The Albany Prize has been awarded annually since 2001 and was established by the late Morris “Marty” Silverman, whose vision was to celebrate scientists whose work exemplifies the “bench to bedside” arc of modern biomedical research: fundamental discoveries made at the laboratory bench that ultimately translate into treatments that measurably improve the lives of patients across the country and around the globe. That mission is underwritten by a $50 million gift commitment from the Marty and Dorothy Silverman Foundation to Albany Medical Center, a commitment that guarantees the prize can be conferred for 100 years and has helped build its reputation to a level often described as approaching that of the Nobel Prize. Past recipients read like a roster of modern biomedical history, including former National Institute of Allergy and Infectious Disease director Anthony Fauci, CRISPR pioneers and Nobel Laureates Emmanuelle Charpentier and Jennifer Doudna, and mRNA vaccine pioneers and Nobel Laureates Katalin Karikó and Drew Weissman, among many others. Hunter’s inclusion in that company reflects the sheer reach of a single biochemical insight made more than four decades ago.

That insight concerns a molecular switch known as tyrosine phosphorylation. Phosphorylation, the process by which enzymes attach phosphate groups to amino acids within proteins, is one of the cell’s most fundamental control mechanisms, a way of flipping proteins between functional states in response to signals. For years, scientists knew that phosphate groups could be attached to the amino acids serine and threonine. What Hunter discovered in 1979, quite by accident, was that phosphate could also be linked to a third amino acid: tyrosine. The finding revealed an entirely new class of regulatory enzymes, the tyrosine kinases, which add phosphate groups to tyrosine residues and in doing so help govern how cells grow, divide, and communicate with their surroundings.

The discovery itself is a textbook example of serendipity rewarding careful observation. Hunter was conducting an experiment to separate the amino acids in a viral protein, a routine analytical procedure that depended on a buffer, a solution used to control acidity. Unknowingly, he used a buffer with a pH of 1.7 instead of the intended 1.9. That tiny difference in acidity, a shift of just two-tenths of a pH unit, altered the chemical behavior of the phosphorylated amino acid in his sample just enough to expose what had previously been hidden: a phosphate group sitting on a tyrosine residue. Had the pH been exactly as planned, the modification might have gone undetected. “A gratifying outcome of this set of experiments on a simple chicken tumor virus,” Hunter later wrote of the episode in a 2015 perspective published in the Proceedings of the National Academy of Sciences, a wry acknowledgment that a humble reagent error had opened a vast new field of cancer biology.

What followed the 1979 landmark study was a career of persistent, systematic elaboration. Hunter went on to write and publish many additional papers on this new protein kinase family, methodically characterizing how tyrosine kinases work and how they are controlled. Through that sustained curiosity, he came to a realization that would transform medicine: tyrosine kinases become overactive in many human cancers. When the molecular switches that regulate cell growth become stuck in the on position, cells proliferate uncontrollably. Identifying tyrosine phosphorylation therefore did more than add a line to biochemistry textbooks; it handed cancer researchers a specific, druggable target. If overactive tyrosine kinases drive malignancy, then molecules designed to block those enzymes might stop tumors in their tracks.

That logic produced one of the great success stories of modern oncology. In 2001, the U.S. Food and Drug Administration approved imatinib, known commercially as Gleevec, the first in a revolutionary class of drugs called tyrosine kinase inhibitors. Imatinib transformed the treatment of chronic myelogenous leukemia, converting what had been a terminal disease into a highly manageable condition for many patients. It was the proof of principle that Hunter’s foundational discovery could be turned directly into lifesaving therapy. Today, more than 100 cancer drugs that block overactive tyrosine kinases exist, all of them tracing their conceptual origin to Hunter’s identification and characterization of the tyrosine kinase family. Few basic science discoveries can claim a pharmacological legacy of that scale, and it is precisely this bench-to-bedside trajectory that the Albany Prize was created to honor.

Hunter shares the 2026 prize with Dennis Slamon of UC Los Angeles, whose own cancer biology discoveries have likewise translated into therapies with global impact. The pairing of the two laureates underscores a theme that runs through the Albany Prize’s history: the award seeks scientists whose laboratory insights have demonstrably reached patients. In Hunter’s case, the chain of translation runs from a chicken tumor virus experiment in 1979, through decades of enzymology and signal transduction research, to a pharmacopoeia of kinase inhibitors now deployed in clinics worldwide. Gerald Joyce, MD, PhD, president of the Salk Institute, praised Hunter’s approach to science in announcing the honor. “Tony’s dedication to curiosity-driven research has made him an irreplaceable asset at Salk and in science at large,” Joyce said. “His commitment to foundational discovery has transformed cancer biology and treatment, and we look forward to celebrating this honor with him.”

