The Mark Foundation Awards $12 Million to Cross-Disciplinary Cancer Research Teams

Four New Endeavor Awards Unite Global Experts to Fight Cancer

Key Takeaways

• Enabling International Collaboration: As funding uncertainties persist for multidisciplinary and international scientific partnerships, The Mark Foundation is purposefully connecting global teams to take on big research challenges. 
• A $50+ Million Commitment to Team Science: This $12 million investment brings the Endeavor Awards portfolio to 15 grants totaling over $50 million since 2021, a commitment that has fast-tracked dozens of breakthrough publications, patents, and clinical trials.
• Science at the Frontiers: Moving beyond traditional research boundaries, this cohort of new grants bridges diverse fields—including structural biophysics, spatial transcriptomics, and generative AI—to dismantle the mechanisms of invasive and treatment-resistant cancers.

NEW YORK, Oct. 7, 2026 /PRNewswire/ -- The Mark Foundation for Cancer Research today announced its latest Endeavor Award recipients, providing a total of $12 million in funding to four multi-institutional teams. Selected from a highly competitive pool of hundreds of applicant teams, the 2026 awardees represent 11 premier academic research institutions across five countries.

This funding arrives at a critical juncture for the international scientific community. At a time when collaboration across disciplines, institutions, and borders is becoming ever more challenging, The Mark Foundation is purposefully bridging those gaps to bring together scientists with the best ideas from around the world to work boldly together in taking on the most urgent and difficult problems in cancer research today.

By giving these collaborative teams the financial freedom and operational flexibility to explore complex challenges through diverse lenses, these three-year, $3 million grants enable global experts to integrate distinct technologies and significantly accelerate the path from laboratory discovery to active clinical treatment.

Hacking Liver Metastases
Sarah-Maria Fendt, PhD, and Colinda Scheele, PhD, VIB, Belgium
Peter Siegel, PhD, McGill University, Canada

Of the 10 million people who die each year from cancer, roughly a quarter suffer from cancer that has spread to the liver. Once tumors take root in this organ, standard treatments often stop working because the new tumors grow in completely different ways. The deadliest of these growth patterns, called "replacement-type" tumors, physically weaves into existing liver tissue. Colorectal cancer patients, for example, who show this pattern face a 5-year overall survival rate of less than 38%, compared to 77% for patients whose metastases grow as encapsulated tumors, which are distinct, isolated clusters in the liver.

The Strategy and Patient Implications

To find out why some tumors become so aggressive, this Endeavor team is utilizing specialized mouse models that mirror the types of metastatic liver tumors that develop in colorectal cancer patients. They are also building on their previous discovery that if a cancer cell primarily interacts with healthy liver cells, it tends to stay in the less aggressive encapsulated form. However, if a patient has a fatty liver (steatosis), that specific environment can encourage the cancer to switch into the deadlier replacement form.

Using advanced cellular tracking and high-resolution imaging, the team is mapping out and defining these cellular conversations. Their goal is to identify unique blind spots arising from the liver's physical condition, enabling them to design personalized therapies tailored to a patient's specific liver health. Learn more about this project.

Overcoming Immunotherapy Resistance in Stomach Cancer

Brent Hanks, MD, PhD, Jenny Ting, PhD, and Elizabeth Brunk, PhD, University of North Carolina at Chapel Hill
John Strickler, MD, Duke University

Co-funded by the Torrey Coast Foundation

While modern immunotherapies have revolutionized care for many, they still fail most patients with advanced gastric and esophageal cancers. Doctors routinely combine these cutting-edge therapies with standard chemotherapy, but the long-term outcomes remain poor. Unlocking the secret to why these tumors resist treatment is a critical question in oncology.

The Strategy and Patient Implications

This North Carolina-based team recently discovered that high activity within a specific early-warning system inside tumor cells, called the NLRP3 pathway, strongly predicts that immunotherapy will fail. The reason? The team found that when this system fires up, it prevents the tumor from displaying the "flags" that immune cells look for to identify danger and recruits immunosuppressive cells to prevent the immune system from clearing the tumor.

Crucially, this genetic alteration isn't unique to stomach cancer; it is common across various aggressive solid tumors. By using advanced 3D models grown from patient cells (organoids), this team will test a new drug designed to block this cellular invisibility cloak. Preliminary results indicate that shutting down this pathway forces the tumor to reveal itself, allowing immune cells to rush in and destroy it—work that is paving the way for future human clinical trials. Learn more about this project.

