Also check out our latest Beaker post on our CDG research.

Getting to the molecular heart of melanoma

Over the past two decades, Ze’ev Ronai, Ph.D., and his laboratory team have studied protein kinases such as JNK, AKT,  and PDK1. These enzymes are important components of signaling pathways in cells that are commonly down-regulated in melanoma, a type of skin cancer. As a result, the enzymes serve as potential drug targets so they can become active again.

Dr. Ronai’s team also studies a protein called activating transcription factor 2 (ATF2), which is associated with a poor prognosis in melanoma. This protein regulates a vast array of genes important for the healthy functioning of cells. The Ronai team identified a protein kinase named PKCɛ as the component that makes ATF2 cancer-causing in melanoma. In normal tissues, PKCɛ  is not as active, which allows ATF2 to protect the body against the formation of tumors.

Using this information, Dr. Ronai’s team, in collaboration with Sanford-Burnham’s Conrad Prebys Center for Chemical Genomics, is searching for small molecules that would confer the anti-cancer function of ATF2, thereby resuming ATF2’s ability to prevent the development of tumors. This approach could offer new therapeutic options for melanoma, and possibly other tumors where PKCɛ  promotes ATF2’s cancer-causing malfunction.

Targeting drugs for chemotherapy and tumor imaging

For many years, Elena Pasquale, Ph.D., has studied the relationship between a cell-surface receptor called Eph and proteins called ephrin. Eph receptors are like antennae that protrude from the surface of a cell. They foster cell-to-cell communication by binding to ephrin proteins on the surfaces of neighboring cells. Eph receptors, researchers have learned, appear more often in cancer cells than they do in normal ones.

Dr. Pasquale is now creating peptides that attach selectively to Eph receptors. Her collaborator, Maurizio Pellecchia, Ph.D., has developed a way to combine one of these peptides with a chemotherapy drug. The resulting combination amounts to a guided missile with a potent anti-cancer payload. Such specially designed drugs could be made to target cancer tumors, making them more effective while greatly reducing side effects.

In other work, Sanford-Burnham researchers have attached special chemicals to another Eph-targeting peptide that Dr. Pasquale developed to image tumors in mice. This approach might enable physicians to use MRI or PET scans to detect tumors early.

Visit us again next week for the last post in our National Cancer Research Month blog series about therapies to watch. Also go to Facebook.com/CancerResearchMonth to learn more about National Cancer Research Month and follow the conversation on Twitter, #NCRM13.

Targeting childhood brain cancer

Robert Wechsler-Reya, Ph.D., and his colleagues study the relationship between normal human development and cancer. They’re interested in how normal stem cells decide when to divide, when to specialize into other types of cells, and what tissues to become. When those processes break down, cancer can develop.

Dr. Wechsler-Reya’s group was the first to identify a new type of stem cell that develops into many different cell types in the cerebellum. But if this stem cell acquires certain mutations, it can result in medulloblastoma, the most common malignant brain cancer in children. Medulloblastomas are often treatable through surgery, radiation, and chemotherapy, but these treatments can dramatically reduce cognitive function and a child’s overall quality of life.

Dr. Wechsler-Reya’s team is identifying drug candidates that more specifically target tumors seen in medulloblastoma, to avoid the dangerous side effects of radiation and chemotherapy. Over the next few years, they hope to use this information to develop more effective therapies.

Converting cancer stem cells into normal cells

What if the best way to stop a tumor is not to kill it, but to turn it into something else? That’s the idea behind “differentiation therapy,” a new approach that prompts cancer stem cells to change into healthy, functioning cells—stopping tumors at their earliest stages.

In a recent study by Sanford-Burnham’s Robert Oshima, Ph.D., Masanobu Komatsu, Ph.D., and others, a mouse model of aggressive breast cancer was treated with bosutinib (SKI-606), a drug currently under development to treat advanced malignant tumors. The potential drug prevented the appearance of tumors in more than half of the treated mice, and it reduced tumor growth in older animals with pre-existing tumors.

