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Business Wire
a day ago
- Business
- Business Wire
Verastem Oncology to Report Second Quarter 2025 Financial Results on August 7, 2025
BOSTON--(BUSINESS WIRE)--Verastem Oncology (Nasdaq: VSTM), a biopharmaceutical company committed to advancing new medicines for patients with RAS/MAPK pathway-driven cancers, today announced that the Company will host a conference call and webcast to discuss its second quarter 2025 financial results and business updates on Thursday, August 7, 2025, at 4:30 pm ET. To access the conference call, please dial (800) 715-9871 (U.S.) or (646) 307-1963 (international) and enter the passcode 1210516 at least 10 minutes prior to the event start time. A live audio webcast of the call, along with accompanying slides, will be available under "Events & Presentations" in the Investor section of the Company's website, A replay of the webcast will be archived and available following the event. About Verastem Oncology Verastem Oncology (Nasdaq: VSTM) is a biopharmaceutical company committed to developing and commercializing new medicines to improve the lives of patients diagnosed with RAS/MAPK pathway-driven cancers. Verastem markets AVMAPKI™ FAKZYNJA™ CO-PACK in the U.S. Our pipeline is focused on novel small molecule drugs that inhibit critical signaling pathways in cancer that promote cancer cell survival and tumor growth, including RAF/MEK inhibition, FAK inhibition, and KRAS G12D inhibition. For more information, please visit and follow us on LinkedIn.
Miami Herald
03-07-2025
- Health
- Miami Herald
Science seek to tap amazing healing powers of the mouth's interior
ST. PAUL, Minn., July 2 (UPI) -- The cellular action that enables the mouth's interior lining to heal quicky and without scarring has always been a mystery but a new study suggests it may be linked to a specific "signaling pathway." That new knowledge is raising hopes the mouth lining's healing powers could be applied to other skin wounds, which take far longer to heal and often leave permanent, unsightly scars, according to a preclinical study published Wednesday by Cedars-Sinai Medical Center and University of California-San Francisco researchers. The study on mice provides evidence that the "Gas6/AXL" protein/enzyme signaling pathway is likely responsible for the mouth's amazing ability to heal itself completely from even deep bite wounds within a matter of days with no leftover scarring, the authors wrote in the journal Science Translational Medicine. Known as the oral mucosa, the mouth's interior lining heals fast and cleanly, even though it is continuously exposed to different types of microbes, abrasion from foods, motion and tension. This unique regenerative capacity is made possible by specialized gene programs activated during injury, but just how those mechanisms work has been unknown. In the study reported Wednesday, a research team led by Dr. Ophir Klein, executive vice dean of Children's Health at Cedars-Sinai and executive director of Cedars-Sinai Guerin Children's in Los Angeles, found that by manipulating levels of the AXL enzyme they could affect how wounds healed. For instance, if they inhibited AXL in mice, the healing of oral mucosa wounds worsened, making them more like skin wounds. Conversely, when they stimulated AXL in facial skin wounds, they healed more efficiently and with reduced scarring, much like the oral mucosa. Boosting the levels of AXL suppresses the expression of another protein called Focal Adhesion Kinase, or FAK, which plays a significant role in scar formation during wound healing. Should future research validate the benefits for humans, the new knowledge could aid in developing new therapies to heal skin wounds with reduced scarring, Klein said. "We are actively thinking about harnessing AXL-driven repair in both the mouth and the skin, and perhaps in other tissues as well," he told UPI in emailed comments. "One application that comes to mind is to improve healing and reduce scarring in the skin for burn victims or those with other cutaneous disorders. "Another is that there are a number of diseases of the mouth, many of them autoimmune, in which severe oral ulcers form and heal poorly or not at all. These are different from canker sores, also known as aphthous ulcers, which many people get and which typically heal on their own; the more severe ulcers are difficult to treat and cause very significant illnesses, and we currently do not have good therapies for them." A related direction for research could focus on "obtaining a deeper understanding of the effects of AXL signaling on scarring and regeneration at a molecular level, in terms of other components of the signaling pathways," Klein added. "It will also be interesting to explore the role of this pathway in other tissues and organs, and in the context of distinct injuries and perturbations --for example, physical cuts vs heat burns vs irradiation versus chemical insults." Meanwhile, a pair of recent animal studies led by the University of Arizona in Tucson similarly have shown that the use of FAK inhibitors can make skin grafts look more like healthy skin and produce less scarring, raising hopes for a potential new treatment for survivors of blast wounds, burns and other major injuries. Kellen Chen, an assistant research professor in the university's Department of Surgery and lead author of those papers, said the current Cedars-Sinai study appears to add to a mounting list of evidence that "FAK acts as a central mediator of scarring in the oral mucosa gives additional credence to the importance of this factor." Chen was not involved with the new study. "A better understanding of how the oral mucosa heals without scarring through the FAK pathway will allow us to better develop therapies to target FAK for healing in the future," he told UPI. Chen said his team has the funding to pursue Food and Drug Administration approval for a FAK inhibitor, or FAKI, hydrogel therapy and expects to conduct human trials soon. The growing evidence that wound healing can be accelerated at the cellular level "could have strong clinical implications for the treatment of severe injuries for humans and animals, especially because there are zero FDA-approved treatments that reduce scar formation," he added. "Patients with severe injuries or burns can suffer a lifetime of pain and disfigurement from scarring. The potential to heal burn injuries with regeneration, rather than scarring, would dramatically change the lives of these patients." Copyright 2025 UPI News Corporation. All Rights Reserved.
