exciting new approaches in targeting deadly cancers is chimeric antigen receptor (CAR) T-cell therapy, using the patient’s own immune system cells that have been re-engineered to help them fight back against the tumor.

Today we are profiling City of Hope’s Christine Brown, Ph.D., who is using CAR-T cells in a CIRM-funded Phase 1 clinical trial for an aggressive brain cancer called malignant glioma.

“Brain tumors are the hardest to treat solid tumors. This is a project that CIRM has supported from an early, pre-clinical stage. What was exciting was we finished our first milestone in record time and were able to translate that research out of the lab and into the clinic. That really allowed us to accelerate treatment to glioblastoma patients.

I think there are glimmers of hope that immune based therapies and CAR-T based therapies will revolutionize therapy for patients with brain tumors. We’ve seen evidence that these cells can travel to the central nervous system and eliminate tumors in the brain.

We now have evidence that this approach produces a powerful, therapeutic response in one group of patients. We are looking at why other patients don’t respond as well and the CIRM funding enables us to ask the questions that will, we hope, provide the answers.

Because our clinical trial is a being carried out at the CIRM-supported City of Hope Alpha Stem Cell Clinic this is a great example of how CIRM supports all the different ways of advancing therapy from early stage research through translation and into clinical trials in the CIRM Alpha Clinic network.

There are lots of ways the tumor tries to evade the immune system and we are looking at different approaches to combine this therapy with different approaches to see which combination will be best.

It’s a challenging problem and it’s not going to be solved with one approach. If it were easy we’d have solved it by now. That’s why I love science, it’s one big puzzle about how do we understand this and how do we make this work.

I don’t think we would be where we are at without CIRM’s support, it really gave the funding to bring this to the next level.”

Dr. Brown’s work is also creating interest among investors. She recently partnered with Mustang Bio in a $94.5 million agreement to help advance this therapy.

CIRM-Funded Clinical Trials Targeting Cancers

Welcome to the Month of CIRM!

As we mentioned in last Thursday’s blog, during the month of October we’ll be looking back at what CIRM has done since the agency was created by the people of California back in 2004. To start things off, we’ll be focusing on CIRM-funded clinical trials this week. Supporting clinical trials through our funding and partnership is a critical cornerstone to achieving our mission: to accelerate stem cell treatments to patients with unmet medical needs.

Over the next four days, we will post infographics that summarize CIRM-funded trials focused on therapies for cancer, neurologic disorders, heart and metabolic disease, and blood disorders. Today, we review the nine CIRM-funded clinical trial projects that target cancer. The therapeutic strategies are as varied as the types of cancers the researchers are trying to eradicate. But the common element is developing cutting edge methods to outsmart the cancer cell’s ability to evade standard treatment.

For more details about all CIRM-funded clinical trials, visit our clinical trials page and read our clinical trials brochure which provides brief overviews of each trial.

Genetically engineered immune cells melt away deadly brain tumors

MRI scan of patient with glioblastoma tumor. (wikicommons)

MRI scan of patient with glioblastoma. (wikicommons)

Cancers come in many different forms. Some are treatable if caught early and other aren’t. One of the most deadly types of cancers are glioblastomas – a particularly aggressive form of brain tumor.  Patients diagnosed with glioblastoma have an average life expectancy of 12-15 months and there is no cure or effective treatment that extends life.

While a glioblastoma diagnosis has pretty much been a death sentence, now there could be a silver lining to this deadly, fast-paced disease. Last week, scientists from the City of Hope in southern California reported in the New England Journal of Medicine, a new cell-based therapy that melted away brain tumors in a patient with an advanced stage of glioblastoma.

An Immunotherapy Approach to Glioblastoma

The patient is a 50-year-old man named Richard Grady who was participating in an investigational clinical trial run out of the City of Hope’s CIRM Alpha Stem Cell Clinic. A brain scan revealed a brightly lit tumor on the right side of Richard’s brain. Doctors surgically removed the tumor and treated him with radiation in an attempt to staunch further growth. But after six months, the tumors came back with a vengeance, spreading to other parts of his brain, lighting up his MRI scan like a Christmas tree.