Bosutinib was successful not because it killed cancer cells, but because it induced them to change into normal functioning cells. Unlike chemotherapy and radiation, which kill every cell they encounter, differentiation therapy disarms cancer cells without the dangerous side effects. Dr. Oshima’s team is now searching for other drug candidates that might induce cancer stem cell differentiation.

Carbohydrates that are good for you

One of the ways that tumors develop is when carbohydrates on a cell’s surface, which influence many cellular functions, become misplaced or malfunction.

Minoru Fukuda, Ph.D., and his team found that one type of carbohydrate, called “core 3 O-glycans,” suppresses tumor formation and metastasis—and it’s this same carbodydrate that’s seen at abnormally low levels in cancer cells.

Dr. Fukuda’s lab found that when core 3 O-glycans were artificially expressed on human prostate cancer cells, those cells produced much smaller tumors and almost no metastases. Parent cancer cells that do not express core 3 O-glycans, in contrast, produce robust tumors. Dr. Fukuda’s team also learned that the expression of core 3 O-glycans decreases the formation of integrin complexes, which play a role in a cell’s ability to migrate—a defining feature of cancer metastasis.

This means that certain carbohydrates on normal cells, such as core 3 O-glycans, and the enzymes that synthesize them, can act as tumor suppressors. Drug therapies that boost the activity of those enzymes may prove effective in treating cancer tumors.

Visit us again next week to learn about our research into how cell signaling is leading to new cancer treatment approaches. Also go to Facebook.com/CancerResearchMonth to learn more about National Cancer Research Month and follow the conversation on Twitter, #NCRM13.

“Sanford-Burnham can really make an impact in the field,” said Vipul Patel, M.D., FACS, founder of the IPCF and internationally renowned prostate cancer surgeon at Florida Hospital’s Global Robotics Institute, as he acknowledged Dr. Perera’s work to identify molecular markers for prostate cancer. Given IPCF and Sanford-Burnham’s shared goal to develop better diagnoses and treatments, this postdoc grant will hopefully only be a first step in a long and mutually beneficial partnership.

In Sanford-Burnham’s Lake Nona labs, Dr. Perera and his team are currently working on early prognostic markers for prostate cancer. The goal is to be able to diagnose prostate cancer earlier, through a simple urine or blood test instead of an invasive biopsy. “This research is urgently needed as professionals from all aspects of the field have been calling for these molecular markers. Not just for prostate cancer, but other malignant tumors as well,” explained Perera.

But how would these molecular markers work? Dr. Perera and others have found that the 97 percent of RNAs (messenger molecules) in the human cell that are not coding for a protein actually do have functional roles. Some non-coding RNAs perform important functions, such as switching genes on and off. However, they are also involved in the development of cancer. Higher or lower levels of certain RNAs have been found to play a role in the development of prostate cancer. Measuring these elevated or lowered RNA levels in the blood could consequently be an early marker for the disease.

As Dr. Patel pointed out during the ceremony, “We at Florida Hospital have operated on thousands of prostate cancer patients with various states of disease. We have a large database and a diverse pool of patient samples while Sanford-Burnham has deep basic medical research expertise.” When clinicians and medical researchers work together new therapies and diagnostic tools can be developed more rapidly.

You can read more about Dr. Perera’s research in a recent Florida Trend article, which you can find here. More information about the Dr. Patel and the International Prostate Cancer Foundation can be found here.

Their study was published online today by Arteriosclerosis, Thrombosis, and Vascular Biology. The findings suggest that the development of drug therapies to selectively inhibit endothelial Dkk1 signaling may help limit arteriosclerotic disease.

