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A new study led by UCLA investigators may help explain why certain liver tumors return quickly after thermal ablation, a widely used minimally-invasive, image-guided technique that kills cancer cells by applying intense heat through a needle-like probe. The team found that the sugar-binding protein Galectin-1 (Gal-1) plays a critical role in helping hepatocellular carcinoma, the most common form of primary liver cancer, resist thermal ablation and even thrive after being treated with high heat. “We found that Gal-1 fuels cancer cells by boosting their ability to produce energy through sugar metabolism, allowing them to resist the effects of thermal stress,” said Dr. Jason Chiang, assistant professor of Radiological Sciences at the David Geffen School of Medicine at UCLA and senior author of the study. “It facilitates production of the additional energy required for liver cancer cells to continue growing, even after being exposed to thermal ablation. This helps the cells not only bounce back quickly after ablation but progress even faster on follow up imaging.”

The Alfred P. Sloan Foundation has named Dr. Albrecht a Sloan Research Fellow for her innovative work in cell and chemical biology. She is one of 126 early-career scientists to be recognized this year by the foundation as next-generation leaders. Dr. Albrecht’s research explores how cells regulate protein function and degradation through methylation – a process previously overlooked in lysosomal proteolysis. This discovery has the potential to reshape our understanding of cell signaling and protein homeostasis, with implications from genetic heart disease to new therapeutic strategies.

The annual Highly Cited Researchers list, compiled by the international data and analytics firm Clarivate, identifies scholars whose work has been cited most often in papers published by other researchers in their fields over the past decade. Those chosen for the 2024 list have authored multiple studies that rank in the top 1% in the number of scholarly citations worldwide. Congratulations to Drs. Aldons J. "Jake" Lusis and Richard S. Finn. Read more in UCLA Newsroom and see full list of UCLA faculty members and researchers who were recognized

People with chronic liver disease can be categorized into four distinct risk groups based on the different barriers they face in obtaining outpatient care, barriers that increase their odds of requiring hospitalization, a new UCLA study finds. The findings, published November 20 in the peer-reviewed PLOS ONE, point to the need for interventions aimed at reducing possibly avoidable hospitalizations among the highest-risk people with chronic liver disease (CLD). Previous research has found that people with CLD on average need more hospital-based care than those with other chronic diseases. About 4 million adults in the US have CLD, said Carrie R. Wong, MD, PhD, assistant professor of medicine in the division of digestive diseases at the David Geffen School of Medicine at UCLA) and the study’s lead author.

The Liver Meeting is a global conference organized by the American Association for the Study of Liver Diseases (AASLD) that brings together clinicians, scientists, and associates to exchange information on the latest research in the field of hepatology. Members of the Comprehensive Liver Research Center and David Geffen School of Medicine will present abstracts on the latest research taking place at UCLA.

Researchers at UCLA Health uncovered new information about the role inflammation plays in mitigating liver fibrosis, which is associated with metabolic-associated fatty liver disease (MAFLD), one of the most common diseases in the world affecting up to 40 percent of U.S. adults. While inflammation in the liver has long been considered a prerequisite to developing liver fibrosis, the scarring and thickening of tissue that can impair the liver’s ability to function, this new research suggests that reducing inflammation may not influence the extent of fibrosis. “Liver fibrosis is the critical feature that creates chronic liver disease and liver cancer. If we can keep fibrosis in check then we can meaningfully impact liver disease,” said Tamer Sallam, MD, PhD, corresponding author of the study and vice chair and associate professor in the Division of Cardiology, David Geffen School of Medicine at UCLA.

Dr. Nguyen, assistant clinical professor of medicine, was awarded a K08 Clinical Investigator Award from the National Institute of Diabetes and Digestive and Kidney Diseases. This five-year award of $853,000 supports Dr. Nguyen’s research on the “Role of a Novel Methyltransferase in Liver Lipid Metabolism.” His work aims to characterize how a methyltransferase regulates cellular cholesterol metabolism and contributes to the development of steatotic liver disease.

Researchers from the UCLA Health Jonsson Comprehensive Cancer Center and UCLA Liver Basic Research Center have received two grants totaling $9.1 million from the National Cancer Institute to advance liquid biopsy technologies for the early detection of cancer, which can significantly improve treatment outcomes and reduce the number of deaths caused by the disease. A liquid biopsy is a promising non-invasive medical test using a small volume of blood that gives scientists insight into the genetic makeup of tumors. By analyzing these components, researchers can gain valuable information about the genetic mutations, alterations and other molecular changes associated with the presence of cancer.

Dr. Benhammou, assistant clinical professor of medicine, was awarded a seed grant from the UCLA Health Jonsson Comprehensive Cancer Center and UCLA Jonsson Cancer Center Foundation for her project, The Impact of Statins on Immune Checkpoint Inhibitors for the Treatment of Hepatocellular Carcinoma. The cancer research project was funded in the amount of $49,562 and the award period is February 1, 2024 - January 31, 2025.

UCLA researchers found that fasting increases the splitting of mitochondria, which may have implications for metabolic and aging-related diseases. In the study published in June, scientists examined the livers of mice that had been starved and identified the activated proteins, said Nuria Martinez-Lopez, PhD, adjunct assistant professor, the paper’s first author. They found that proteins in the mTORC2 cellular signaling pathway – known to be related to cell growth and metabolism – were activated by fasting, she added. These proteins increased the splitting of the mitochondria during fasting, which might allow cells to more efficiently burn fatty acids to cope with starvation, said Rajat Singh, MD, MBBS, professor of medicine, the paper’s corresponding author. 

Dr. Sammy Saab, medical director of the Pfleger Liver Institute and medical director of the Adult Liver Transplant Program, commented in a NBC News story on a recently published analysis of data on 32,726 adults who participated in the National Health and Nutrition Examination Survey. The analysis showed that overall, NAFLD rose from 16% in 1988 to 37% in 2018. Among Mexican Americans, the rate of NAFLD rose from 36% in 1988 to 58% in 2018, an increase of 61%. Among African Americans, it rose from 11% in 1988 to 25% in 2018, a 127% increase. Among white Americans, the rate rose from 15% in 1988 to 35% in 2018, for a 133% increase. The new study was co-authored by Dr. Theodore Friedman, an endocrinologist and professor of medicine at both the Charles R. Drew University of Medicine and Science and the UCLA David Geffen School of Medicine.

A new study sheds light on how autophagy, the body’s process for removing damaged cell parts, when impaired, can play a role in causing heart failure. The research team led by Dr. E. Dale Abel, chair of the Department of Medicine at UCLA, and Dr. Quanjiang Zhang, adjunct assistant professor of medicine at UCLA, identified a signaling pathway that links autophagy to the control of cellular levels of a key coenzyme known as NAD+, which is found in all living cells and is central to how our metabolism works. Researchers say these findings may have implications for heart failure treatment.