Rewiring Cancer's Protectors into Active Tumor-Killers
Miriam Merad, MD, PhD, and Brian Brown, PhD, Icahn School of Medicine at Mount Sinai
Leonard Zon, MD, Harvard University
Brent Stockwell, PhD, Columbia University
Martin Guilliams, PhD, Ghent University, Belgium

In many cancers, the tumor microenvironment—the immediate neighborhood surrounding a tumor—is manipulated by cancer cells to overcome the body's natural defenses. A primary culprit is the corruption of macrophages, specialized white blood cells which are normally the body's frontline immune defenders. Instead of attacking cancer cells and alerting the immune system, these corrupted cells protect the tumor and shield it from treatment.

The Strategy and Patient Implications

This transatlantic team recently overturned old assumptions through its discovery that this corruption is actually a two-part process. First, the tumor sends signals through the bloodstream to alter how these immune cells are born inside the bone marrow, making them highly resistant to stress. Second, once those cells travel to the tumor, direct physical contact completes their transformation into deceptive tumor allies.

Using genetic tools and specialized antibodies to intercept this assembly line, the team has already achieved remarkable tumor clearing in early lab models. By combining human tumor profiling with functional genomics in mouse and zebrafish models, they aim to disrupt these systemic cues. Their ultimate goal is to permanently rewrite the programming of these corrupted defenders, transforming them back into potent, anti-cancer effectors that can destroy malignant cells entirely on their own. Learn more about this project.

BOLTS: Locking Down "Undruggable" Cancer Drivers

Georg Winter, PhD, AITHYRA Institute, Austria
Nicolas Thomä, PhD, and Bruno Correia, PhD, EPFL, Switzerland Nathanael Gray, PhD, Stanford University

Many of the most aggressive cancers are driven by overactivated transcription factors— master control switches that cause tumor cells to divide uncontrollably. Historically, directly targeting these switches with therapeutic agents has been deemed impossible because they constantly change their shape and lack the deep structural pockets to which traditional drugs bind.

The Strategy and Patient Implications

This project (named BOLTS for Blocking Oncogenic transcription via Ligand-Triggered SUMOylation), was born from an accidental discovery. While studying an existing class of breast cancer therapeutics called SERDs (Selective Estrogen Receptor Degraders), the team realized that those drugs weren't directly destroying their targets as previously thought. Instead, they were triggering a natural cellular process called SUMOylation. This process acts like a biochemical padlock, physically freezing the shape-shifting cancer switch onto the cell's DNA and rendering it completely silent.

Uniting the disciplines of chemical biology, biophysics, and AI-enabled structural biology across research labs in Austria, Switzerland, and the United States, the team is building a pipeline to intentionally design new, drug-like padlocks. Rather than destroying these elusive transcription factor targets, these new drugs will freeze them in an "off" state—silencing notorious cancer drivers in treatment-resistant prostate, pancreatic, gastric, and brain cancers. Learn more about this project.

Building Momentum Across a Legacy of Scientific Agility

The initiation of these four new projects builds directly upon the foundational success of the Endeavor Award program. Since its launch in 2021, the program has consistently prioritized high-risk, collaborative synergy to solve problems that a single lab cannot tackle alone.

By bypassing rigid, localized frameworks in favor of an agile, international funding network, The Mark Foundation ensures that the world's best minds remain unified in the accelerating fight to eradicate cancer.

About the Mark Foundation for Cancer Research

The Mark Foundation for Cancer Research, a charitable organization based in New York City, actively partners with scientists worldwide to accelerate research that will transform cancer prevention, diagnosis, and treatment. Since 2017, The Mark Foundation has awarded over $300 million in grants to investigators at more than 120 academic institutions across 18 countries, with research programs focusing on early career support, team science collaboration, new technology innovation, and therapeutics discovery. Additionally, The Mark Foundation maintains a growing portfolio of investments in early-stage cancer diagnostics and therapeutics companies, including several that have transitioned from grantee projects into commercial development. To learn more, please visit www.themarkfoundation.org.

Contact: Rachel Hastings, [email protected] 

SOURCE The Mark Foundation for Cancer Research