German Cancer Research Center

Theator's advanced AI technology sets a new standard in surgical safety, outperforming competitors in the SAGES CVS Challenge and showcasing its commitment to transparency and innovation. PALO ALTO, Calif., Dec. 5, 2024 /PRNewswire/ -- Theator Inc., a leader in AI-driven surgical intelligence, has won the Society of American Gastrointestinal and Endoscopic Surgeons (SAGES) Critical View of Safety (CVS) Challenge at the prestigious MICCAI 2024 conference. In addition to winning the overall challenge, Theator excelled in the subchallenges, securing first place in the Uncertainty Quantification subchallenge and second in CVS Classification and Robustness. Theator's success in this rigorous competition, which included industry and leading academic centers such as Stanford, highlights the company's cutting-edge AI and its dedication to advancing surgical safety and transparency in medical technology. SAGES, a leading surgical society whose mission is to innovate, educate, and collaborate to improve patient care, created the world's first global competition focused on the computational assessment of the Critical View of Safety during laparoscopic cholecystectomy, a widely performed minimally invasive procedure for gallbladder removal. Recognized as an international safety standard, the CVS was initially proposed in 2010 and adopted by leading professional societies such as SAGES. Achieving the CVS has been shown to mitigate the risk of bile duct injuries significantly, one of the most severe complications in gallbladder surgeries. This challenge required participants to train AI algorithms to accurately assess the CVS visual criteria, enhancing surgeons' decision-making capacity and overall surgical safety. Theator's proprietary AI technology, recognized for its unique ability to capture and analyze minimally invasive surgical (MIS) videos, excelled in the challenge due to its precise CVS criteria detection and robust uncertainty quantification. Theator's solutions were tested on a globally diverse dataset of 1,000 annotated laparoscopic cholecystectomy videos, reflecting real-world complexities across various demographics, surgical techniques, and equipment. "Understanding and applying the critical view of safety is arguably the single most important strategy surgeons can employ to enhance the safety of laparoscopic cholecystectomy and reduce the risk of bile duct injury," said Dr. Michael Brunt, past President of SAGES, Professor of Surgery and Co-Director, Washington University Institute for Minimally Invasive Surgery, and a pioneer in the field of MIS. Notably, Dr. Brunt is one of the original architects of CVS. "As technology evolves, modalities like artificial intelligence have the potential to provide real-time feedback to surgeons about achieving the CVS and further add a safety element to this common operation. The recent CVS AI challenge held by SAGES that involved industry and academic institutions testing their CVS identification ability moves the needle further in this direction. Congratulations to Theator on achieving 1st place overall in the competition across a diverse array of images and clinical scenarios by ranking highly in every subcategory of the challenge. While much work is yet to be done, this important step will set the stage for real-world clinical applications with potential future benefits to the surgical community and for our patients. We look forward to continued collaborations between AI partners, surgical societies, and surgeons in this exciting new era." "Winning this challenge is a testament to our team's relentless pursuit of excellence in AI-driven surgical intelligence. Our commitment to transparency in AI technology is vital for building trust in the medical community," said Dotan Asselmann, Co-founder and CTO of Theator. "We also want to congratulate the second and third-place winners, the German Cancer Research Center and Stanford University. We are deeply grateful to SAGES for organizing this challenge and advancing the development of AI technologies that will make surgery safer worldwide." Leveraging AI technology to advance surgical care is becoming increasingly prevalent and is poised to address significant unmet needs in the field. Theator's achievements in the CVS Challenge underscore its leadership in applying AI to surgery, reflecting its vast and unique MIS dataset. CVS is one of numerous best practices in various specialties that are visually identifiable using Theator's technology, allowing for safer surgery. Combining world-class AI models with comprehensive surgical data from tens of thousands of cases, Theator is poised to continue delivering actionable insights that improve patient outcomes, support surgical decision-making, and reduce procedural variability. About Theator Theator is transforming surgical care through its AI-powered Surgical Intelligence Platform, enhancing quality, safety, and efficiency across health systems. By standardizing surgical video capture and analysis with advanced computer vision and AI, Theator provides much-needed actionable visibility at scale to impact quality, safety, operational efficiency, education, and documentation workflows. For surgeons, this means continuous improvement through data-driven insights and shared best practices. For health system leaders, the platform surfaces variability and enables standardization of care, reducing operational inefficiencies while improving quality metrics. For patients, the platform ensures equitable, high-quality care regardless of geography. Theator is committed to addressing disparities in surgical outcomes, advancing the standard of care, and creating a transparent, more data-driven surgical ecosystem. Based in Palo Alto, California, Theator partners with leading healthcare systems, professional societies, and research institutions to pave the way for better healthcare outcomes worldwide. Discover more at theator.io. Media Contact: Theator, Inc. Natalie Holger Email: [email protected] Phone: +1 (937) 901-6459 SOURCE Theator, Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