With few treatment options and little time left, Richard was enrolled in the City of Hope trial that was testing a cell-based immunotherapy that recognizes and attacks cancer cells. It’s called CAR T-cell therapy – a term that you probably have heard in the news as a promising and cutting-edge treatment for cancer. Scientists extract immune cells, called T-cells, from a patient’s blood and reengineer them in the laboratory to recognize unique surface markers on cancer cells. These specialized CAR T-cells are then put back into the patient to attack and kill off cancer cells.

In Richard’s case, CAR-T cells were first infused into his brain through a tube in an area where a tumor was recently removed. No new tumors grew in that location of his brain, but tumors in other areas continued to grow and spread to his spinal cord. At this point, the scientists decided to place a second tube into a cavity of the brain called the ventricles, which contain a clear liquid called cerebrospinal fluid. Directly infusing into the spinal fluid allowed the cancer fighting cells to travel to different parts of the brain and spinal cord to attack the tumors.

Behnam Badie, senior author on the study and neurosurgery chief at the City of Hope, explained in a news release,

Benham Badie, City of Hope

Benham Badie, City of Hope

“By injecting the reengineered CAR-T cells directly into the tumor site and the ventricles, where the spinal fluid is made, the treatment could be delivered throughout the patient’s brain and also to the spinal cord, where this particular patient had a large metastatic tumor.”

 

Bye Bye Brain Tumors? Almost…

Three infusions of the CAR T-cell treatment shrunk Richard’s tumors noticeably, and a total of ten infusions was enough to melt away Richard’s tumors completely. Amazingly, Richard was able to reduce his medications and go back to work.

TESt

CAR T-cell therapy reduces brain tumors when infused into the spinal fluid. (NEJM)

The effects of the immunotherapy lasted for seven-and-a-half months. Unfortunately, his glioblastoma did come back, and he is now undergoing radiation treatment. Instead of being discouraged by these results, we should be encouraged. Patients with advanced cases of glioblastoma like Richard often have only weeks left to live, and the prospect of another seven months of life with family and friends is a gift.

Following these promising results in a single patient, the City of Hope team has now treated a total of nine patients in their clinical trial. Their initial results indicate that the immunotherapy is relatively safe. Further studies will be done to determine whether this therapy will be effective at treating other types of cancers.

CIRM Alpha Clinics Advance Stem Cell Treatments

The findings in this study are particularly exciting to CIRM, not only because they offer a new treatment option for a deadly brain cancer, but also because the clinical trial testing this treatment is housed at one of our own Alpha Clinics. In 2014, CIRM funded three stem cell-focused clinics at the City of Hope, UC San Diego, and a joint clinic between UC Los Angeles and UC Irvine. These clinics are specialized to support high quality trials focused on stem cell treatments for various diseases. The CIRM team will be bringing a new Alpha Clinics concept plan to its governing Board for approval in February.

Geoff Lomax, Senior Officer of Strategic Infrastructure at CIRM who oversees the CIRM Alpha Clinics, commented on the importance of City of Hope’s glioblastoma trial,

“Treating this form of brain cancer is one of the most vexing challenges in medicine. With the support and expertise of the CIRM Alpha Stem Cell Clinic, City of Hope is harnessing the power of patients’ immune cells to treat this deadly disease.”

Neil Littman, CIRM Director of Business Development and Strategic Infrastructure added,

“This study provides important proof-of-concept that CAR-T cells can be used to target hard-to-treat solid tumors and is precisely the type of trial the CIRM Alpha Stem Cell Clinic Network is designed to support.”

For more details on this study, watch the video below from City of Hope:

Scientists use human stem cell models to target deadly brain cancer

Malignant brain cancer is a devastating disease and it’s estimated that more than 16,000 patients will die of it this year. One of the most aggressive forms of brain cancer is gliomas, which originate from the support cells in the brain or spine that keep nerve cells happy and functioning. Unfortunately, there is no cure for gliomas and common treatments involving surgery, radiation and chemotherapy are not effective in fully eradicating these tumors.

