This week, our guests are Bryan McClellan, who conducted research on pancreatic cancer as a postdoctoral fellow at Dell Medical School, and William Matsui, the study’s senior author and former executive vice dean for research at Dell Medical School; and Theialife president and CEO, Thomas Ruggia, about myopia.
02:26 Theialife
27:38 University of Texas
Theialife
Theialife is a global ophthalmology drug development company focused on advancing first-in-class therapies that aim to address major unmet needs in eye diseases.
The company’s lead asset, ND10 (7-Methylxanthine), is an oral therapy designed to slow paediatric myopia progression, for which phase 3 clinical trial planning is currently under way.
Theialife is building a pipeline of differentiated ophthalmic programmes targeting indications that include dry eye disease, wet age-related macular degeneration, and corneal blindness.
Thealife’s mission is to develop transformative therapies to address significant unmet needs of vision care worldwide.
Research uncovers new driver of immunotherapy resistance in pancreatic cancer
Pancreatic tumours can resist immunotherapy by recruiting nearby immune cells to help protect them, according to researchers at The University of Texas at Austin. The findings, published in Nature Communications, point to a potential new strategy for overcoming resistance and improving cellular therapies.
Pancreatic ductal adenocarcinoma, the most common type of pancreatic cancer, is projected to become the second leading cause of cancer death in the US by 2030. CAR T-cell therapy, which re-engineers a patient’s own T cells to hunt tumours, has transformed treatment for several blood cancers but has repeatedly stalled against solid tumours such as pancreatic cancer, where early responses fade and tumours return.
Researchers found dormant tumour cells protected themselves by recruiting other immune cells. The cells released a protein called EREG that activated nearby macrophages, immune cells that help coordinate the body’s immune response. Those macrophages then suppressed CAR T cells, reducing the therapy’s effectiveness. When macrophages were removed, the protective effect disappeared.
Blocking EREG changed outcomes in mice. Median survival increased from about five weeks to more than four months, and tumours were eradicated in half of the treated animals. The approach prevented relapses.
Researchers also saw similar results when they used an antibody to block EREG instead of preventing tumour cells from producing it. Because antibodies can be developed as medicines, the findings suggest the approach could have potential for patients.
The researchers found the same pattern in human tissue. Across 23 patient tumour samples, EREG was concentrated in dormant cancer cells, and tumours rich in those cells contained fewer cancer-killing T cells. In a separate national tumour database, patients with high EREG expression had a five-year survival rate of zero, compared with 33% among patients with low expression.
Because EREG appears to shield tumours from immune attack rather than drive their growth, they suggest it could serve two roles: as a target to improve cellular therapies already in clinical testing for pancreatic cancer, and as a biomarker to identify tumours that are keeping immune cells out.
McClellan and Matsui are now in the Department of Stem Cell Transplantation and Cellular Therapy at UT MD.
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