Sanford-Burnham Science Blog
Garth Powis, Ph.D., has been appointed professor and director of Sanford-Burnham's Cancer Center,...
Researchers discover that a protein called Siah2 helps prostate cancer cells resist hormone...
Sanford-Burnham is excited to be part of the first Pedal the Cause--San Diego, in partnership with...
Sanford-Burnham at Lake Nona announced today the selection of the first five research organizations...
May is National Cancer Research Month
May is National Cancer Research Month, so we thought we’d highlight exciting cancer research underway at Sanford-Burnham. Today, we focus on a few of the strategies our researchers are pursuing to better understand the pathologies of cancer tumors—and stop them in their tracks.
Drs. Perera (left) and Patel during the "A Celebration of Collaboration" ceremony on May 10
During a ceremony at Sanford-Burnham at Lake Nona on May 10, the International Prostate Cancer Foundation (IPCF) awarded Ranjan Perera, Ph.D., scientific director of analytical genomics and bioinformatics at our Lake Nona campus, $60,000 to fund a postdoctoral fellow in Dr. Perera’s lab.
“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.
Congratulations to these Sanford-Burnham golfers (pictured above left to right): Peter Teriete (staff scientist), Jochen Maurer (postdoctoral researcher), Eric Tabanico (safety technician), and Robert Oshima (professor).
The Florida Translational Research Program provides Florida-based scientists with access to Sanford-Burnham's drug-discovery technology and expertise.
We announced today the selection of the first five research organizations that will participate in the Florida Translational Research Program (FTRP) to advance drug discovery in the state. The projects focus on cancer, diabetes, and obesity, and are led by scientists from the University of Central Florida, the University of Florida, the University of Miami, Scripps Florida, and a team of our own Lake Nona scientists. The Florida Department of Health and Sanford-Burnham established the FTRP as a competitive grant program that provides funding for collaborative drug discovery projects. The overall goal of the program is to translate research discoveries made in Florida laboratories into the medicines of tomorrow.
Prostate cancer cells expressing a mutant form of c-Myc that cannot be altered by PKCzeta (left) are more aggressive and more invasive than prostate cancer cells in which PKCzeta is able to keep tabs on c-Myc (right).
The enzyme PKCζ acts as a tumor suppressor by keeping the pro-tumor c-Myc gene in check, in both mice and humans.
Researchers have identified how an enzyme called PKCζ suppresses prostate tumor formation. The finding, which also describes a molecular chain of events that controls cell growth and metastasis, could lead to novel ways to control disease progression.
Siah2 levels (brown staining) are high in human castration-resistant prostate cancer (left), as compared to benign prostate growths (right)
Researchers discover that a protein called Siah2 helps prostate cancer cells resist hormone therapy—making it an attractive biomarker and therapeutic target.
Hormonal therapies can help control advanced prostate cancer for a time. However, for most men, at some point their prostate cancer eventually stops responding to further hormonal treatment. This stage of the disease is called androgen-insensitive or castration-resistant prostate cancer. In a study published March 18 in Cancer Cell, a research team found a mechanism at play in androgen-insensitive cells that enables them to survive treatment. They discovered that a protein called Siah2 keeps a portion of androgen receptors constantly active in these prostate cancer cells. Androgen receptors—sensors that receive and respond to the hormone androgen—play a critical role in prostate cancer development and progression.
Pedal the Cause–San Diego, the region’s only multi-day cycling fundraiser for cancer research, will announce their first annual event today at 11 a.m. PT, on our La Jolla campus.
Sanford-Burnham is excited to be part of this new fundraising event for cancer research, in partnership with our two “neighbor” National Cancer Institute (NCI)-designated cancer centers, UC San Diego Moores Cancer Center and the Salk Institute for Biological Studies.
San Diego is a powerhouse for cancer research, home to two National Cancer Institute (NCI)-designated centers for basic research—our Cancer Center and the Salk Institute Cancer Center—and the University of California, San Diego Moores Cancer Center, the region’s only NCI-designated comprehensive cancer center.
L to R: Peter Preuss, Peggy Preuss and Peter Preuss, Jr., whose family foundation provides generous support for cancer research and brain cancer seminars in San Diego.
Napoleone Ferrara, Ph.D., was propelled into the national spotlight last week, when he was named one of 11 winners of the first Breakthrough Prizes in Life Sciences. This new prize—awarding a no-strings-attached $3 million to each recipient—was bestowed by Silicon Valley innovators Sergey Brin, Anne Wojcicki, Mark Zuckerberg and Yuri Milner. One goal of the prize is to make household names out of the country’s top scientists.
Ze'ev Ronai, Ph.D.
Editor’s note: below is a message that Kristiina Vuori, M.D., Ph.D., our President and Interim CEO, sent to Sanford-Burnham scientists and staff today.
Dear All:
I’m pleased to announce the appointment of Dr. Ze’ev Ronai to the position of Scientific Director of the La Jolla campus. As many of you are aware, such position was held by Dr. John Reed in 1995-2001, while I held a similar position of Executive Vice President for Scientific Affairs prior to my appointment as President in 2010.
Garth Powis, Ph.D.
