Dr. Carl Ware

Dr. Carl Ware has joined Sanford-Burnham’s faculty as Director of the Infectious and Inflammatory Disease Center (IIDC). Although, this is the first time Dr. Ware has been employed at Sanford-Burnham, his roots with the Institute go back to 1996. That’s  when he, Dr. John Reed, Dr. Guy Salvesen and others began a collaborative project to study apoptosis and cell death. That same year, Dr. Ware joined the La Jolla Institute for Allergy and Immunology, where he led the Division of Molecular Immunology. Over the years, he has maintained strong ties with Sanford-Burnham.

Dr. Ware’s research focuses on the fundamental pathways that control cytokines, a family of proteins involved in immune signaling. One group of cytokines, called tumor necrosis factors or TNF, are part of an intricate communication network between immune system cells.

“They’re complicated circuits,” says Dr. Ware. “There are more than two dozen proteins in this family and an equal number of receptors. The pathways involve hundreds of proteins. In infectious disease, these pathways are amplified in a very dramatic fashion. In autoimmune disease the pathways escape regulatory control entirely. Something just goes haywire. However, with any circuit, theoretically, you can rewire around it.”

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Sanford-Burnham at Lake Nona

The real estate section of today’s New York Times features Orlando’s Medical City in Lake Nona, an emerging research hub that was founded in part with Sanford-Burnham’s  campus:

As soon as the [University of Central Florida] medical school was approved in 2006, the Burnham Institute (now called the Sanford-Burnham Medical Research Institute after a recent $50 million donation by the billionaire T. Denny Sanford) chose Lake Nona for its new home. The building, which opened last year, contains one of the country’s few robotic high-throughput screening centers — machines that can run a huge number of biological tests very quickly.

In addition to Sanford-Burnham and the University of Central Florida’s College of Medicine, Lake Nona’s Medical City currently includes MD Anderson Cancer Center Orlando. The hub will also soon welcome the University of Florida Academic and Research Center, a new Veteran’s Affairs Medical Center and Nemours Children’s Hospital.

While Medical City has been a boon for economic development, it’s also been great for scientific collaboration:

“A lot of Sanford-Burnham researchers have similar interests with ours,” said Roger Oxendale, the chief executive of Nemours. “A lot of the questions they’ll be asking about diabetes and obesity, they’ll be asking with respect to childhood diseases. I think we haven’t realized the potential of these partnerships.”

For a more complete history of Medical City at Lake Nona, read the entire New York Times article, “Orlando’s Newest Attraction is Medical”.

Dr. Robert Oshima

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 novel concept that targets cancer stem cells.

Scientists at Sanford-Burnham and elsewhere are beginning to think that stem cells may be the culprit behind tumor formation in some cancers. Much like other types of stem cells, cancer stem cells are presumably able to do two things: 1) self-renew, generating more new stem cells and 2) differentiate, giving rise to a variety of cell types. Differentiation therapy attempts to end the cycle of self-renewal by encouraging the cells to settle down and become a specific cell type, such as a skin cell.

“It seems to me that if we are smart enough to know all the genes in a cell, we should be smart enough to tell the cell what to do,” says Dr. Robert Oshima, co-director of the Sanford-Burnham Cancer Center’s Tumor Development Program. “In differentiation therapy, we are essentially telling cells: ‘Don’t become criminals, become productive members of society. If you stay legal, we’ll leave you alone.’”

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Dr. Sheila Collins

How is fat tissue from an obese person different from a thin person’s fat tissue? Dr. Sheila Collins and her colleagues at Sanford-Burnham’s Diabetes and Obesity Research Center recently discovered one major distinguishing feature – fat tissue from obese people doesn’t oxidize fatty acids as well as that from thinner people.

Fat cells use fatty acids for energy. But in response to adrenaline, fat tissue can also release fatty acids into the bloodstream for use by other tissues, such as heart and muscle. This latest study, published in the journal Diabetes, revealed that obese fat tissue was not as good as non-obese fat tissue at consuming fatty acids for energy. This might be one of the reasons why obese fat tissue releases more fatty acids into the bloodstream.  And although fatty acids are an important source of energy for other tissues, too much of it in the blood – a condition frequently seen in obesity – is believed to lead to type 2 diabetes and cause detrimental heart problems.

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Nanotechnology is solving some key drug delivery issues. In addition to learning how drugs and fluids move through tissue, researchers are developing needle-free drug delivery mechanisms, as shown here. Image by Peter Allen, UCSB.

Earlier this week, U.S. Congresswoman Lois Capps spent an afternoon touring the Center for Nanomedicine, Sanford-Burnham’s joint venture with the University of California, Santa Barbara (UCSB).

As Santa Barbara’s Daily Sound reports:

When asked why she came to see the center, Capps answered simply, “to be inspired.”

The Center for Nanomedicine, home to the laboratories of Sanford-Burnham’s Dr. Erkki Ruoslahti and Dr. Jamey Marth, focuses on the convergence of biology, nanotechnology and engineering, promising a new generation of solutions that address unmet needs in medicine and human health.