According to the recent announcement on the CDE (China's Center for Drug Evaluation) website, Bayer has successfully obtained clinical trial approvals for two of its novel Class 1 drugs, which are aimed at addressing the treatment needs of patients with late-stage solid tumors and acute ischemic stroke.   Based on Bayer's public information, one of the new drugs is a DGKα inhibitor, and the other is a protein-based drug targeting α2AP. These two candidates are currently in Phase 1 and Phase 2 clinical development stages, respectively, at the international level.   BAY 2862789 oral solution, a small-molecule DGKα inhibitor co-developed by Bayer and the German Cancer Research Center (DKFZ), is now undergoing the first-in-human Phase 1 clinical trial globally. Its research and development target is the treatment of solid tumors. The diacylglycerol kinase (DGK) family plays a crucial role in the development, differentiation, and functional regulation of T cells and NK cells, with DGKα and DGKζ being the predominant isoforms. Studies have shown that DGKα is significantly expressed in various refractory cancers, promoting cell proliferation and inhibiting apoptosis. Its high expression is closely related to T-cell exhaustion, which is a key factor in the evasion of immune surveillance by late-stage cancers. Therefore, the specific inhibition of DGKα holds great potential in the field of cancer therapy, as it can effectively suppress cancer cell proliferation and activate T-cell functions, achieving a dual anti-cancer effect. Furthermore, the synergistic effect of this inhibitor with PD-1/PD-L1 inhibitors offers new hope for the treatment of refractory cancers.   The other new drug, BAY 3018250, is a protein-based drug targeting α2AP, which is part of Bayer's cardiovascular disease research and development pipeline. It aims to treat acute ischemic stroke and pulmonary embolism. Currently, this drug has made significant progress in the international Phase 2 clinical trial for the treatment of deep vein thrombosis (DVT). DVT is a serious health issue that can lead to life-threatening blockage of blood flow in the lungs. BAY 3018250 exerts its therapeutic effect by dissolving blood clots. Thrombotic vascular occlusion is a key factor in the development of ischemic stroke, and α2-antiplasmin (α2AP), a member of the serine protease inhibitor family, is closely associated with an increased risk of ischemic stroke and the failure of recombinant tissue plasminogen activator (rt-PA) treatment. Research has shown that anti-α2AP therapy can significantly reduce the formation of microvascular thrombosis, ischemic brain injury, brain edema, intracerebral hemorrhage, and mortality after ischemic stroke, suggesting that the temporary inactivation of α2AP may have potential therapeutic value for ischemic stroke. With the approval for clinical trials in China, BAY 3018250 will now be evaluated for the specific indication of acute ischemic stroke, bringing new hope for the treatment of this condition.

Cancer genomes are the result of diverse mutation processes that have often accumulated over decades. Scientists have analyzed the molecular evolution of tumors after exposure to mutagenic chemicals. DNA lesions that persists unrepaired over several cell generations lead to sequence variations at the site of damage, the quantification of which provides insights into the kinetics and mechanisms of DNA repair. This enabled the researchers to distinguish the contribution of the triggering lesion from that of the subsequent repair in shaping the mutation pattern. Cancer genomes are the result of diverse mutation processes that have often accumulated over decades. Scientists from the German Cancer Research Center (DKFZ) and the Universities of Cambridge and Edinburgh have analyzed the molecular evolution of tumors after exposure to mutagenic chemicals. DNA lesions that persists unrepaired over several cell generations lead to sequence variations at the site of damage, the quantification of which provides insights into the kinetics and mechanisms of DNA repair. This enabled the researchers to distinguish the contribution of the triggering lesion from that of the subsequent repair in shaping the mutation pattern. These results have now been published in the journal Nature. After DNA damage, for example by chemicals, the damaged and undamaged DNA strands are separated from each other during cell division. The cells often do not repair the DNA damage immediately; the lesions persist over several rounds of cell division. The damaged DNA can be copied by specialized enzymes known as translesion polymerases. However, these enzymes incorporate DNA building blocks (nucleotides) at random or simply skip the damaged nucleotide. The daughter cells develop different mutation profiles as a result. Researchers refer to this as "lesion segregation." This results in complex mutation patterns in a clonal cell population such as a tumor, and can reveal which damaged DNA strand a cancer cell inherited from its "ancestors." Researchers led by Duncan Odom, DKFZ, Sarah Aitken, University of Cambridge and Martin Taylor, University of Edinburgh, investigated the question of how this asymmetry of DNA damage and DNA repair comes about. In particular, they wanted to clarify whether it plays a role in the mutation rate which of the two DNA strands is damaged. Despite the symmetry of both strands of the DNA ladder, they differ in many respects: only one of the strands is read into RNA, different machinery copies each of the two strands during replication, and both strands are differently accessible to repair enzymes. The team used a mouse model to investigate how diethylnitrosamine damages liver cells and ultimately causes liver cancer. The substance damages the genetic material by chemically bonding with a base. Experts refer to such stable attachments as small DNA adducts. For their current study, the researchers examined 237 tumors from 98 mice and analyzed over seven million mutations. Contrary to expectations, they found no significant differences in the mutation rates of the two strands of DNA (leading and lagging strand) despite their replication being performed by different processes. They went on to show that on encountering damage, both processes recruit the same damage bypass machinery with the same efficiency. This stands in stark contrast to the asymmetric strand tolerance of the much more space-consuming UV light-induced adducts and gives new insight into how cells deal with the DNA damage caused by smoking and cancer treatments. The accumulation of several different mutations at the site of persistently unrepaired DNA lesions can be used to measure the efficiency of repair processes -- in the entire genome and with a resolution of single nucleotides. The researchers found that the mutations induced by DNA damage are largely shaped by the influence of DNA accessibility on repair efficiency rather than where damage occurs. Finally, they reveal specific genomic conditions that actively drive cancer-promoting mutagenesis by impairing the reliability of a specific repair mechanism called "nucleotide excision repair." Duncan Odom, one of the senior authors of the study, summarizes: "Our results shed light on how strand-asymmetric mechanisms of DNA damage generation, tolerance and repair underlie the evolution of the cancer genome."