“I think the strategy going forward is to find ways to modulate or inhibit Dkk1 function, but we’re going to have to do it in a time-sensitive and cell type-specific fashion,” said Dwight A. Towler, M.D., Ph.D., director of the Cardiovascular Pathobiology Program at our Lake Nona campus and senior author of the study. “In diseases such as chronic renal deficiency or diabetes, where unregulated Dkk1 signaling can be destructive, it may be appropriate to restrain the action of Dkk1 for a prolonged period of time,” Dr. Towler added.

When the inflammatory response goes awry

The Dkk1 protein, when functioning normally, is important for aiding in wound repair. But inflammatory responses triggered inside artery walls after the onset of hyperglycemia, and other metabolic injuries associated with diseases like diabetes, can trigger prolonged and destructive Dkk1 signaling.

Dkk1 triggers the conversion of cells that line the interior surface of artery walls, called endothelial cells, into mesenchymal cells, which can direct connective tissue formation. This process is known as the endothelial-mesenchymal transition. The resulting fibrosis inside arterial walls leads to a dangerous stiffening of vessels that increases systolic blood pressure and ultimately impairs distal blood flow.

Drug therapy strategies to target Dkk1

Drug therapies should focus on the places where Dkk1 inhibition is called for—the arteries, in the case of atherosclerosis—because healthy Dkk1 signaling regulates normal processes such as cartilage and joint remodeling. To enable this targeted approach, Dr. Towler said he hopes to develop a therapeutic drug that would include a Dkk1 inhibitor and a peptide—a short chain of amino acids—engineered to target specific vascular tissues.

Longtime Sanford-Burnham researcher and past president Erkki Ruoslahti, M.D., Ph.D., developed these homing peptides, which have been used to deliver cancer drugs to where they’re most needed. “If we can target a Dkk1 antagonist to endothelial cells using the Ruoslahti peptides—or a similar strategy—that would be very, very powerful,” Dr. Towler said.

Dkk1 is from a family of molecules that arose during the development of vertebrates and is involved in heart formation in embryos. Researchers initially thought the protein’s only role was to inhibit a molecular pathway known as canonical Wnt signaling, which controls cell differentiation. However, these new data identify surprising “cross-talk” between Dkk1 and a bone-inducing pathway previously shown to promote the endothelial-mesenchymal transition.

Dr. Towler and his team will continue to study Dkk1 and Wnt signaling to identify potential drug targets to prevent the hardening of arteries in patients with atherosclerosis.

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This research was funded by the U.S. National Institutes of Health (grants HL81138, HL69229, and HL88651) and the Barnes-Jewish Hospital Foundation.

Cheng, S., Shao, J., Behrmann, A., Krchma, K., & Towler, D. (2013). Dkk1 and Msx2-Wnt7b Signaling Reciprocally Regulate the Endothelial-Mesenchymal Transition in Aortic Endothelial Cells Arteriosclerosis, Thrombosis, and Vascular Biology DOI: 10.1161/ATVBAHA.113.300647

“László is an international expert in studies of how genes are turned on and off in different cell types and at different times, particularly in response to hormones. He’s also made valuable contributions to our understanding of the roles these processes play in the development of common metabolic diseases,” said Daniel Kelly, M.D., director of our Diabetes and Obesity Research Center and scientific director of the Lake Nona campus. “He will apply his expertise in genomics to decipher the complexity of processes driving cancer, cardiovascular disease, and diabetes, a first step toward personalizing our approach to therapies.”

About László Nagy

Nagy uses systems-based molecular biology approaches, including epigenetics, to unravel the cellular communication networks regulated by nuclear hormone receptors. Nuclear hormone receptors are proteins that directly bind to DNA to turn genes on or off in response to hormones or other signals. Some of these receptors play key roles in immunity and inflammation. Nagy’s team is looking for ways to influence nuclear hormone receptors as a therapeutic strategy to alleviate infectious and chronic inflammatory diseases.

“I am thrilled about the opportunity to join Sanford-Burnham. The Institute’s commitment to technology-driven research programs and deep basic research expertise perfectly complement my background in genomics and nuclear hormone receptor research,” Nagy said. “As head of the new research program, I hope to help advance the Institute’s goal of developing new treatment strategies for metabolic diseases.”

