Cold Spring Harbor Biological Laboratory

COLD SPRING HARBOR, N.Y., April 2, 2025 /PRNewswire/ -- Pancreatic cancer is projected to become the second-deadliest cancer by 2030. By the time it's diagnosed, it's often difficult to treat. So, for both individual patients and the general population, fighting pancreatic cancer can feel like a race against time. Cold Spring Harbor Laboratory (CSHL) Professor and Cancer Center Director David Tuveson offers a telling analogy: Continue Reading A new study from Cold Spring Harbor Laboratory, published in Cancer Research, shows that inhibiting the FGFR2 and EGFR proteins in pancreatic cells can delay or even prevent tumor formation. "We all have moles on our skin. Most of your moles are fine. But some of your moles you have a dermatologist looking at to make sure it's always fine. They may take it out and send it to the pathologist to ask, 'Is this an early melanoma, a melanoma in situ?' Now, that's just what you can see. Imagine that in your pancreas—because that's the reality. We all have early versions of cancer in many tissues at all times." Now imagine treating those "early versions" in the pancreas—before they become cancerous. A new discovery at the CSHL Cancer Center could help make this possible. Tuveson and Research Investigator Claudia Tonelli have found a way to effectively "intercept" pancreatic cancer. To understand how it works, we need to first understand a little bit about pancreatic cancer genetics. "Over 95% of pancreatic cancer patients have mutations in KRAS," Tonelli explains. "It's the driving oncogene in this disease. We discovered that another gene, FGFR2, plays a role in enhancing mutant KRAS signaling in pancreatic cancer. When that happens, those 'early versions' of pancreatic cancer become much more aggressive." Tonelli and Tuveson observed this outcome in mice and organoids—lab-grown versions of human pancreatic tissue. Of course, the researchers weren't just having a look. Their goal was to stop the pancreatic tissue from becoming cancerous. Because FGFR2 is a known oncogene in other cancers, several inhibitors are already used in the clinic today. When Tonelli and her colleagues inhibited FGFR2 at precisely the right moment, they got the results they wanted. Tumor formation slowed significantly. When they targeted FGFR2 along with EGFR—a protein known to be overactive in pancreatic cancer—they saw even better results. Fewer "early versions of cancer" formed in the first place. "With an increasing number of FGFR2 inhibitors entering the clinic, our study lays the foundation to explore their use in combination with EGFR inhibitors for pancreatic cancer interception," Tonelli says. Patients with a family history of pancreatic cancer would likely be among the first candidates to receive such treatments. For now, fighting pancreatic cancer remains a race against time. But with this discovery, the day may soon come when time is on our side. About Cold Spring Harbor Laboratory Founded in 1890, Cold Spring Harbor Laboratory has shaped contemporary biomedical research and education with programs in cancer, neuroscience, plant biology and quantitative biology. Home to eight Nobel Prize winners, the private, not-for-profit Laboratory employs 1,000 people including 600 scientists, students and technicians. For more information, visit . SOURCE Cold Spring Harbor Laboratory WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

