Onco Preventer

Category: Uncategorized

  • health reminders

    In today's fast-paced world, prioritizing health can often be challenging. However, maintaining regular health check-ups and screenings is crucial for early detection and prevention of serious illnesses, including cancer. Health reminders serve as an essential tool to help individuals stay on track with their health goals by providing timely prompts for medical appointments, screenings, and lifestyle management. One innovative solution that revolutionizes this approach is OncoPreventer, an AI-powered assistant designed specifically for cancer prevention and early detection.

    Cancer remains one of the leading causes of death worldwide, with many cases being diagnosed at advanced stages when treatment options are limited and outcomes less favorable. Early detection through routine screening significantly improves survival rates, making it imperative for individuals to adhere to personalized screening schedules. This is where OncoPreventer steps in as a vital health companion.

    OncoPreventer leverages advanced artificial intelligence combined with expert medical knowledge to create custom screening plans tailored to each individual's unique profile. Factors such as age, gender, family history, and lifestyle habits are considered to develop a personalized schedule that maximizes the effectiveness of preventive care. This personalized approach ensures that users receive recommendations that are relevant and timely, helping to address their specific risk factors.

    A standout feature of OncoPreventer is its intelligent reminder system. Users receive smart notifications for upcoming check-ups, lab tests, and annual visits, eliminating the possibility of missed appointments. These reminders are designed to seamlessly fit into users' busy lives, ensuring that health maintenance does not become a stressful or forgettable chore.

    Beyond reminders, OncoPreventer offers a user-friendly interface that provides clear, trusted answers to health-related questions. This feature helps demystify medical jargon, making health information accessible and easy to understand for everyone. Users can feel confident and informed as they navigate their health journey, empowered by accurate and reliable information.

    Tracking health progress is made simple through OncoPreventer's interactive timelines and summaries. Users can visualize their health milestones and screening history, which promotes accountability and reinforces proactive care. This transparent view aids in spotting trends and areas that may require additional attention.

    What sets OncoPreventer apart is its versatility and convenience. Available across multiple platforms including web, Telegram, and WhatsApp, it ensures users can stay connected to their health assistant wherever they are. Whether at home or on the go, managing health reminders and screening plans becomes effortless.

    In essence, OncoPreventer stands as a beacon of proactive healthcare, emphasizing prevention and early detection without the stress or confusion. Its AI-driven, personalized approach caters to the modern individual's needs, fostering healthier lifestyles through education, timely reminders, and continuous support.

    Embracing health reminders like those offered by OncoPreventer can transform how people approach cancer prevention. By integrating technology with medical expertise, OncoPreventer helps reduce cancer risk and enhances the quality of life. Individuals no longer need to navigate the complexities of healthcare alone; instead, they have a trusted, intelligent companion guiding every step toward wellness.

    In summary, maintaining health is not just about reacting to illness but actively preventing it. OncoPreventer provides the tools to achieve this by delivering tailored screening schedules, smart reminders, helpful information, and progress tracking—all in one user-friendly platform. For anyone committed to safeguarding their health and reducing cancer risk, OncoPreventer offers an indispensable solution that combines technology and medical insight for smarter, stress-free health management.

  • how to monitor your health

    Monitoring your health is a proactive approach to maintaining well-being and preventing potential health issues. With advancements in technology, individuals now have access to various tools and strategies to track and manage their health effectively. This article explores methods to monitor your health and introduces OncoPreventer, an AI-powered assistant designed to assist in cancer prevention and early detection.

  • AI health assistant

    In the rapidly advancing world of healthcare, where technology continuously reshapes the ways we diagnose, treat, and prevent diseases, one innovation stands out prominently in the battle against cancer: OncoPreventer. Designed as an AI-powered assistant, OncoPreventer is not just another health app. It is a transformative tool that harnesses the power of artificial intelligence to revolutionize cancer prevention and early detection by tailoring care to individual health profiles. Early detection has long been recognized as one of the most critical factors in increasing survival rates for cancer patients, and OncoPreventer takes this principle to new heights by enabling proactive and personalized interventions that fit each user’s unique risk factors.

    Artificial intelligence has dramatically changed numerous industries, and healthcare has been a major beneficiary. Specifically, in oncology, AI's capabilities are revealing a new frontier of diagnostic precision and preventive strategies. Machine learning algorithms can evaluate complex medical imaging, such as CT scans and MRIs, to detect minuscule abnormalities that may signify the beginnings of cancer—often far earlier than human clinicians can spot. According to institutions like Massachusetts General Hospital, this ability to pinpoint cancer in its nascent stages means treatments can begin sooner, improving outcomes dramatically. AI’s power doesn’t stop at imaging analysis; it extends to predictive risk modeling, aiding healthcare providers in understanding which patients are at higher risk based on demographic data, genetics, and lifestyle habits. This multifaceted use of AI transforms what was once reactive cancer care into a proactive, anticipatory approach.

    OncoPreventer taps into this transformative potential with a plethora of user-friendly features that emphasize personalization and convenience. At its core lies the ability to generate personalized screening plans; by analyzing crucial factors including age, gender, family history, and lifestyle choices such as diet and activity levels, it schedules optimal screening intervals customized for each user. This tailored approach is essential because cancer risk varies widely among individuals, and one-size-fits-all screening protocols often lead to delays or unnecessary tests. To maintain ongoing engagement, the app employs intelligent, non-intrusive reminders for check-ups, lab work, and annual wellness visits. Beyond scheduling, OncoPreventer offers expert-backed recommendations drawn from an extensive medical knowledge base, ensuring that users receive reliable answers to health-related queries, fostering informed decision-making. Progress tracking through interactive timelines offers visual insight into one’s health journey, motivating users with tangible data on their screening adherence and overall wellness. Perhaps most impressively, the platform embraces cross-platform accessibility, working seamlessly via web browsers, Telegram, and WhatsApp, meeting users exactly where they are most comfortable and active.

    The application of AI in early cancer detection is making headlines worldwide, and OncoPreventer is riding this wave with enthusiasm and scientific rigor. AI-driven approaches have increasingly been adopted for analyzing imaging indicative of lung and pancreatic cancers, among others. Lung cancer, a historically deadly disease often detected in advanced stages, has seen improved diagnostic times thanks to AI’s ability to discern subtle CT scan irregularities. Similarly, pancreatic cancer, infamous for its stealthy progression and poor prognosis, stands to benefit massively from AI’s nuanced analysis, which can reveal early-stage tumors that might otherwise remain hidden until too late for effective surgery. These breakthroughs are more than technological marvels; they translate into lives saved and families spared from profound loss. By aligning with such state-of-the-art tools, OncoPreventer offers users on-demand insight into their health trajectories and empowers them to act early when it counts most.

    In conclusion, OncoPreventer embodies the exciting fusion of artificial intelligence with personalized medicine, charting a new course for cancer prevention and early detection. This powerful assistant offers individuals an unparalleled level of control and clarity over their health, making expert guidance accessible through intuitive, timely interactions that shape proactive health habits. Amid a landscape where early intervention can tip the scales towards survival, platforms like OncoPreventer aren’t just apps—they are vital partners in the personal and public health crusade against cancer. As AI continues driving innovations in healthcare, OncoPreventer exemplifies the promise of technology not only to save lives but to enhance the quality of those lives through smarter, simpler, and more effective care strategies.

    #CancerPrevention #AIinHealthcare #EarlyDetection #OncoPreventer #HealthTechInnovation #PersonalizedMedicine #CancerAwareness

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  • Communication Between Leadership and Clinicians Improves Cancer Care

    In May 2025, a significant milestone was reached in the fight against cancer with the grand opening of a new, state-of-the-art cancer center at Hackensack Meridian Health John F. Kennedy (JFK) University Medical Center. This expansion represents a bold step forward in providing advanced cancer care, bringing cutting-edge treatments and multidisciplinary collaboration under one roof. The opening ceremony drew attention not only because of the facility’s impressive capabilities but also due to the insightful perspectives shared by key leaders within Hackensack Meridian Health. Robert C. Garrett, the CEO of Hackensack Meridian Health, and Joseph C. Landolfi, DO, CPE, chief medical officer and vice president of JFK University Medical Center, offered their thoughts on how effective communication and collaboration are crucial for enhancing patient outcomes and driving healthcare innovations.

    One of the most compelling points raised by Garrett during the ceremony was the vital role of communication between healthcare leaders and frontline clinicians. Garrett emphasized that occupying a leadership role enables him to advocate directly with elected officials to shape policies that impact the broader healthcare system. However, he pointed out that this responsibility demands staying deeply connected with those delivering day-to-day care. Such dialogue ensures that the perspectives and challenges experienced by clinicians inform the policy decisions he champions. This type of engagement is critical when addressing issues like budget cuts. In fact, Garrett was preparing for an upcoming trip to Washington, D.C., where he planned to meet with senators and representatives to discuss potentially detrimental budget reductions. Through these interactions, Garrett strives to build a solid case grounded in real-world clinical input, highlighting the ripple effects legislative decisions can have on patient care quality.

    Adding another layer to the center’s vision for the future, Landolfi focused on enhancing multidisciplinary collaboration across cancer care teams. He put forth the idea of hosting conferences that bring together specialists from various fields to work cohesively in patient treatment planning. This approach promotes a holistic understanding of cancer care, enabling experts from oncology, radiology, surgery, pathology, nursing, and supportive care services to pool their expertise. Landolfi’s vision goes even further by proposing the integration of departments statewide, linking resources and knowledge bases from the new JFK cancer center with other esteemed institutions such as John Theurer Cancer Center and HOPE Tower at Jersey Shore University Medical Center. This statewide network aspires to expand access to comprehensive cancer care and foster continual innovation through shared research and clinical trials. Such interconnectedness could serve as a model for other regions aiming to bridge gaps in specialized healthcare.

    The importance of multidisciplinary care cannot be overstated in modern oncology. Cancer treatment often requires navigating complex therapies that must be tailored to individual patient needs—ranging from chemotherapy and radiation to surgical interventions and emerging immunotherapies. By establishing forums for cross-specialty collaboration, the new center aims to ensure that patients benefit from the combined wisdom of diverse experts, leading to more personalized and effective treatment protocols. Moreover, this approach can help accelerate clinical research by enabling seamless data sharing and cooperative study designs across multiple centers. It’s fascinating to note that the concept of multidisciplinary cancer care has roots dating back to the 1960s but has gained enormous traction only in recent decades with advances in medical technology and data analytics. The JFK cancer center’s initiative highlights the ongoing transformation of cancer treatment from siloed efforts to integrated care ecosystems.

    In addition to its clinical mission, the new cancer center embodies a broader commitment to community health and patient education. Facilities like these often serve as hubs for outreach programs, early detection campaigns, and survivorship support networks. In fact, there is growing evidence that community engagement, including preventive education and psychosocial support, plays a crucial role in improving overall cancer outcomes. As healthcare continues to evolve, centers like the one at JFK University Medical Center stand as beacons of hope, illustrating how collaboration, leadership communication, and patient-centric innovations converge to tackle one of humanity’s most formidable health challenges. The opening of this center not only marks a new chapter for Hackensack Meridian Health but also sets a precedent for how healthcare organizations can balance cutting-edge technology with empathetic, integrated patient care.

    #CancerCareInnovation #MultidisciplinaryMedicine #HealthcareLeadership #HackensackMeridian #OncologyAdvancements #PatientCenteredCare #NewJerseyHealthcare

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  • ALX Oncology won’t seek approval for CD47 drug in gastric cancer; Korro Bio’s layoffs

    In the ever-advancing world of biotechnology and pharmaceuticals, constant developments ensure that the landscape remains dynamic, brimming with promise and possibilities. Recently, a series of intriguing shifts have surfaced among several noteworthy companies including ALX Oncology, Cognition Therapeutics, Sagimet Biosciences, BeiGene, Hikma, and Rallybio. These organizations stand at the cutting edge of pioneering treatments and medical innovations, each making strategic choices that shape the future trajectory of healthcare and significantly impact patient outcomes around the globe. Their efforts not only aim to tackle some of the most challenging diseases but also push the boundaries of what medicine can achieve in the 21st century.

    ALX Oncology, a company renowned for its focus on groundbreaking cancer therapies, has recently made a pivotal decision regarding its portfolio. The firm decided to halt efforts toward gaining approval for a gastric cancer treatment that it had been actively developing. Gastric cancer, commonly referred to as stomach cancer, remains a formidable adversary in oncology, with limited therapeutic options contributing to persistent high mortality rates worldwide. ALX Oncology’s strategic withdrawal signals a recalibration of priorities, likely redirecting resources toward other therapeutic candidates within their pipeline that may have more immediate or promising potential. This decision underscores the rigorous evaluation processes that companies navigate to ensure that any drug introduced to the market offers the optimal chance for clinical success and commercial viability, highlighting the tough balancing act between hope and reality in drug development.

    Meanwhile, several other key players continue to forge ahead in their specialized medical fields. Cognition Therapeutics, for example, focuses intensely on neurodegenerative diseases such as Alzheimer’s, with efforts aimed at targeting root causes rather than merely alleviating symptoms. This approach represents a hopeful shift in managing conditions that have long been considered intractable. Sagimet Biosciences is advancing treatments for metabolic and cardiovascular diseases, a crucial arena given the global surge in lifestyle-related chronic illnesses like diabetes and heart disease. BeiGene distinguishes itself as a global biopharmaceutical powerhouse, expanding its work in immunotherapies and precision-targeted cancer treatments, which are rapidly transforming oncology care. Hikma Pharmaceuticals, meanwhile, has become a vital provider of a broad range of medications worldwide, supplying everything from essential generics to complex specialty drugs. Rallybio’s focus on rare and serious diseases places it at the forefront of developing transformative therapies aimed at populations often underserved and overlooked in the healthcare system. Together, these companies illustrate the multifaceted innovation ongoing in the biotech and pharmaceutical sectors.

    The biotech industry fascinates not only because of the breakthrough science but also due to the strategic business maneuvers companies employ, often influenced by clinical trial outcomes, regulatory frameworks, and shifting market demands. For instance, ALX Oncology’s decision to withdraw from pursuing gastric cancer approval is not a retreat but rather a strategic realignment that could accelerate development in other potentially groundbreaking treatments. This highlights the complex yet thrilling interplay biotech firms must manage—which combines scientific potential, patient needs, and business pragmatism to steer toward success. It is also a testament to the resilience and adaptability that characterize the sector, where setbacks are often the gateways to innovation and new directions.

    Adding a lighthearted twist to this serious field, the biotechnology sector is full of quirky and fascinating tidbits. Did you know that the first successful lab-grown meat — which has recently piqued considerable public interest — was developed using principles closely aligned with those in therapeutic biotechnology? Similarly, some of the techniques currently employed in cancer research have surprising origins in the study of obscure organisms such as deep-sea bacteria and Arctic fungi. These organisms possess unique biochemical pathways and survival mechanisms that inspired novel approaches in drug discovery and development. Such odd yet inspiring roots beautifully illustrate the interdisciplinary and inventive spirit of biotech research, where breakthroughs arise from the most unexpected corners of the natural world. This melding of creativity and science not only gives hope to patients but suggests that medicine’s future innovations may come from the most unusual sources.

    #BiotechInnovation #PharmaNews #CancerResearch #NeurodegenerativeDiseases #RareDiseases #HealthcareTrends #Biotechnology

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  • digital doctor

    In today's fast-paced world, taking control of your health can often feel overwhelming, especially when it comes to preventing serious diseases like cancer. Early detection and proactive prevention are critical in the fight against cancer, but navigating the myriad of recommendations, screenings, and lifestyle adjustments can be daunting. Enter OncoPreventer, a cutting-edge digital doctor designed to revolutionize how we approach cancer prevention and early detection.

    ### What is OncoPreventer?
    OncoPreventer is an AI-powered digital assistant created specifically to help individuals reduce their cancer risk through personalized, proactive healthcare. By combining advanced artificial intelligence with extensive medical expertise, OncoPreventer offers a seamless, user-friendly experience that tailors cancer prevention strategies to each user's unique profile.

    ### Personalized Screening Plans
    One of the standout features of OncoPreventer is its ability to create customized screening schedules. These plans take into account various factors such as age, gender, family history, and lifestyle, ensuring that each screening is timely and relevant. This personalized approach means users are not subjected to generic recommendations but receive care that is precisely aligned with their personal risk factors.

    ### Timely Reminders to Stay on Track
    A crucial challenge in preventive care is adherence to screening and check-up schedules. OncoPreventer addresses this by sending smart reminders for medical appointments, lab tests, and annual health visits. Whether you prefer to receive alerts on the app or via popular messaging platforms like Telegram and WhatsApp, OncoPreventer ensures you never miss an important health milestone.

    ### Expert-Backed Recommendations and Clear Communication
    Navigating health information can often be confusing, filled with medical jargon and uncertainty. OncoPreventer cuts through the complexity by providing clear, trusted answers to health-related questions. Users can interact with the system to gain insights backed by medical experts, empowering them to make informed decisions without the stress.

    ### Tracking Progress with Interactive Tools
    Understanding your health journey is vital to maintaining motivation and making adjustments when necessary. OncoPreventer includes interactive timelines and health summaries that allow users to visualize their progress, see upcoming screenings, and review past results. This holistic view keeps users engaged and proactive about their health.

    ### Seamless Integration Across Platforms
    Recognizing the importance of accessibility, OncoPreventer operates smoothly across multiple platforms — from web interfaces to popular messaging apps like Telegram and WhatsApp. This flexibility lets users integrate cancer prevention into their daily routines without disruption.

    ### Why Choose OncoPreventer?
    OncoPreventer stands out as more than just a health app; it is your intelligent companion in the journey towards cancer prevention. With its personalized care plans and AI-driven insights, the app transforms a traditionally complex healthcare process into a manageable, stress-free experience.

    In conclusion, OncoPreventer offers tremendous value in today's healthcare landscape by empowering individuals to proactively manage their cancer risk. By delivering expert-backed recommendations, tailored screening plans, and smart reminders all through an easy-to-use interface, it makes cancer prevention accessible to everyone. If you're looking to take control of your health with confidence and ease, OncoPreventer is an indispensable digital doctor that guides you every step of the way.

  • prevention chatbot

    **OncoPreventer: Revolutionizing Cancer Prevention with AI-Powered Chatbot Technology**

    Cancer remains one of the leading causes of death worldwide, with early detection and prevention being crucial in improving survival rates. Advancements in technology have paved the way for innovative solutions in healthcare, and one such innovation is the integration of artificial intelligence (AI) through chatbots to enhance cancer prevention efforts. OncoPreventer stands at the forefront of this revolution, offering a personalized, accessible, and efficient approach to cancer risk reduction.

    **The Role of Chatbots in Healthcare**

    Chatbots have emerged as transformative tools in the healthcare sector, providing patients with immediate access to information, reminders, and support. Their ability to deliver personalized care, coupled with 24/7 availability, makes them invaluable in managing health proactively. In the realm of oncology, chatbots have been utilized for various purposes, including patient education, symptom monitoring, and facilitating early detection.

    **OncoPreventer: Your AI-Powered Health Companion**

    OncoPreventer leverages AI technology to offer a comprehensive suite of features designed to empower individuals in their cancer prevention journey:

    – **Personalized Screening Plans**: By analyzing factors such as age, gender, family history, and lifestyle, OncoPreventer crafts individualized screening schedules, ensuring that users undergo appropriate tests at optimal intervals.

    – **Timely Reminders**: The chatbot sends smart notifications for upcoming check-ups, lab tests, and annual visits, promoting adherence to preventive care protocols.

    – **Expert-Backed Recommendations**: Users receive clear, trusted answers to health-related questions, backed by medical expertise, facilitating informed decision-making.

    – **Progress Tracking**: Interactive timelines and health summaries allow users to monitor their health status and the effectiveness of their preventive measures.

    – **Seamless Integration**: OncoPreventer operates across multiple platforms, including web interfaces, Telegram, and WhatsApp, ensuring accessibility and convenience.

    **The Value Proposition of OncoPreventer**

    OncoPreventer is more than just a chatbot; it is an intelligent health companion dedicated to reducing cancer risk through proactive, personalized care. By combining medical expertise with AI technology, it offers several key benefits:

    – **Enhanced Patient Engagement**: The interactive nature of OncoPreventer fosters active participation in health management, leading to better health outcomes. Studies have shown that chatbots can significantly improve patient engagement by providing personalized guidance and support. ([yellow.ai](https://yellow.ai/blog/healthcare-chatbot/?utm_source=openai))

    – **Improved Accessibility and Convenience**: With 24/7 availability and multi-platform support, OncoPreventer ensures that users have continuous access to health information and reminders, reducing barriers to care. This constant availability means patients can receive immediate answers to urgent questions, guidance for minor health issues, or directions on when to seek emergency care, thereby reducing unnecessary hospital visits and easing the burden on healthcare systems. ([yellow.ai](https://yellow.ai/blog/healthcare-chatbot/?utm_source=openai))

    – **Cost-Effectiveness**: By automating routine tasks such as appointment scheduling, medication reminders, and information dissemination, OncoPreventer reduces administrative burdens and associated costs, allowing healthcare providers to allocate resources more efficiently. Chatbots in healthcare contribute to significant cost savings by automating routine tasks and providing initial consultations. ([yellow.ai](https://yellow.ai/blog/healthcare-chatbot/?utm_source=openai))

    – **Health Education and Empowerment**: OncoPreventer delivers accurate, easy-to-understand information about cancer prevention, empowering users to make informed health decisions and adopt preventive measures. They provide personalized, easy-to-understand information about diseases, treatments, and preventive measures. ([yellow.ai](https://yellow.ai/blog/healthcare-chatbot/?utm_source=openai))

    – **Scalability**: The AI-driven nature of OncoPreventer allows it to handle a large volume of interactions simultaneously, ensuring that all users receive timely assistance, which is particularly beneficial during health crises or peak times. The scalability of healthcare chatbots is a significant advantage. ([yellow.ai](https://yellow.ai/blog/healthcare-chatbot/?utm_source=openai))

    **Evidence Supporting Chatbots in Cancer Prevention**

    Research has demonstrated the efficacy of chatbots in enhancing cancer prevention efforts:

    – **Patient Education**: A systematic review and meta-analysis found that chatbot interventions for breast cancer education led to high user satisfaction (85% to 99%) and significantly improved knowledge acquisition compared to routine care. ([pubmed.ncbi.nlm.nih.gov](https://pubmed.ncbi.nlm.nih.gov/39730943/?utm_source=openai))

    – **Health Behavior Change**: AI chatbots have been effective in promoting healthy lifestyles, including physical activity and diet, smoking cessation, and treatment adherence, thereby contributing to cancer prevention. ([ncbi.nlm.nih.gov](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10007007/?utm_source=openai))

    – **Cost Savings**: The integration of chatbots in healthcare has been associated with significant cost savings by automating routine tasks and providing initial consultations, reducing the need for staff to handle basic inquiries and administrative duties. ([yellow.ai](https://yellow.ai/blog/healthcare-chatbot/?utm_source=openai))

    **Conclusion**

    OncoPreventer exemplifies the transformative potential of AI-powered chatbots in cancer prevention. By offering personalized, accessible, and efficient health management tools, it empowers individuals to take proactive steps in reducing their cancer risk. As healthcare continues to evolve, integrating AI technologies like OncoPreventer will play a pivotal role in enhancing patient engagement, improving outcomes, and optimizing resource utilization.

  • Improving outcomes of patients with pancreatic cancer

    Huang, J. et al. Worldwide burden of, risk factors for, and trends in pancreatic cancer. Gastroenterology 160, 744–754 (2021).

    Abboud, Y. et al. Increasing pancreatic cancer incidence in young women in the United States: a population-based time-trend analysis, 2001–2018. Gastroenterology 164, 978–989.e6 (2023).