Nagy received his M.D. and Ph.D. from the University of Debrecen’s Faculty of Medicine in Hungary. He received postdoctoral training at The University of Texas Health Science Center at Houston, and later at the Salk Institute for Biological Studies in La Jolla, Calif. Nagy has held appointments at the University of Debrecen since 1999. He will remain on the faculty there as an adjunct professor.

Nagy is the recipient of numerous awards, including a Boehringer Ingelheim Research Award, a Wellcome Trust Senior Research Fellowship in Biomedical Sciences, and three Howard Hughes Medical Institute International Research Scholar Awards. He was also elected EMBO (European Molecular Biology Organization) Young Investigator in 2000 and a member of EMBO and the Hungarian Academy of Sciences in 2007. He became a member of Academia Europaea (The Academy of Europe) in 2012.

Ballistics injuries that penetrate the skull have amounted to 18 percent of battlefield wounds sustained by men and women who served in the campaigns in Iraq and Afghanistan, according to the most recent estimate from the Joint Theater Trauma Registry, a compilation of data collected during Operation Iraqi Freedom and Operation Enduring Freedom. “A major contributor to the mortality associated with a penetrating brain injury is the elevated risk of intracranial infection,” said Chen, a neurosurgeon with UC San Diego Health System, noting that projectiles drive contaminated foreign materials into neural tissue. Under normal conditions, the brain is protected from infection by a physiological system called the blood-brain barrier. “Unfortunately, those same natural defense mechanisms make it difficult to get antibiotics to the brain once an infection has taken hold,” said Chen.

DARPA hopes to meet these challenges with nanotechnology. The agency awarded this grant under its In Vivo Nanoplatforms for Therapeutics program to construct nanoparticles that can find and treat infections and other damage associated with traumatic brain injuries. “Our approach is focused on porous nanoparticles that contain highly effective therapeutics on the inside and targeting molecules on the outside,” said Sailor, the UC San Diego materials chemist who leads the team. “When injected into the blood stream, we have found that these silicon-based particles can target certain tissues very effectively.”

Several types of nanoparticles have already been approved for clinical use in patients, but none for treatment of trauma or diseases in the brain. This is due in part to the inability of nanoparticle formulations to cross the blood-brain barrier and reach their intended targets. “Poor penetration into tissues limits the application of nanoparticles to the treatment of many types of diseases,” said Ruoslahti, distinguished professor in our NCI-designated Cancer Center. “We are trying to overcome this limitation using targeting molecules that activate tissue-specific transport pathways to deliver nanoparticles.” Ruoslahti’s team has already developed peptide-based biomolecules that can specifically target tissues such as brain tumors, atherosclerotic plaques and blood clots in the heart. Now they have set their sights on infections of the brain.

Treating brain infections is becoming more difficult as drug-resistant strains of viruses and bacteria have emerged. Because drug-resistant strains mutate and evolve rapidly, researchers must constantly adjust their approach to treatment. In an attempt to hit this moving target, the team is making their systems modular, so they can be reconfigured “on the fly” with the latest therapeutic advances. Nanocomplexes that contain genetic material known as short interfering RNA, or siRNA, developed by Bhatia’s research group at MIT, will be key to this aspect of the team’s approach. “The function of this type of RNA is that it specifically interferes with processes in a diseased cell. The advantage of RNA therapies are that they can be quickly and easily modified when a new disease target emerges,” said Bhatia, a bioengineering professor at MIT and partner in the research.

But effective delivery of siRNA-based therapeutics in the body has proven to be a challenge because the negative charge and chemical structure of naked siRNA makes it very unstable in the body and it has difficulty crossing into diseased cells. To solve these problems, Bhatia has developed nanoparticles that form a protective coating around siRNA. “The nanocomplexes we are developing shield the negative charge of RNA and protect it from nucleases that would normally destroy it. Adding Erkki’s tissue homing and cell-penetrating peptides allows the nanocomplex to transport deep into tissue and enter the diseased cells,” she said.