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Brain CT scan of human glioma.

In hopes of finding a cure, scientists have turned to animal models and human cell models derived from tumor biopsies or fetal tissue, to gain understanding of how gliomas form and what makes these type of tumors so deadly and resistant to normal cancer treatments.  These models have their limitations, and scientists continue to develop more relevant models in hopes of identifying new potential treatments for brain cancer.

Speaking of which, a CIRM-funded research team from the Salk Institute recently reported a new human stem cell-based model for studying gliomas in Nature Communications. The team figured out how to transform human induced pluripotent stem cells (iPS cells) into glioma tumor-initiating cells (GTICs) that they used to model how gliomas develop and to screen for drugs that specifically target this deadly form of cancer.

Making the Model

One theory for how gliomas form is that neural progenitor cells (brain stem cells) can transform and take on new properties that turn them into glioma tumor-initiating cells or GTICs, which are a subpopulation of cancer stem cells that are really good at staying alive and reproducing themselves into nasty tumors.

The Salk team created a stem cell model for glioma by generating GTICs in a dish from human iPS cells. They genetically manipulated brain progenitor cells (which they called induced neural progenitor cells or iNPCs) derived from human iPS cells to look and behave like GTICs. Building off of previous studies reporting that a majority of human gliomas have genetic mutations in the p53 and Src-family kinase (SFK) genes, they developed different iNPC lines that either turned off expression of p53, a potent tumor suppressor, or that ramped up expression of SFKs, whose abnormal expression are associated with tumor expansion.

The team then compared the transformed iNPC lines to primary GTICs isolated from human glioma tissue. They found that the transformed iNPCs shared many similar characteristics to primary GTICs including the surface markers they expressed, the genes they expressed, and their metabolic profiles.

Their final test of their stem cell model determined whether transformed iNPCs could make gliomas in an animal model. They transplanted normal and transformed iNPC lines into the brains of mice and saw aggressive tumors develop only in mice that received transformed cells. When they dissected the gliomas, they found a mixture of GTICs, more mature brain cells produced from GTICs, and areas of dead cells. This cellular makeup was very similar to that of advanced grade IV primary glioblastomas.

Screening for drugs that target glioma initiating cells

Now comes the applied part of this study. After developing a new and relevant stem cell model for glioma, the team screened their transformed iNPC lines with a panel of 101 FDA-approved anti-cancer drugs to see if any of them were effective at stopping the growth and expansion of GTICs. They identified three compounds that were able to target and kill both transformed iNPCs and primary GTICs in a dish. They also tested these compounds on living brain slices that were injected with GTICs to form tumors and saw that the drugs worked well at reducing tumor size.

The authors concluded that their transformed iNPCs are appropriate for modeling certain features of how GTICs develop into adult gliomas. Their hope is that this model will be useful for developing new targeted therapies for aggressive forms of brain cancer.

“Our results highlight the potential of hiPSCs for studying human tumourigenesis. Similar to conventional disease modeling strategies based on the use of hiPSCs, the establishment of hiPSC cancer models might facilitate the future development of novel therapeutics.”


Related Links:

Funding a clinical trial for deadly cancer is a no brainer

The beast of cancers
For a disease that is supposedly quite rare, glioblastoma seems to be awfully common. I have lost two friends to the deadly brain cancer in the last few years. Talking to colleagues and friends here at CIRM, it’s hard to find anyone who doesn’t know someone who has died of it.

Immunocellular

Imagery of glioblastoma, a deadly brain cancer,  from ImmunoCellular’s website

So when we got an application to fund a Phase 3 clinical trial to target the cancer stem cells that help fuel glioblastoma, it was really a no brainer to say yes. Of course it helped that the scientific reviewers – our Grants Working Group or GWG – who looked at the application voted unanimously to approve it. For them, it was great science for an important cause.

Today our Board agreed with the GWG and voted to award $19.9 million to LA-based ImmunoCellular Therapeutics to carry out a clinical trial that targets glioblastoma cancer stem cells. They’re hoping to begin the trial very soon, recruiting around 400 newly diagnosed patients at some 120 clinical sites around the US, Canada and Europe.

