cancer metabolism Archives - Sanford Burnham Prebys
Institute News

Southern California metabolism scientists meet on the Mesa

AuthorGreg Calhoun
Date

March 30, 2026

The fourth annual SoCal Metabolism Symposium brought together hundreds of experts and trainees to share the latest advances

SoCal Metabolism Symposium co-organizer Brooke Emerling, PhD, opened the meeting held at Sanford Burnham Prebys Medical Discovery Institute on Friday, March 20, 2026, by celebrating the event’s momentum.

“In 2023, when it started, we had about 12 talks, 28 posters, about 120 attendees and three sponsors, and now we’re up to 18 talks, 64 posters, more than 200 attendees and six sponsors,” said Emerling, director of and associate professor in the Sanford Burnham Prebys Cancer Metabolism and Microenvironment Program.

Speakers were mostly postdoctoral researchers and graduate students from Sanford Burnham Prebys, the Salk Institute, the University of California Irvine, the University of Southern California, the University of California Los Angeles and the University of California San Diego.

The event began with a session of scientific talks focused on the theme of cancer metabolism. Aaliyah Balagtas, a graduate student in the lab of Cosimo Commisso, PhD, at Sanford Burnham Prebys, discussed her research on a cellular scavenging process known as macropinocytosis that pancreatic tumors use to survive and grow when resources are scarce. The morning continued with a second thematic session focused on metabolism in aging and cell fate.

Before the event’s lunch break and poster viewing, Emerling introduced the symposium’s first-ever guest speaker from outside Southern California, Navdeep Chandel, PhD, the David W. Cugell, MD, Professor and professor of Medicine (Pulmonary and Critical Care), Biochemistry and Molecular Genetics at Northwestern University.

Chandel began by sharing his delight that the speakers in the morning sessions showed genuine enthusiasm and interest in studying mitochondria and targeting metabolism to improve human health and treat disease. He thinks there is a significant opportunity to use the fundamental knowledge we’re learning about intermediary metabolism in mitochondria and translate it into concrete advances for human health.

Brooke Emerling, PhD, is the director of the Sanford Burnham Prebys Cancer Metabolism and Microenvironment Program.

Brooke Emerling, PhD, is director of and associate professor in the Cancer Metabolism and Microenvironment Program at Sanford Burnham Prebys. Image credit: Sanford Burnham Prebys.

Chandel focused on one of his lab’s translational projects studying metformin, a longstanding, widely used, cheap and safe drug for treating high blood sugar in prediabetes and type 2 diabetes. Various studies have suggested that metformin also has anti-cancer effects and may reduce inflammation, but it was not clear how the drug worked in our bodies or cells to cause any of this to occur. Chandel shared soon-to-be-published data regarding how metformin builds up in the gut after being taken as a pill, and how it influences mitochondria there to systemically lower blood sugar.

The afternoon opened with a third set of thematic podium presentations centered on the topic of physiological metabolism and new techniques. The fourth and final session of scientific talks were grouped around the theme of immunometabolism.

Cosimo Commisso, PhD, is the deputy director of the National Cancer Institute-designated Cancer Center at Sanford Burnham Prebys. He currently serves as the interim director while a national search is conducted for a new center director.

Cosimo Commisso, PhD, is the deputy director of the institute’s NCI-Designated Cancer Center and a professor in the Cancer Metabolism and Microenvironment Program. Image credit: Sanford Burnham Prebys.

The symposium’s closing podium talk was the Gina Lee Memorial Keynote, a lecture honoring cancer signaling and metabolism expert Gina Lee, PhD, an assistant professor of Microbiology and Molecular Genetics at the University of California Irvine, who passed away on June 23, 2024, at the age of 39.

Cosimo Commisso, PhD, the deputy director of the institute’s NCI-Designated Cancer Center and a professor in the Cancer Metabolism and Microenvironment Program, delivered the 2026 Gina Lee Memorial Keynote and focused on a new direction for his lab. Aging is a major risk factor for pancreatic cancer that also can limit treatment options if a patient is too frail to be safely treated with surgery or other alternatives.

The average age of a patient diagnosed with pancreatic cancer is 70, and nearly two-thirds of cases are in people over the age of 65. Commisso and his lab members are rethinking how therapies in development will work for a frail and aging population that represents the majority of patients.

Following Commisso’s keynote address, the 2026 SoCal Metabolism Symposium concluded with a reception and second poster session. The next SoCal Metabolism Symposium will be held in March 2027 at the University of California Irvine.

Emerling organized the event in partnership with Peter James Mullen, PhD, assistant professor of Microbiology and Immunology in the Keck School of Medicine at the University of Southern California, and Cholsoon Jang, PhD, assistant professor of Biological Chemistry at the University of California Irvine School of Medicine.