Bhatia has previously used the cell-penetrating nanocomplex to deliver siRNA to a tumor cell and shut down its protein production machinery. Although her group’s effort has focused on cancer, the team is now going after two other hard-to-treat cell types: drug-resistant bacteria and inflammatory cells in the brain. “The work proposed by this multi-disciplinary team should provide new tools to mitigate the debilitating effects of penetrating brain injuries and offer our warfighters the best chance of meaningful recovery,” Chen said. Team leader Sailor adds, “The DARPA funding agency often uses the term ‘DARPA-hard’ to refer to problems that are extremely tough to solve. What makes this a DARPA-hard problem is the fact that it is so difficult to deliver therapeutics to the brain. This is an underserved area of research.”

But researchers at Sanford-Burnham recently discovered three children (pictured above) with CDG who are mosaics—only some cells in some tissues have the mutation. For that reason, standard exome sequencing initially missed their mutations, highlighting the technique’s diagnostic limitations in some rare cases. These findings were published April 4 in the American Journal of Human Genetics.

“This study was one surprise after another,” said Hudson Freeze, Ph.D., director of Sanford-Burnham’s Genetic Disease Program and senior author of the study. “What we learned is that you have to be careful—you can’t simply trust that you’ll get all the answers from gene sequencing alone.”

Searching for a rare disease mutation

Complicated arrangements of sugar molecules decorate almost every protein and cell in the body. These sugars are crucial for cellular growth, communication, and many other processes. As a result of a mutation in an enzyme that assembles these sugars, children with CDG experience a wide variety of symptoms, including intellectual disability, digestive problems, seizures, and low blood sugar.

To diagnose CDG, researchers will test the sugar arrangements on a common protein called transferrin. Increasingly, they’ll also look for known CDG-related mutations by whole-exome sequencing, a technique that sequences only the small portion of the genome that encodes proteins. The patients are typically three to five years old.

A cautionary tale for genomic diagnostics

In this study, our researchers observed different proportions and representations of sugar arrangements depending on which tissues were examined. In other words, these children have the first demonstrated cases of CDG “mosaicism”—their mutations only appear in some cell types throughout the body, not all. As a result, the usual diagnostic tests, like whole-exome sequencing, missed the mutations. It was only when Freeze’s team took a closer look, examining proteins by hand using biochemical methods, did they identify the CDG mutations in these three children.

The team then went back to the three original children and examined their transferrin again. Surprisingly, these readings, which had previously shown abnormalities, had become normal. Freeze and his team believe this is because mutated cells in the children’s livers died and were replaced by normal cells over time. However, better transferrin did not reverse all symptoms.

“If the transferrin test hadn’t been performed early on for these children, we never would’ve picked up these cases of CDG. We got lucky in this case, but it just shows that we can’t rely on any one test by itself in isolation,” Freeze said.

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This research was funded by The Rocket Fund at Sanford-Burnham and the U.S. National Institutes of Health—National Institute of Diabetes and Digestive and Kidney Diseases grant R01DK55615 and National Human Genome Research Institute grant 1U54HG006493.

Ng, B., Buckingham, K., Raymond, K., Kircher, M., Turner, E., He, M., Smith, J., Eroshkin, A., Szybowska, M., Losfeld, M., Chong, J., Kozenko, M., Li, C., Patterson, M., Gilbert, R., Nickerson, D., Shendure, J., Bamshad, M., & Freeze, H. (2013). Mosaicism of the UDP-Galactose Transporter SLC35A2 Causes a Congenital Disorder of Glycosylation The American Journal of Human Genetics, 92 (4), 632-636 DOI: 10.1016/j.ajhg.2013.03.012

Researchers discovered that small pieces of genetic material called microRNAs link the two defining characteristics of fit muscles: the ability to burn sugar and fat and the ability to switch between slow- and fast-twitch muscle fibers. The team used two complementary mouse models—the “marathon mouse” and the “couch potato mouse”—to make this discovery. But what’s more, they also found that active people have higher levels of one of these microRNAs than sedentary people. These findings, published May 8 in The Journal of Clinical Investigation, suggest microRNAs could be targeted for the development of new medical interventions aimed at improving muscle fitness in people with chronic illness or injury.