Remarkably, the discovery that anchors this award is not the endpoint of Hunter’s career but a chapter in its middle. The year 2025 marked his 50th at the Salk Institute, where he remains an active researcher, pursuing his own collaborations and projects while taking evident pride in training the next generation of cancer biologists and life sciences researchers. His perspective on the unfinished nature of biology is one he shares directly with his students. “When I’m teaching students, I say an awful lot has already been discovered, but an awful lot remains unknown. I’m sure that new biological principles will emerge that we can’t even imagine right now,” Hunter said in a 2023 feature in Inside Salk magazine. “I’m excited because there will always be new things to be discovered for as long as I’m alive.” It is a sentiment that captures the ethos of curiosity-driven research that colleagues credit for his longevity and productivity at the bench.

The Albany Prize adds a distinguished new item to an already crowded shelf of accolades. Hunter’s earlier honors include the Wolf Prize in Medicine, the Gairdner Foundation International Award, the Louisa Gross Horwitz Prize, the National Cancer Institute Outstanding Investigator Award, the American Association for Cancer Research Lifetime Achievement Award in Cancer Research, the Sjöberg Prize for Cancer Research, the Prince Mahidol Award, and the Dr. Paul Janssen Award for Biomedical Research. He has also been elected a fellow of the American Association for Cancer Research, a Member of the American Philosophical Society, a fellow of the Royal Society of London, a Member of the National Academy of Sciences, a fellow of the American Academy of Arts and Sciences, and a Member of the National Academy of Medicine. Each of these recognitions, like the Albany Prize itself, circles back to the same origin: a two-tenths-of-a-pH-unit error in 1979 that revealed how a phosphate group on a single amino acid could unlock the molecular logic of cancer, and ultimately the drugs that hold it in check for millions of patients.

Subject of Research: Recognition of Tony Hunter's discovery of tyrosine phosphorylation and its role in targeted cancer drug development

Article Title: Salk scientist Tony Hunter receives 2026 Albany Prize

Article References: Salk scientist Tony Hunter receives 2026 Albany Prize. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: Tony Hunter, Albany Prize, tyrosine phosphorylation, tyrosine kinases, cancer drugs, imatinib, Gleevec, Salk Institute, chronic myelogenous leukemia, signal transduction, biomedical research award, Dennis Slamon

The prize itself carries a layered history. Known previously as the Yergin-New International Prize for Biomedical Research, it was renamed this year in recognition of the Yergin family’s longstanding support of the program. It commemorates Maria I. New, MD, the groundbreaking Mount Sinai pediatric endocrinologist who passed away in 2024 and whose six-decade career transformed the understanding and treatment of adrenal steroid disorders. The prize, now in its fifth year, is awarded annually to a distinguished physician-scientist whose lifetime achievements have led, or may lead, to new ways to prevent and treat human disease, and it has quickly become regarded as one of the foremost international honors in medical research.

Ferrara will receive a $50,000 award and deliver the Yergin Family Distinguished Lecture during a ceremony at Mount Sinai in New York City on Wednesday, November 18. The recognition caps a career that has already earned election to both the National Academy of Sciences and the National Academy of Medicine, along with the 2010 Lasker-DeBakey Clinical Medical Research Award, the 2013 Breakthrough Prize in Life Sciences, and the 2014 Canada Gairdner International Award. Together, these honors trace an unusually complete arc from basic discovery to clinical revolution.

The scientific story began in earnest in 1989, when Ferrara and his colleagues isolated and cloned VEGF, finally pinning down the biological signal responsible for angiogenesis, the formation of new blood vessels. The problem they tackled had puzzled vascular biologists for decades. Tumors, embryonic tissues, and healing wounds all emit some diffusible factor that coaxes nearby capillaries to extend toward them, but the identity of that factor remained elusive. By purifying and cloning the molecule, Ferrara’s team gave the field both a concrete target and a powerful set of experimental tools, including antibodies and genetic models that could test what VEGF actually does in living organisms.

Subsequent work revealed a biology of elegant duality. VEGF is indispensable for normal blood-vessel development, guiding the vascular system as it wires the embryo and maintains tissue health in adulthood. Yet the same signaling pathway, when overactive, becomes an engine of disease. Ferrara’s laboratory demonstrated that tumors exploit VEGF to sustain angiogenesis, supplying themselves with the oxygen and nutrients needed to grow beyond a few millimeters. In the eye, excessive VEGF drives the abnormal, leaky vessel growth that destroys vision in neovascular age-related macular degeneration, diabetic retinopathy, and other retinal diseases. The insight that a single pathway could be both essential and pathological set the stage for a new therapeutic strategy: block the signal, and starve the disease.