Institute News

Raising awareness of breast cancer research at Sanford Burnham Prebys

AuthorGreg Calhoun
Date

October 31, 2024

The October Science Connect Series event was themed around Breast Cancer Awareness Month and featured two cancer research experts.

The Sanford Burnham Prebys Wellness Ambassadors hosted a Science Connect event on Wednesday, October 30, 2024, featuring two faculty experts discussing their breast cancer research and its implications.

The Science Connect Series provides a forum for Sanford Burnham Prebys principal investigators to share their research with administrative personnel. Faculty members gain experience in communicating their science to a lay audience, and administrators gain a better understanding of research conducted at the institute so they can become better advocates and ambassadors of the shared mission to translate science into health.

Kelly Kersten, PhD, an assistant professor in the Cancer Metabolism and Microenvironment Program, opened the event by focusing on the importance of finding new treatments —such as immunotherapies — for the one-third of breast cancer patients that are diagnosed after the early stages of the disease when surgery is less effective.

The immune system is one of the main defenses of the human body to fend off harmful pathogens and invasive cells, such as cancer. Among all white blood cells, a particular cell type, called a T cell, can directly kill cancer cells and therefore plays an essential role in building anti-tumor immune responses.

Many types of cancer are confronted and infiltrated by T cells, only to be suppressed by the local tumor environment.

“While immunotherapies that boost the immune system have revolutionized the way we treat cancer, many patients do not respond to the treatments, and the mechanisms of resistance remain largely unclear,” said Kersten.

Kersten’s goal is to understand why T cells enter a state known as exhaustion and lose their tumor-killing capacity. This knowledge will help her team find potential future therapies that could prevent T-cell exhaustion and improve immunotherapies for cancer patients.

Kevin Tharp, PhD, also an assistant professor in the Cancer Metabolism and Microenvironment Program, shared that his lab’s focus is on how cancer cells adapt their metabolism to generate the energy needed to spread to other tissues through metastasis. He presented his team’s work with the Kersten lab on another aspect of potential resistance to immunotherapy in breast cancer.

Tharp and Kersten are studying the hypothesis that part of the reason why these therapies fail is due to tumor-associated fibrosis, the creation of a thick layer of fibrous collagen (like scar tissue) that acts as a barrier against the anti-tumor immune response. They published a paper on June 3, 2024, in Nature Cancer,  discussing how tumor-associated macrophages, a type of immune cell found abundantly in the tumor microenvironment, respond to the physical properties of fibrosis.

By synthesizing injury-associated collagens that facilitate wound closure, TAMs experience metabolic changes and generate metabolic byproducts that suppress the anti-tumor function of immune cells.

“The metabolic changes in the microenvironment present more of a challenge to anti-tumor responses than the physical barrier,” said Tharp. “Our study provides an alternative explanation for why anti-tumor immunity is impaired in fibrotic solid tumors.”

To follow up on these results, Tharp is collaborating with Sarah Blair, MD, a professor of surgery at the University of California San Diego, to fund and initiate a clinical trial testing the potential of dietary supplements to counteract the suppressive effects of TAM metabolic byproducts as an adjunct therapy to surgery.

Institute News

Preeminent scientists present at SBP’s Cancer Metabolism Symposium

AuthorSusan Gammon
Date

June 27, 2018

SBP’s 4th Cancer Metabolism Symposium attracted nearly 150 attendees—all eager to learn more about how the nation’s top-tier cancer scientists are looking to target tumor metabolism.

Research on cancer metabolism is critical to identify new therapeutic targets to starve tumors of the fuels and building blocks they need to grow. Recognition and understanding of the impact of cancer metabolism will increasingly and positively affect the development of novel anti-cancer therapeutics.

The event featured 21 speakers who presented the latest concepts and models in the field of tumor metabolism, which expands to other areas of cancer biology, including microenvironment, immunometabolism and cell bioenergetics. All of the presentations addressed fundamental mechanisms of cancer as well as how this emerging field of science is impacting translational research and personalized medicine. 

“It’s an honor to host the top experts in the field and discuss what we know about metabolic wiring in tumors and their environment,” said Jorge Moscat, PhD, conference co-organizer and director and professor of the Cancer Metabolism and Signaling Networks Program at SBP. “These events will lead us to strategies to exploit tumor vulnerabilities and better ways to treat cancer.”

Keynote speaker M. Celeste Simon, PhD, who studies cancer metabolism and the influence of oxygen availability on tumor growth, presented her recent data on “Metabolic Symbiosis in the Hypoxic Tumor Microenvironment.” Simon, a recipient of a National Cancer Institute Outstanding Investigator Award, is a leader in biomedical research on cancer metabolism, specifically renal cancer, which is one of the 10 most common cancers in both men and women. She is scientific director of the Abramson Family Cancer Research Institute of the Perelman School of Medicine at the University of Pennsylvania.