There’s a real urgency to this work. More than 50 percent of those diagnosed with glioblastoma die within 15 months, and more than 90 percent within three years. There are no cures and no effective long-term treatments.

As our President and CEO, Dr. Randy Mills, said in a news release:

 “This kind of deadly disease is precisely why we created CIRM 2.0, our new approval process to accelerate the development of therapies for patients with unmet medical needs. People battling glioblastoma cannot afford to wait years for us to agree to fund a treatment when their survival can often be measured in just months. We wanted a process that was more responsive to the needs of patients, and that could help companies like ImmunoCellular get their potentially life-saving therapies into clinical trials as quickly as possible.”

The science
The proposed treatment involves some rather cool science. Glioblastoma stem cells can evade standard treatments like chemotherapy and cause the recurrence and growth of the tumors. The ImmunoCellular therapy addresses this issue and targets six cell surface proteins that are found on glioblastoma cancer stem cells.

The researchers take immune cells from the patient’s own immune system and expose them to fragments of these cancer stem cell surface proteins in the lab. By re-engineering the immune cells in this way they are then able to recognize the cancer stem cells.

My colleague Todd Dubnicoff likened it to letting a bloodhound sniff a piece of clothing from a burglar so it’s able to recognize the scent and hunt the burglar down.  When the newly trained immune system cells are returned to the patient’s body, they can now help “sniff out” and hopefully kill the cancer stem cells responsible for the tumor’s recurrence and growth.

Like a bloodhound picking up the scent of a burglar, ImmunoCellular's therapy helps the immune system track down brain cancer stem cells (source: wikimedia commons)

Like a bloodhound picking up the scent of a burglar, ImmunoCellular’s therapy helps the immune system track down brain cancer stem cells (source: Wikimedia Commons)

Results from both ImmunoCellular’s Phase 1 and 2 trials using this approach were encouraging, showing that patients given the therapy lived longer than those who got standard treatment and experienced only minimal side effects.

Turning the corner against glioblastoma
There’s a moment immediately after the Board votes “yes” to fund a project like this. It’s almost like a buzz, where you feel that you have just witnessed something momentous, a moment where you may have turned the corner against a deadly disease.

We have a saying at the stem cell agency: “Come to work every day as if lives depend on it, because lives depend on it.” On days like this, you feel that we’ve done something that could ultimately help save some of those lives.

Brain’s Own Activity Can Fuel Growth of Deadly Brain Tumors, CIRM-Funded Study Finds

Not all brain tumors are created equal—some are far more deadly than others. Among the most deadly is a type of tumor called high-grade glioma or HGG. Most distressingly, HGG’s are the leading cause of brain tumor death in both children and adults. And despite extraordinary progress in cancer research as a whole, survival rates for those diagnosed with an HGG have yet to improve.

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But recent research from Stanford University scientists could one day help move the needle—and give renewed hope to the patients and their families affected by this devastating disease.

The study, published today in the journal Cell, found that one key driver for HGG’s deadly diagnosis is that the tumor can be stimulated to grow by the brain’s own neural activity—specifically the nerve activity in the brain’s cerebral cortex.

Michelle Monje, senior author of the study that was funded in part by two grants from CIRM, was initially surprised by these results, as they run counter to how most types of tumors grow. As she explained in today’s press release:

“We don’t think about bile production promoting liver cancer growth, or breathing promoting the growth of lung cancer. But we’ve shown that brain function is driving these brain cancers.”
 


By analyzing tumor cells extracted from HGG patients, and engrafting it onto mouse models in the lab, the researchers were able to pinpoint how the brain’s own activity was driving tumor growth.

The culprit: a protein called neuroligin-3 that appeared to be calling the shots. There are four distinct types of HGGs that affect the brain in vastly different ways—and have vastly different molecular and genetic characteristics. Interestingly, says Monje, neuroligin-3 played the same role in all of them.