Read more about the Center and Rep. Capp’s visit in the Daily Sound.

Dr. John Reed

Sanford-Burnham CEO Dr. John Reed recently visited Beijing, where he toured a number of facilities and presented to the Institute of Genetic and Development Biology of the Chinese Academy of Sciences. The goal was to enhance Sanford-Burnham’s relationship with the Chinese scientific community and foster new opportunities for collaboration.

During his presentation, Dr. Reed highlighted the Institute’s scientific capabilities, leadership in basic research, advances in drug discovery and culture of collaboration. In particular, he pointed to the impact Sanford-Burnham publications have on the scientific community and the efficiency with which the Institute converts grant dollars into new discoveries. He also pointed out that Sanford-Burnham has the most advanced infrastructure for small molecule drug discovery in the non-profit world.

In addition, Dr. Reed noted that the non-profit biomedical research community in San Diego, which includes Sanford-Burnham, The Scripps Research Institute, the Salk Institute for Biological Studies, UC San Diego and others, has led to the creation of more than 500 biotechnology and pharmaceutical companies in the San Diego region.

The hope is that increased collaboration with China will lead to new discoveries and help new medicines move through the pipeline more rapidly.

Metastasis is a word no one wants to hear. Cells that should never leave their biological home migrate to distant parts of the body. Many things have to go wrong with cellular checks and balances for this to happen, yet it happens all too frequently.

To metastasize, cells must acquire a number of properties, including the abilities to move, survive in the bloodstream, cross tissue boundaries and grow in foreign organs. These last two properties require the activity of proteases, enzymatic proteins that break down other proteins. Dr. Sara Courtneidge, director of Sanford-Burnham’s Tumor Microenvironment Program, studies how the activity of these proteases is controlled by cell surface structures called invadopodia. These finger-like projections from the cell membrane are found in metastatic cancer cells but not in non-invasive cells. Dr. Courtneidge’s laboratory discovered a protein, called Tks5, which controls the formation of these invadopodia in cancer cells.

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Dr. Heather Buschman with daughter Avery

Hello! Heather here, science writer at Sanford-Burnham and frequent contributor to Beaker. We’re going to do something a little different today. I’m still going to discuss some of the cool research going on here at Sanford-Burnham, but since it affects me personally, this time it’ll be in the context of my own story…

Early one morning eleven years ago, I was visiting some friends while enjoying a break from college, when my dad called to tell me that my mom had died. It was sudden and completely unexpected. She was only 46 years old, healthy and seemingly full of life. My mom just went to work one evening (alone on the late shift) and never came home. As my dad tried to explain to me at the time, she just collapsed and that was it – nobody else was there to know what really happened. It was devastating to me and my family and our lives were forever changed. Not only was she gone, but we never had much of an explanation as to why. What caused her death and could it have been prevented? This was one of the hardest parts for me as both a daughter and as a young scientist. I read the medical examiner’s report myself. It wasn’t a heart attack and it wasn’t a stroke. The cause of death was simply listed as ‘heart failure’.

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Dr. Evan Snyder

In 2001, President George W. Bush limited federal funding for research on embryonic stem cells to just 21 federally approved cell lines. Shortly after taking office, President Barack Obama signed an executive order that removed that restriction, allowing scientists to apply for government funding to work with hundreds of new embryonic stem cell lines. Now, in a surprise announcement this week, a judge from the U.S. District Court in Washington, D.C. put the brakes on embryonic stem cell research once again by ruling that President Obama’s order violated a budget rider that bars federal funding for research in which an embryo is destroyed.

Last night, Dr. Evan Snyder, director of Sanford-Burnham’s program in stem cells and regenerative biology, debated this latest blow on PBS NewsHour, where he said:

“The biology that we are learning and the therapies that we are getting under our control from using these amazingly important cells could change the face of medical care. [Embryonic stem cells] and other stem cells like it have given rise to the entire field called regenerative medicine. In a way, this [ruling] has put a halt to the progress of regenerative medicine, one of the most promising areas of research of this century.”

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Dr. Sepideh Khorasanizadeh

Each of our cells contains a lot of DNA. So much DNA, in fact, that it has to be elaborately condensed and organized into chromosomes, which are then packed into the cell’s nucleus. If completely unraveled, the genetic material from just one of our 46 chromosome would stretch out to 1.5 centimeters – 10,000 times the length of the packed chromosome.

To condense all of this genetic material, long strands of DNA are tightly wound around proteins called histones. All this packing, however, can present a problem when our cellular machinery needs to access our DNA to read genes and produce proteins. As a result, chromosome packing is dynamic – some areas stay tightly wound while others are looser.  Just how accessible a particular region is can vary, depending on the tissue type, stage of development, disease state and other factors.

Dr. Sepideh Khorasanizadeh, one of Sanford-Burnham’s newest faculty members in Lake Nona, Florida, studies the cellular signals that influence chromosome packing to turn genes on and off. While much is known about how cells receive signals from the environment and carry those signals across into the cytoplasm, what happens when they reach the nucleus remains a mystery.

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