“In this study, we wanted to determine, on a molecular level, what makes a muscle fit during development or following exercise. This information is relevant to our efforts to improve muscle fitness in many health conditions, such as aging, cancer, and heart failure. These findings may also prove useful for our active members of the military, who become ‘detrained’ during injury and recovery time,” said Daniel P. Kelly, M.D., director of Sanford-Burnham’s Diabetes and Obesity Research Center and senior author of the study.

Marathon vs. couch potato mice

Fit muscle is known for its ability to do two things: 1) burn fat and sugars and 2) switch between slow-twitch and fast-twitch muscles. According to Kelly, muscle fitness only occurs if both are functioning properly.

Increased muscle endurance cannot occur without boosting both of these muscle components.  Kelly and his team set out to determine what connects muscle metabolism and structure. To do this, they turned to two different mouse models, each specially engineered to produce distinct but related proteins that turn muscle-specific genes on and off.

The first model, dubbed the “marathon mouse,” has a muscle-gene regulator called PPARβ/δ. These mice can run much further than normal mice. The second model, known as the “couch potato mouse,” produces a different muscle-gene regulator, called PPARα. These mice are able to burn a lot of fuel, but they can’t run very far.

MicroRNAs in muscle fitness

To identify the link between muscle metabolism and muscle fiber type-switching, Kelly’s team compared the molecular differences between these two disparate mouse models.

First, the team found that PPARα couch potato mice have the optimal metabolic switch, but lack the muscle fiber switch. In contrast, PPARβ/δ marathon mice have the whole package necessary for muscle fitness.

The two mouse models also differed in molecular profiling, according to this study. The team discovered that marathon mice produce certain microRNAs that are capable of activating the fiber switch. By comparison, this same circuitry is suppressed in couch potato mice.

Digging a little deeper, Kelly’s team determined that PPARβ/δ is connected to microRNAs via an intermediary called estrogen-related receptor (ERRγ). This protein collaborates with PPARβ/δ to turn on microRNAs. That’s why marathon mice are fitter and have more type I muscle fibers than couch potato mice—their PPARβ/δ and ERRγ induce the right microRNAs.

Muscle-boosting potential for patients

To determine if their findings were relevant to human health, Kelly and his team worked with Steven R. Smith, M.D., director of the Florida Hospital—Sanford-Burnham Translational Research Institute for Metabolism and Diabetes. From there, the team obtained muscle tissue from sedentary people (those who don’t exercise regularly) and active people in good shape.

Sure enough, ERRγ and one of the microRNAs elevated in PPARβ/δ marathon mice were also increased in active people, but not the sedentary group.

“We’re now conducting additional human studies to further investigate the ERRγ-microRNA circuit as a potential avenue for improving fitness in people with chronic illness or injury,” Kelly said. “For example, next we want to know what happens to this circuit during exercise and what effect it has on the cardiovascular system.”

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This research was funded by the U.S. National Institutes of Health (grants RO1DK045416, R01DK095686, R01AR41928, R01AG030226), American Heart Association, Robert A. Welch Foundation, Jon Holden DeHaan Foundation, Fondation Leducq TransAtlantic Network of Excellence in Cardiovascular Research Program, ERC, Ecole Polytechnique Fédérale de Lausanne, Swiss National Science Foundation, and Novartis Clinical Innovation Fund.