What was so disturbing to the research team, says Monje, is that neuroligin-3 is an essential protein for overall brain development. Specifically, it helps maintain healthy growth and repair of brain tissue over time. In order to grow, HGG tumors hijack this critical protein.

The research team came to this conclusion after a series of experiments that delved deep into the molecular mechanisms that guide both brain activity and brain tumor development. They first employed a technique called optogenetics, whereby scientists use genetic manipulation to insert light-sensitive proteins into the brain cells, or neurons, of interest. This allowed scientists to activate these neurons—or deactivate them—at the ‘flick of a switch.’

When applying this technique to the tumor-engrafted mouse models, the team could then see that tumors grew significantly better when the neurons were switched on. The next step was to narrow it down to why. Additional biochemical analyses and testing on the mouse models confirmed that neuroligin-3 was being hijacked by the tumor to spur growth.

And when they dug deeper into the connection between neuroligin-3 and cancer, they found something even more disturbing. A detailed look at the Cancer Genome Atlas (a large public database of the genetics of human cancers), they found that HGG patients with higher levels of neuroligin-3 in their brain had shorter survival rates than those with lower levels of the same protein.

These results, while highlighting the particularly nefarious nature of this class of brain tumors, also presents enormous opportunity for researchers. Specifically, Monje hopes her team and others can find a way to block or nullify the presence of neuroligin-3 in the regions surrounding the tumor, creating a kind of barrier that can keep the size of the tumor in check. 


The Man Behind the Curtain: Protein Helps Keep Cancer Cells Alive and Kicking

Being diagnosed with brain cancer comes with a sobering sentence: even with the most aggressive treatments, life expectancy for the most common form of brain cancer—called glioblastoma—is less than two years.

One of the key culprits, many scientists now believe, are cancer stem cells. Cancer stem cells are a subset of cancer cells that have three very unique properties: they can self-renew, they can propagate (or multiply) the cancer, and they can transform into the many types of cells that are found in a tumor.

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Cancer stem cells are a relatively new concept, but they have generated a lot of excitement among cancer researchers because they could lead to the design of more effective therapies. And while whether or not they even existed has long been a source of debate among experts, a series of recent research findings have bolstered the notion not only that they exist, but also that they play a significant role in the recurrence of some forms of cancer—including glioblastoma.

Researchers have been identifying, step by step, the many proteins and chemical pathways that form the path from cancer stem cell to tumor. Previous research had found the CDK class of proteins to be present in large quantities in mature cancer cells in patients suffering from glioblastoma. But they suspected something else was at play, helping to keep the CDK proteins switched on in mature cancer cells.

So scientists at McGill University in Canada, led by neurologist Dr. Anita Bellail, dug deeper. In their report, published this week in the journal Nature Communications, the team has pinpointed a new class of proteins at play behind the scenes called SUMO.

Specifically, Bellail and her team observed that the SUMO1 protein in particular modifies a CDK protein called CDK6 in a process the team has dubbed ‘sumylation.’ As Bellail explained in this week’s news release:

“CDK6 sumylation inhibits its degradation and thus stabilizes the CDK6 protein in the cancer.”

In other words, the CDK6 protein does not by itself maintain a presence in the cancer cells. Instead, it requires a little help from SUMO1. As Bellail continued:

“We found that CDK6 sumylation is required for the renewal and growth of the cancer stem cells in glioblastoma.”

It stands to reason, therefore, that shutting off SUMO1 could do the reverse—thus destabilizing CDK6 and, potentially, block the progression of the cancer.

And in further experiments by Bellail and her team, they found exactly that.

These results hold significant promise for finding new ways to treat glioblastoma because now the team has a target: SUMO1. In fact, the research team is now screening for drugs that can target SUMO1 and block it, thus reducing CDK6 levels and, as a result, cancer cells—and one day offering a more optimistic outcome for those diagnosed with glioblastoma.

Want to learn more about cancer stem cells? Check out our 2009 “Spotlight on Cancer Stem Cells” video starring Dr. Michael Clarke, associate director of the Stanford Institute for Stem Cell and Regenerative Medicine.