We’re happy to announce that Garth Powis, Ph.D., has been appointed professor and director of our Cancer Center, one of seven National Cancer Institute (NCI)-designated basic research cancer centers in the U.S. He will also assume the Jeanne and Gary Herberger Leadership Chair in Cancer Research. Powis previously held leadership positions at MD Anderson Cancer Center in Texas. He will join our faculty May 1.
Cells proliferating in an intestinal tumor
Researchers discover that tumors lacking the protein PKCζ are good at surviving when nutrients are scarce—opening a new therapeutic avenue that targets cancer metabolism.
Cancer cells need food to survive and grow. They’re very good at getting it, too, even when nutrients are scarce. Many scientists have tried killing cancer cells by taking away their favorite food, a sugar called glucose. Unfortunately, this treatment approach not only fails to work, it backfires—glucose-starved tumors actually get more aggressive. In a study published January 31 in the journal Cell, researchers discovered that a protein called PKCζ is responsible for this paradox. The research suggests that glucose depletion therapies might work against tumors as long as the cancer cells are producing PKCζ.
PKCζ: critical regulator of tumor metabolism
According to this study, when PKCζ is missing from cancer cells, tumors are able to use alternative nutrients. What’s more, the lower the PKCζ levels, the more aggressive the tumor.
“We found an interesting correlation in colon cancers—if a patient’s tumor doesn’t produce PKCζ, he has a poorer prognosis than a similar patient with the protein. We looked specifically at colon cancer in this study, but it’s likely also true for other tumor types,” said Jorge Moscat, Ph.D., a professor at Sanford-Burnham. Moscat led the study in close collaboration with colleague Maria Diaz-Meco, Ph.D.
Potential cancer drug sabutoclax blocks Bcl-2 protein family members that help keep cancer cells alive. This image shows the structure of one Bcl-2 protein, known as Bcl-Xl. (Image courtesy of the Pellecchia laboratory)
Researchers find that certain types of drug-resistant leukemia stem cells are vulnerable to sabutoclax, a novel cancer stem cell-targeting drug based on Sanford-Burnham research.
New experiments show that sabutoclax, a novel cancer stem cell-targeting drug that grew out of research at Sanford-Burnham Medical Research Institute, in combination with other therapies, could effectively treat diseases like chronic myeloid leukemia (CML). Sabutoclax might also lower the chance of relapse.
“The demonstration of sabutoclax’s preclinical activity in mouse models of CML is exciting and encourages further evaluation of this promising drug candidate for aggressive leukemias. We look forward to continuing our collaborative studies of sabutoclax, as we move this drug closer to the clinic,” said John Reed, M.D., Ph.D., professor and Donald Bren Chief Executive Chair at Sanford-Burnham.
Sabutoclax was first discovered as a result of research in the laboratories of Reed and his Sanford-Burnham colleague, Maurizio Pellecchia, Ph.D. The pair is now working with biotechnology company Oncothyreon Inc to develop sabutoclax into a potential anti-cancer drug. This latest study of sabutoclax’s efficacy, published January 17 in the journal Cell Stem Cell, was led by Catriona Jamieson, M.D., Ph.D., at UC San Diego Moores Cancer Center, in collaboration with Reed, Pellecchia and others.
![3D structure of CXCR1, a G protein-coupled receptor that transmits inflammatory signals [Image courtesy of Stanley Opella, UCSD]](http://beaker.sanfordburnham.org/wp-content/uploads/2012/12/CXCR11_top10.jpg)
3D structure of CXCR1, a G protein-coupled receptor that transmits inflammatory signals [Image courtesy of Stanley Opella, UCSD]
Originally published October 23, 2012
Scientists have, for the first time, determined the three-dimensional structure of a complete, unmodified G-protein-coupled receptor (GPCR) in its native environment: embedded in a lipid membrane.
The team, led by Stanley Opella, Ph.D. at the University of California, San Diego and Francesca Marassi, Ph.D. at Sanford-Burnham Medical Research Institute, used a technique called NMR spectroscopy to map the arrangement of atoms in one particular GPCR, called CXCR1. Their finding was published by Nature on October 21.
Lung X-ray, with a possible tumor shown on the right (Image courtesy of National Cancer Institute)
Originally published June 18, 2012
Sanford-Burnham researchers and their collaborators uncovered a new mechanism that may lead to unique treatments for lung cancer, one of the leading causes of death worldwide.
In the study, published May 15 in the journal Genes & Development, the team discovered that a protein called Bax Inhibitor-1 (BI-1) protects lung cancer cells and promotes tumor growth by regulating autophagy, a mechanism by which cells break down their own components and recycle the parts. Autophagy, which literally means “to eat oneself,” is essential to cell survival, particularly when food is scarce.
“Cancer cells are remarkably adaptive and depend on a variety of mechanisms to ensure their survival and continued growth when challenged by their environment,” says John C. Reed, M.D., Ph.D., Sanford-Burnham’s CEO and senior author of the study. “By reducing levels of BI-1, it appears we were able to modulate intracellular signals and starve lung cancer cells of the energy needed to carry out one of their most important survival mechanisms—autophagy.”