That strategy bore fruit in oncology first. Ferrara’s group showed that neutralizing VEGF could slow tumor growth in preclinical models, an achievement that led directly to bevacizumab, a monoclonal antibody designed to bind VEGF and prevent it from activating its receptors on blood-vessel cells. In 2004, the U.S. Food and Drug Administration approved bevacizumab for metastatic colorectal cancer, making it the first anti-angiogenic cancer therapy ever approved. Anti-VEGF approaches have since become part of standard treatment for several malignancies, including colorectal, kidney, lung, cervical, and ovarian cancers. In hepatocellular carcinoma, combinations of anti-VEGF drugs with immunotherapy are now standard of care, reflecting a growing understanding that pruning a tumor’s vasculature can also reshape the immune environment around it.

The ophthalmic branch of the story proved equally transformative. Ferrara and his collaborators established that VEGF is a key driver of neovascular age-related macular degeneration, in which rogue vessels invade the retina and leak fluid into tissue that must remain dry and precisely layered to support sight. Their work led to ranibizumab, an antibody fragment engineered for intraocular use, and helped establish anti-VEGF injection therapy as the standard of care for several serious eye disorders. For patients who once faced inevitable central vision loss, the ability to preserve or even improve sight through regular treatment has been one of the most consequential clinical advances of the past two decades.

Leaders at Mount Sinai framed the award as a case study in the value of fundamental research. “Dr. Ferrara’s work is a remarkable example of how a fundamental discovery in biology can change the course of medicine,” said Mone Zaidi, MD, PhD, MACP, Director of Mount Sinai’s Institute for Translational Medicine and Pharmacology and Mount Sinai Professor of Clinical Medicine. “By identifying VEGF and demonstrating its role in blood-vessel growth, he opened the door to treatments that have changed outcomes for patients with cancer and serious eye diseases around the world.” Daniel Yergin, PhD, the Pulitzer Prize-winning author and economic historian who endowed the prize along with his wife, foreign policy expert Angela Stent, PhD, echoed that theme: “Napoleone Ferrara’s discovery demonstrates the extraordinary impact that fundamental biomedical research can have on human health. His work has transformed the treatment of cancer and blinding eye diseases and continues to influence the development of new therapies.”

Ferrara’s laboratory has not rested on its accomplishments. His current research continues to probe VEGF and other pathways governing blood-vessel growth, with two clinical problems in sharp focus. The first is treatment burden: patients with retinal disease typically require frequent intraocular injections, and his team is developing longer-acting therapies that could extend the interval between treatments. The second is geographic atrophy, the advanced, dry form of age-related macular degeneration, for which treatment options remain limited and which represents one of the largest unmet needs in ophthalmology. Both efforts extend the same logic that produced the original breakthrough, namely that understanding the molecular machinery of the vasculature reveals new points of therapeutic intervention.

The selection process behind the award reflects its international ambitions. Winners are chosen by a jury of distinguished physician-scientists chaired by Dr. Zaidi. The 2026 jury included Nobel laureate Aaron Ciechanover of the Technion in Haifa; Nancy Andrews of Boston Children’s Hospital; Michael J. Welsh of the University of Iowa; Jeffrey Friedman of The Rockefeller University and the Howard Hughes Medical Institute; and Anna Wedell of the Karolinska Institutet in Stockholm. “We are grateful to the distinguished members of the international jury for dedicating their time and expertise to reviewing this year’s exceptional group of nominees and selecting Dr. Ferrara as the recipient,” Dr. Zaidi said. Eric J. Nestler, MD, PhD, Dean of the Icahn School of Medicine at Mount Sinai and Chief Scientific Officer of the Mount Sinai Health System, noted that the award was first established in honor of Dr. New and her extraordinary legacy, and expressed gratitude for the vision of Daniel Yergin and Angela Stent in endowing the program to live in perpetuity. “Dr. Ferrara’s achievements reflect the lasting impact of research that begins with fundamental questions and ultimately changes the way diseases are treated,” Nestler said. Administered by Mount Sinai’s Institute for Translational Medicine and Pharmacology, the prize stands as both a tribute to Maria New’s legacy and a reminder that the path from a cloned molecule to medicines used around the world often begins with a single, persistent question about how life works.

Subject of Research: Award of the 2026 Yergin Family International Prize for Biomedical Research to VEGF discoverer Napoleone Ferrara

Article Title: Napoleone Ferrara, MD, receives 2026 Yergin Family International Prize for Biomedical Research

Article References: Napoleone Ferrara, MD, receives 2026 Yergin Family International Prize for Biomedical Research. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: Napoleone Ferrara, VEGF, angiogenesis, Yergin Family Prize, Mount Sinai, bevacizumab, ranibizumab, age-related macular degeneration, cancer therapy, anti-angiogenic treatment, retinal disease, biomedical research award