COLD SPRING HARBOR, N.Y., Jan. 2, 2025 /PRNewswire/ -- Fighting cancer can seem like a deadly game of chance. While some patients may respond well to certain treatments, others might not be as fortunate. Doctors and scientists have long struggled to explain why. Now, Cold Spring Harbor Laboratory (CSHL) Assistant Professor Katherine Alexander and University of Pennsylvania Professor Shelley Berger have found a possible source of this variability in clear cell renal cell carcinoma (ccRCC)—the most common kidney cancer diagnosed in adults. Continue Reading CSHL Assistant Professor Katherine Alexander and colleagues at the University of Pennsylvania have identified two different patterns of cellular structures known as nuclear speckles (red) in the most common form of renal cancer. They’ve also spotted a possible connection between these patterns and patient survival rates. Their work is published in Nature Cell Biology. Alexander has identified two different patterns of cellular structures known as nuclear speckles in kidney tumors. Even more exciting, Alexander's research, conducted in Berger's lab at the University of Pennsylvania, shows a potential correlation between speckle patterns and patient outcomes. Alexander explains: "We found that different therapies are more or less effective depending on how the speckles look. This means potentially if a patient comes in with a normal or aberrant speckle state, they might be more responsive to one drug or another. Of course, more research needs to be done." Discovered over 100 years ago, nuclear speckles are tiny cellular structures that reside in the nucleus. Here, they're thought to intermingle with DNA and help regulate gene activity. Alexander's research reveals that nuclear speckles have two different signatures in ccRCC: normal-like and aberrant. It's a matter of positioning. Normal-like speckles tend to congregate toward the center of the nucleus. Aberrant speckles are more dispersed. "How these signatures affect patient outcomes remains a mystery for now," Berger says. "However, the search for answers may lead to more personalized treatments. This discovery offers a new starting point in ccRCC." Alexander adds: "It's the first suggestion that this would be potentially applicable to giving someone [diagnosed with ccRCC] one drug or another. That's huge because cancer therapy has a lot of horrible side effects. To be able to tell a patient, 'Your tumor looks like this, so we think this drug will work better than this drug,' is something we really need." The team didn't just look at kidney cancer. They analyzed speckles in over 20 different types of cancers, from melanomas to breast cancer. However, only ccRCC showed a correlation between speckle patterns and patient outcomes. What makes this cancer special? Alexander's findings point to HIF-2𝛼, a protein typically overactive in ccRCC. The Alexander lab aims to pursue this lead alongside other researchers at CSHL's Cancer Center. For now, Alexander continues to investigate the mystery of nuclear speckles' role in cancer. Though she's in uncharted territory, the object of her search is clear. Her work seeks to help stack the odds in cancer patients' favor. About Cold Spring Harbor Laboratory Founded in 1890, Cold Spring Harbor Laboratory has shaped contemporary biomedical research and education with programs in cancer, neuroscience, plant biology and quantitative biology. Home to eight Nobel Prize winners, the private, not-for-profit Laboratory employs 1,000 people including 600 scientists, students and technicians. For more information, visit SOURCE Cold Spring Harbor Laboratory WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

COLD SPRING HARBOR, N.Y., Oct. 24, 2024 /PRNewswire/ -- Prostate cancer is a quiet killer. In most men, it's treatable. However, in some cases, it resists all known therapies and turns extremely deadly. A new discovery at Cold Spring Harbor Laboratory (CSHL) points to a potentially groundbreaking solution. CSHL Professor Lloyd Trotman's lab has found that the pro-oxidant supplement menadione slows prostate cancer progression in mice. The supplement is a precursor to vitamin K, commonly found in leafy greens. The story begins more than two decades ago. Continue Reading A new study from Cold Spring Harbor Laboratory Professor Lloyd Trotman and colleagues, published in Science, shows that menadione significantly slows prostate cancer growth in mice and in human-derived cancer cells, as seen here. In 2001, the National Cancer Institute's SELECT trial sought to determine if an antioxidant vitamin E supplement could successfully treat or prevent prostate cancer. The trial involving 35,000 men was planned to last up to 12 years. However, after just three years, participants were told to stop taking their supplements. Not only had vitamin E failed to slow or prevent prostate cancer—more men taking the supplement started to get the disease. Seeing these results, Trotman thought, 'If an antioxidant failed, maybe a pro-oxidant would work.' His new findings in mice show just that. When mice with prostate cancer are given menadione, it messes with the cancer's survival processes. Trotman's team has discovered that menadione kills prostate cancer cells by depleting a lipid called PI(3)P, which works like an ID tag. Without it, the cells stop recycling incoming materials and eventually explode. Trotman explains: "It's like a transport hub, like JFK. If everything that goes in is immediately de-identified, nobody knows where the airplanes should go next. New stuff keeps coming in, and the hub starts to swell. This ultimately leads to the cell bursting." This causes the cancer's progression to slow significantly in mice. Trotman now hopes to see the experiment translated to pilot studies in human prostate cancer patients: "Our target group would be men who get biopsies and have an early form of the disease diagnosed. We wonder if they start to take the supplement, whether we would be able to slow that disease down." Amazingly, Trotman's research suggests menadione may also prove effective against myotubular myopathy, a rare condition that prevents muscle growth in infant boys. Those diagnosed rarely live beyond early childhood. Trotman's lab has found that depleting PI(3)P with menadione can double the lifespan of mice with this condition. If the results hold up in humans, it would mean that men with prostate cancer can enjoy a better quality of life and more time with their families. It could also mean more precious time for children born with an incurable disease. About Cold Spring Harbor Laboratory Founded in 1890, Cold Spring Harbor Laboratory has shaped contemporary biomedical research and education with programs in cancer, neuroscience, plant biology and quantitative biology. Home to eight Nobel Prize winners, the private, not-for-profit Laboratory employs 1,000 people including 600 scientists, students and technicians. For more information, visit SOURCE Cold Spring Harbor Laboratory WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED