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.