Gan, Z., Rumsey, J., Hazen, B., Lai, L., Leone, T., Vega, R., Xie, H., Conley, K., Auwerx, J., Smith, S., Olson, E., Kralli, A., & Kelly, D. (2013). Nuclear receptor/microRNA circuitry links muscle fiber type to energy metabolism Journal of Clinical Investigation DOI: 10.1172/JCI67652

To reserve your spot on the 10 a.m. or 2 p.m. PT tours, please contact Molly Townsend at (858) 795-5111 or mtownsend@sanfordburnham.org.

Mrs. Fishman and her late husband, Dr. William Fishman, moved to San Diego in 1976 to establish a research organization with a unique mission: “Our big idea was to create an independent medical research institute dedicated to the emerging field of oncodevelopmental biology. We wanted to hire bright young scientists and give them the freedom to do their research, unencumbered by administrative bureaucracy and departmental politics,” she said. With a meager budget, the Foundation’s scientists took a joint-effort approach to medical research challenges, and worked collaboratively to advance discoveries effectively, a means that the Institute prides itself on today.

One of the scientists who has worked closely with the Fishmans is Dr. José Luis Millán, professor in our Sanford Children’s Health Research Center. “Throughout the 37 years that I have known Lil, I have always admired her ability to focus on the good in people, never lingering on the bad, and to praise successes, small as they might be. I’ve often invited Lil to have lunch with my lab members and they all admired her young spirit and energy and the can-do attitude that very likely was instrumental in enabling Bill and Lil to found this Institution,” he reflects on the decades the two have been close partners.

Sanford-Burnham’s commitment to the pursuit of improving human health can be attributed to the founding principles the Fishmans had originally established for the Institute. Mrs. Fishman explains, “when we started the La Jolla Cancer Research Foundation in our retirement years, we lived it, we ate it, and we slept it. It was a part of us. We were determined to find solutions that would help cure human diseases. I believe the Institute is still true to its core mission. We are trying to uncover new knowledge about being human beings and the mystery of life itself.” This firm dedication to seeking cures is what makes breakthrough discoveries possible at Sanford-Burnham. Mrs. Fishman’s reflections of the Institute’s past offer a valuable perspective of the Institute’s mission to meet the challenges of accelerating advancements in medical research.

The evening began with a lively reception to get our guests into the camping spirit: They sang along to campfire songs and tested their skills at beer and wine toss games. They then enjoyed dinner and a warm welcome from the event’s co-chairs, Stath and Terry Karras, along with former San Diego mayor Jerry Sanders and his wife Rana Sampson who geared up the crowd for a night of friendly competition. Before the camp games began, guests participated in a live auction and “fund-a-need” drive where bid paddles were raised to support our stem cell research to tackle diseases like diabetes, Alzheimer’s, ALS, brain tumors, and heart disease, as well as spinal cord and brain injuries.

Finally, guests from each table were invited to participate in six rounds of interactive challenges, where they showcased their camping expertise in fishing, hiking, and scavenger hunting. The night proved to incite a uniquely “un-gala” energy that carried with it the promise of furthering medical research.

The campers also heard from Robert Wechsler-Reya, Ph.D., professor and director of the Tumor Development Program in Sanford-Burnham’s NCI-designated Cancer Center, who offered a reflection on his laboratory and their efforts to study the relationship between brain development and brain tumor formation. Additionally, Pamela Itkin-Ansari, Ph.D., adjunct assistant professor in our Del E. Webb Center for Neuroscience, Aging, and Stem Cell Research discussed her work studying the signaling pathways controlling growth and differentiation in the human pancreas and touched upon her first-hand experience working with patients with type 1 (juvenile) diabetes.

Visit our Facebook page in the coming days to see more photos from Camp Bring It!, and follow our Events feed on Twitter to stay up-to-date about other events.

Learn more about Sanford-Burnham’s Stem Cell Research Center.

Camp Bring It! would not have been possible without the generous support of our sponsors: Alexandria Real Estate Equities, Lisa & Steve Altman, Bernstein Global Wealth Management, Malin & Roberta Burnham, CONNECT, Cooley, Creative Fusion, Cruzan Monroe, Cuatro Cuatros Winery, Cushman & Wakefield, San Diego Regional EDC, DLA Piper, Marleigh & Alan Gleicher, Jeanne & Gary Herberger, Terry & Stath Karras, Life Technologies, Mintz Levin, NAIOP, Eric Northbrook, Pegasus Building Services, Erin & Peter J. Preuss, Sempra Energy, Underground Elephant, and Willis Insurance Services.

Their team, sponsored by Technical Safety Services, Inc., won the American Cancer Society Relay For Life 9th Annual Golf Tournament in Oceanside, Calif. on April 12. These golfers spend their day jobs conducting and supporting cancer research, and now, by participating in this event, they are also helping to raise money, celebrate the lives of cancer survivors, and remember loved ones lost. Way to go!

What: 14th International Tumor Necrosis Factor Conference
When: July 7-10, 2013
Where: Loews Le Concorde, Quebec City, Canada
Who: Hosted by the International Cytokine Society; attended by more than 300 academic and biopharma industry scientists from around the world
Registration: Visit www.tnf2013.com

The Tumor Necrosis Factor Conference is a biennial meeting focused on the biology of the tumor necrosis factor (TNF) family of ligands and receptors. TNF family members are cytokines, signaling molecules that help direct the immune system. TNF inhibitors are sometimes used to treat autoimmune diseases such as rheumatoid arthritis. 

Conference attendees will discuss new findings on the roles TNF family members play in normal and disease processes, including cellular communication, tissue development, infectious diseases, innate and adaptive immunity, and cancer. The translation of these research advances into new therapies will also be discussed.

The conference is co-organized by Linda Burkly, Ph.D., Biogen Idec, and Jen Gommerman, Ph.D., University of Toronto. Carl Ware, Ph.D., director of Sanford-Burnham’s Infectious and Inflammatory Diseases Center, is a member of the organizing committee.

“This is a generational conference, ongoing since the early 1980s,” Ware said. “This conference continues as the venue  heralding the new discoveries about TNF-related cytokines, and their role in diseases like rheumatoid arthritis.”

Young scientists with new ideas will be able to attend this meeting with funds raised by Ware through the Arthritis National Research Foundation, a non-profit foundation that seeks to support the research of innovative young scientists.

To read more about Ware and his work, check out these blog posts:
Immune system expert takes on leukemia and lymphoma
Ask the experts: What are the risks associated with first FDA-approved HIV prevention drug?
Recruiting new troops in the war on cancer
Breast cancer research: from bench to bedside—and back
A scientist’s life: 10 things Carl Ware has done
Basic research bolsters clinical care
New insights into children’s health
Carl Ware & secrets of the immune system

“We’re looking forward to the valuable information-sharing opportunities and discussions that only occur when stem cell researchers, patient advocates, and representatives of many other stakeholder groups converge at the World Stem Cell Summit. Occasions like these help us advance our research on the basic biology of stem cells and spur the development of new, more personalized, medical applications for this science,” said Evan Snyder, M.D., Ph.D., director of Sanford-Burnham’s Stem Cell and Regenerative Biology Program.

Snyder will co-chair the Summit with TSRI Professor Jeanne Loring, Ph.D., Bernard Siegel of the GPI, Andre Terzic, M.D., Ph.D., of the Mayo Clinic, and Alan Trounson, Ph.D., of CIRM.

The event is expected to attract more than 1,200 attendees from 40 nations, and 200 sponsors, media partners and endorsing organizations. The conference provides an exhibition hall, country pavilions, specialized symposia, networking receptions, awards, and more.

“We are delighted to return to California for our 9th Summit and to showcase San Diego as a global hub for these emerging technologies,” said Siegel, Summit founder and GPI executive director.

The event will be held at the Manchester Grand Hyatt, One Market Place, in downtown San Diego.
To learn more, visit www.worldstemcellsummit.com.