UPI
02-07-2025
- Health
- UPI
Science seek to tap amazing healing powers of the mouth's interior
1 of 2 | The amazing ability of the mouth's lining to quickly heal itself without scarring is likely due to a specific cellular action that could be applied to skin wounds sustained elsewhere on the body, according to a study released Wednesday. File Photo by Molly Riley/UPI | License Photo ST. PAUL, Minn., July 2 (UPI) -- The cellular action that enables the mouth's interior lining to heal quicky and without scarring has always been a mystery but a new study suggests it may be linked to a specific "signaling pathway." That new knowledge is raising hopes the mouth lining's healing powers could be applied to other skin wounds, which take far longer to heal and often leave permanent, unsightly scars, according to a preclinical study published Wednesday by Cedars-Sinai Medical Center and University of California-San Francisco researchers. The study on mice provides evidence that the "Gas6/AXL" protein/enzyme signaling pathway is likely responsible for the mouth's amazing ability to heal itself completely from even deep bite wounds within a matter of days with no leftover scarring, the authors wrote in the journal Science Translational Medicine. Known as the oral mucosa, the mouth's interior lining heals fast and cleanly, even though it is continuously exposed to different types of microbes, abrasion from foods, motion and tension. This unique regenerative capacity is made possible by specialized gene programs activated during injury, but just how those mechanisms work has been unknown. In the study reported Wednesday, a research team led by Dr. Ophir Klein, executive vice dean of Children's Health at Cedars-Sinai and executive director of Cedars-Sinai Guerin Children's in Los Angeles, found that by manipulating levels of the AXL enzyme they could affect how wounds healed. For instance, if they inhibited AXL in mice, the healing of oral mucosa wounds worsened, making them more like skin wounds. Conversely, when they stimulated AXL in facial skin wounds, they healed more efficiently and with reduced scarring, much like the oral mucosa. Boosting the levels of AXL suppresses the expression of another protein called Focal Adhesion Kinase, or FAK, which plays a significant role in scar formation during wound healing. Should future research validate the benefits for humans, the new knowledge could aid in developing new therapies to heal skin wounds with reduced scarring, Klein said. "We are actively thinking about harnessing AXL-driven repair in both the mouth and the skin, and perhaps in other tissues as well," he told UPI in emailed comments. "One application that comes to mind is to improve healing and reduce scarring in the skin for burn victims or those with other cutaneous disorders. "Another is that there are a number of diseases of the mouth, many of them autoimmune, in which severe oral ulcers form and heal poorly or not at all. These are different from canker sores, also known as aphthous ulcers, which many people get and which typically heal on their own; the more severe ulcers are difficult to treat and cause very significant illnesses, and we currently do not have good therapies for them." A related direction for research could focus on "obtaining a deeper understanding of the effects of AXL signaling on scarring and regeneration at a molecular level, in terms of other components of the signaling pathways," Klein added. "It will also be interesting to explore the role of this pathway in other tissues and organs, and in the context of distinct injuries and perturbations --for example, physical cuts vs heat burns vs irradiation versus chemical insults." Meanwhile, a pair of recent animal studies led by the University of Arizona in Tucson similarly have shown that the use of FAK inhibitors can make skin grafts look more like healthy skin and produce less scarring, raising hopes for a potential new treatment for survivors of blast wounds, burns and other major injuries. Kellen Chen, an assistant research professor in the university's Department of Surgery and lead author of those papers, said the current Cedars-Sinai study appears to add to a mounting list of evidence that "FAK acts as a central mediator of scarring in the oral mucosa gives additional credence to the importance of this factor." Chen was not involved with the new study. "A better understanding of how the oral mucosa heals without scarring through the FAK pathway will allow us to better develop therapies to target FAK for healing in the future," he told UPI. Chen said his team has the funding to pursue Food and Drug Administration approval for a FAK inhibitor, or FAKI, hydrogel therapy and expects to conduct human trials soon. The growing evidence that wound healing can be accelerated at the cellular level "could have strong clinical implications for the treatment of severe injuries for humans and animals, especially because there are zero FDA-approved treatments that reduce scar formation," he added. "Patients with severe injuries or burns can suffer a lifetime of pain and disfigurement from scarring. The potential to heal burn injuries with regeneration, rather than scarring, would dramatically change the lives of these patients."
Scientific American
30-06-2025
- Health
- Scientific American
Serenading Cells with Audible Sound Alters Gene Activity
The cells in your ears aren't the only ones listening: recent research suggests that crucial cells throughout the body may respond to audible sound. Experiments described in Communications Biology revealed more than 100 genes whose activity changed in response to these acoustic waves, pointing to possible medical applications. Extensive earlier research has shown that ultrasound—sound at frequencies higher than humans can hear— can affect biology in numerous ways; the new study expands this concept to audible sounds that require no special equipment to produce. Kyoto University biologist Masahiro Kumeta and his colleagues bathed cultured mouse myoblast cells (precursors to muscle tissue) in sound, directly transmitting a low frequency (440 hertz, the A above middle C), a high frequency (14 kilohertz, approaching the top of the perceptible range for humans), or white noise (which contains all audible frequencies) to the culture dishes for either two or 24 hours. The team analyzed the effect these sound waves had on the mouse cells through RNA sequencing, which measures gene activity. The scientists found that activity in 42 genes changed after two hours, and 145 responded after 24 hours. Most showed increased activity, but some were suppressed. 'It's a very extensive, thorough study,' says Lidan You, an engineer at Queen's University in Ontario, who studies how bone cells translate mechanical stimuli into biological signals. On supporting science journalism If you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today. Many of the affected genes have roles in key processes such as cell adhesion and migration, which are known to respond to mechanical forces. The researchers found that sound expanded the size of the sites where cells attached to surrounding tissues, most likely by activating an enzyme called focal adhesion kinase (FAK), which senses mechanical forces and helps to guide tissue development. Sound waves seem to deform molecules in a way that provides easier access for a chemical switch that activates FAK, which in turn influences a chain of other genes' activity. The team also found a strong reaction in fat-cell precursors called preadipocytes: sound suppressed their differentiation into mature fat cells, thereby reducing fat accumulation by 13 to 15 percent. Audible sound is noninvasive and probably safer than drugs, Kumeta says. Although it can't be tightly focused like ultrasound, it is easy to produce and could be useful for bathing large regions of the body in sonic waves. Kumeta and his colleagues have already begun studying such interventions to suppress the development of fat tissue in living mice—and humans could be next, he says: 'If it works well in mice I think this could be achieved in five or 10 years.' Other potential applications include enhancing regenerative medicine and combating cancer growth. 'The next step [could be] using not only human cells but human organoids that model diseases,' You says, 'then moving to clinical studies.'
Yahoo
28-05-2025
- Business
- Yahoo
Verastem Oncology to Present at the Jefferies Global Healthcare Conference
BOSTON, May 28, 2025--(BUSINESS WIRE)--Verastem Oncology (Nasdaq: VSTM), a biopharmaceutical company committed to advancing new medicines for patients with RAS/MAPK pathway-driven cancers, today announced that its management team is scheduled to participate in a fireside chat at the Jefferies Global Healthcare Conference on Wednesday, June 4, 2025, at 4:20 pm ET in New York. A live webcast of the fireside chat can be accessed under "Events & Presentations" on the Company's website at A replay of the webcasts will be archived on the website for approximately 90 days following the presentation. About Verastem Oncology Verastem Oncology (Nasdaq: VSTM) is a biopharmaceutical company committed to developing and commercializing new medicines to improve the lives of patients diagnosed with RAS/MAPK pathway-driven cancers. Verastem markets AVMAPKI™ FAKZYNJA™ CO-PACK in the U.S. Our pipeline is focused on novel small molecule drugs that inhibit critical signaling pathways in cancer that promote cancer cell survival and tumor growth, including RAF/MEK inhibition, FAK inhibition, and KRAS G12D inhibition. For more information, please visit and follow us on LinkedIn. View source version on Contacts For Investor and Media Inquiries: Julissa VianaVice President, Corporate Communications,Investor Relations & Patient Advocacyinvestors@ ormedia@ Sign in to access your portfolio