“These conferences are important because they give scientists an opportunity to share new ideas and promote collaborations that can enhance accelerated discovery and development of new therapeutic approaches to target cancer metabolism,” says conference co-organizer Maria Diaz-Meco, PhD, professor in the Cancer Metabolism and Signaling Networks Program at SBP.

Robert Abraham, PhD, Pfizer Worldwide Research & Development, represented the industry side of research with a presentation titled “Probing Cancer Metabolism with Cancer Drugs.”

Academic biomedical research institute speakers were represented by the Symposium’s organizers, Moscat and Diaz-Meco; and a broad range of acknowledged leaders in cancer research, including Ronald DePinho, MD (MD Anderson Cancer Center); Ramon Parsons, MD, PhD (Mount Sinai); John Blenis, PhD (Weill Cornell Medicine); Reuben Shaw, PhD (Salk Institute); Eileen White, PhD (Rutgers Cancer Institute of New Jersey); Tak Wah Mak, PhD (University of Toronto and The Campbell Family); Alec Kimmelman, MD, PhD (NYU Langone Health); Karen Vousden, PhD (The Crick Institute); Ralph J. DeBerardinis, MD, PhD (University of Texas SW Medical Center); Roberto Zoncu, PhD (UC Berkeley); Christian Metallo, PhD (UC San Diego); Douglas Green, PhD (St. Jude Children’s Research Hospital; Matthew Vander Heiden, MD, PhD (David H. Koch Institute at MIT); Dafna Bar-Sagi, PhD (NYU Langone Health); Michael Karin, PhD (UC San Diego); Jeffrey Rathmell, PhD (Vanderbilt University); and Davide Ruggero, PhD (UC San Francisco).

“We wish to thank all the speakers, attendees and support staff that helped pull this amazing conference together,” said Moscat. “We look forward to planning SBP’s next cancer metabolism conference to continue sharing breakthrough research advances that will ultimately improve the lives of patients.”

Institute News

Research points to possible target to stop cancer stem cells

AuthorJessica Moore
Date

July 28, 2016

When you think of stem cells, you probably think of healing and regeneration—cells that can replace tissue lost to disease or injury. But tumors also arise from stem cells—a specific kind called cancer stem cells. Because these cells can divide indefinitely, while other cancer cells’ proliferation is more limited, therapies that get rid of them would eventually stop a tumor from growing, and from ever coming back.

Researchers in the laboratory of Dieter Wolf, MD, professor in the NCI-Designated Cancer Center, may have found a new way to do this, though in a roundabout way. While examining the function of two proteins found at high levels in tumors, they discovered that these factors are required for a type of metabolism that’s essential for cancer stem cells to survive.

“Our findings suggest that these components, eukaryotic initiation factors (eIFs) 3d and 3e, are novel targets for eliminating cancer stem cells,” said Wolf, senior author of the study, which was published in Cell Reports. “If we could find a way to turn these factors off, we could starve cancer stem cells.”

The details

eIF3d and eIF3e are part of the complex that initiates protein synthesis, also called translation. Specifically, they and other eIFs help bring the ribosome, which builds proteins by linking amino acids one by one, to messenger RNA, the molecules that carry the code the ribosome reads, specifying which amino acid should be added next.

Wolf’s team was interested in whether overproduction of eIF3d and eIF3e promotes cancer progression. To determine their function, they compared the amounts of all proteins made in cells lacking these factors to those in normal cells. A difference that stood out was in the levels of the protein complexes required to produce ATP, the cell’s energy currency, in mitochondria—eIF3d/e-deficient cells produced far lower amounts than normal.

“Cancer stem cells, unlike most tumor cells, rely on mitochondrial metabolism for energy,” Wolf explained. “Since tumor cells have much higher levels of eIF3d/e than normal cells, inhibiting those factors would preferentially block metabolism in cancer stem cells.

“Our results are somewhat surprising because eIF3 has long been thought to control the synthesis of all proteins. Instead, our data suggest that some parts of eIF3 selectively recruit certain mRNAs.”

Next steps

“We’re now examining how eIF3d/e affects cancer metabolism overall to see if these factors might be relevant to more than just cancer stem cells,” added Wolf. “Also, as a step towards advancing this research to the clinic, we’re designing screens to identify small molecule inhibitors of eIF3d/e.”

The paper is available online here.

Institute News

Cancer metabolism symposium highlights hot area in cancer research

AuthorJessica Moore
Date

June 27, 2016

The third Cancer Metabolism Symposium held at Sanford Burnham Prebys Medical Discovery Institute (SBP) June 22-23, 2016, attracted a full house of attendees from across San Diego. Its success likely results from the impressive roster of speakers invited by organizers Jorge Moscat, PhD, professor and director of the Cancer Metabolism and Signaling Networks Program, and Maria Diaz-Meco, PhD, also a professor in that program. The presenters included numerous thought leaders in the field from such prestigious institutions as the Koch Institute for Integrative Cancer Research at MIT, the Dana Farber Cancer Institute at Harvard Medical School, and Memorial Sloan Kettering Cancer Center.

The aim of research on cancer metabolism is simple—to find ways to starve tumors of the fuels and building blocks they need to grow. This strategy is gaining attention (see this recent New York Times feature) because of the increasing evidence that cancer cells obtain and use nutrients differently than normal cells. Plus, there appear to be a few common ways in which cancer cells’ metabolism becomes deranged, making it a much simpler target than oncogenic mutations, which tumor cells accumulate almost exponentially.

Several new drugs that interfere with metabolism have shown promise in clinical trials for numerous types of cancer. Nonetheless, there’s still a lot to learn. Since tumor cells rely on the same metabolic pathways as normal cells, researchers must pinpoint cancer’s weaknesses—the enzymes and nutrients on which cancer cells rely far more than normal cells. Many of these differences were discussed at the symposium, opening doors for new ways to stop cancer.

Institute News

High levels of protein p62 predict liver cancer recurrence

AuthorJessica Moore
Date

May 19, 2016

CANCER METABOLISM AND SIGNALING NETWORKS PROGRAM

New research from SBP and UC San Diego shows that high levels of the protein p62 in human liver samples are strongly associated with cancer recurrence and reduced patient survival. p62 was also found to be required for liver cancer to form in mice. Continue reading “High levels of protein p62 predict liver cancer recurrence”

Institute News

SBP presents at American Association for Cancer Research’s annual meeting

AuthorKristen Cusato
Date

May 10, 2016

Deputy Director of the NCI-designated Cancer Center, Jorge Moscat, PhD, and Cosimo Commisso, PhD, assistant professor in the Center, presented at the AACR conference in New Orleans.

Moscat presented at the session titled “Metabolic Interplay between Tumor and Microenvironment.”

“Cancer cells have to adapt their metabolism to survive nutrient deprivation and several stress conditions in their tumor microenvironment. For this they put in motion a process called autophagy whereby they get rid of toxic intracellular molecules and organelles and generate nutrients that allow them to survive,” said Moscat.

“Central to this process is a protein called p62 that was discovered in collaboration with my SBP colleague Maria Diaz-Meco. This protein is upregulated in, for example, liver cancer, whose mortality has increased dramatically over the last 10 years, in marked contrast to many other neoplasias that have shown a significant decrease in mortality.

“We presented new compelling data from human patients, mouse models and cell culture studies demonstrating that inactivation of p62 in cancer liver cells dramatically reduced the incidence and aggressiveness of hepatocellular carcinoma. Therefore, p62 is a novel and potentially actionable therapeutic target in liver cancer,” added Moscat.

Moscat said he was impressed at AACR by the number and quality of research studies linking the possibility of treating patients by a combined strategy of targeting cancer metabolism and the immunological tumor microenvironment.

He also spoke to ecancer.tv, an online provider of oncology news, about his research. Watch the video here.

Moscat is co-chair of a symposium on related research in cancer metabolism to that will be held June 22-23 at SBP’s La Jolla campus.

Commisso’s presentation was featured in a special session on pancreatic cancer that aimed to stimulate opportunities for collaboration between Pancreatic Cancer Action Network-AACR grantees and others in the field.

“The research that I presented was focused on a novel drug target in pancreatic cancer discovered recently by my lab,” said Commisso.

“We have found that an ion transporter that regulates pH homeostasis is critical to pancreatic cancer cell survival. This previously uncharacterized transporter plays a role in maintaining amino acid supply in tumor cells that harbor a mutation in the oncogene known as Ras, which is mutated in >90% of pancreatic tumors.

“Our future work is focused on exploring the role of this transporter in preclinical models and developing new approaches to inhibit this druggable target,” added Commisso.

He called the AACR meeting “a remarkable opportunity for cancer researchers to come together and share their exciting discoveries.”  Dr. Commisso also said it was a good opportunity to connect with colleagues and friends to develop and nurture scientific collaborations, to create, progress and build.

Commisso will also present at the 2016 PancWest Symposium in September at the Moores Cancer Center at UCSD.

Institute News

Cancer metabolism 101

Authorsgammon
Date

April 21, 2015

“Feed me!” Cancer is caused by the uncontrolled proliferation of cells. Their rapid growth comes with a voracious appetite to support their nutritional demands. To satisfy these demands, cancer cells rewire their metabolism. Increasingly, scientists are looking to exploit the metabolic differences between normal and cancer cells for the development of new anti-cancer therapies. Continue reading “Cancer metabolism 101”