    Koh, B. et al. Patterns in cancer incidence among people younger than 50 years in the US, 2010 to 2019. JAMA Netw. Open. 6, e2328171 (2023).

    Allemani, C. et al. Global surveillance of trends in cancer survival 2000–14 (CONCORD-3): analysis of individual records for 37 513 025 patients diagnosed with one of 18 cancers from 322 population-based registries in 71 countries. Lancet 391, 1023–1075 (2018).

    Siegel, R. L., Giaquinto, A. N. & Jemal, A. Cancer statistics, 2024. CA Cancer J. Clin. 74, 12–49 (2024).

    NHS England. Cancer survival in England, cancers diagnosed 2015 to 2019, followed up to 2020. NHS Digital digital.nhs.uk/data-and-information/publications/statistical/cancer-survival-in-england/cancers-diagnosed-2015-to-2019-followed-up-to-2020 (2022).

    Rahib, L. et al. Projecting cancer incidence and deaths to 2030: the unexpected burden of thyroid, liver, and pancreas cancers in the United States. Cancer Res. 74, 2913–2921 (2014).

    Casolino, R. et al. Reshaping preoperative treatment of pancreatic cancer in the era of precision medicine. Ann. Oncol. 32, 183–196 (2020).

    Conroy, T. et al. FOLFIRINOX versus gemcitabine for metastatic pancreatic cancer. N. Engl. J. Med. 364, 1817–1825 (2011).

    Von Hoff, D. D. et al. Increased survival in pancreatic cancer with nab-paclitaxel plus gemcitabine. N. Engl. J. Med. 369, 1691–1703 (2013).

    Riedl, J. M. et al. Gemcitabine/nab-paclitaxel versus FOLFIRINOX for palliative first-line treatment of advanced pancreatic cancer: a propensity score analysis. Eur. J. Cancer 151, 3–13 (2021).

    Cho, I. R. et al. FOLFIRINOX vs gemcitabine/nab-paclitaxel for treatment of metastatic pancreatic cancer: single-center cohort study. World J. Gastrointest. Oncol. 12, 182–194 (2020).

    Wang-Gillam, A. et al. Nanoliposomal irinotecan with fluorouracil and folinic acid in metastatic pancreatic cancer after previous gemcitabine-based therapy (NAPOLI-1): a global, randomised, open-label, phase 3 trial. Lancet 387, 545–557 (2016).

    Nichetti, F. et al. NALIRIFOX vs FOLFIRINOX vs gemcitabine plus nab-paclitaxel as first-line treatment of advanced pancreatic cancer: an individual patient data pooled analysis of phase 3 registration trials [abstract]. J. Clin. Oncol. 41, e16262 (2023).

    Springfeld, C. et al. Neoadjuvant therapy for pancreatic cancer. Nat. Rev. Clin. Oncol. 20, 318–337 (2023).

    Cameron, J. L. & He, J. Two thousand consecutive pancreaticoduodenectomies. J. Am. Coll. Surg. 220, 530–536 (2015).

    Neoptolemos, J. P. et al. Adjuvant chemotherapy with fluorouracil plus folinic acid vs gemcitabine following pancreatic cancer resection: a randomized controlled trial. JAMA 304, 1073–1081 (2010).

    Neoptolemos, J. P. et al. Comparison of adjuvant gemcitabine and capecitabine with gemcitabine monotherapy in patients with resected pancreatic cancer (ESPAC-4): a multicentre, open-label, randomised, phase 3 trial. Lancet 389, 1011–1024 (2017).

    Neoptolemos, J. P. et al. ESPAC-4: a multicenter, international, open-label randomized controlled phase III trial of adjuvant combination chemotherapy of gemcitabine (GEM) and capecitabine (CAP) versus monotherapy gemcitabine in patients with resected pancreatic ductal adenocarcinoma: five year follow-up [abstract]. J. Clin. Oncol. 38, 4516 (2020).

    Ghaneh, P. et al. ESPAC-5F: four-arm, prospective, multicenter, international randomized phase II trial of immediate surgery compared with neoadjuvant gemcitabine plus capecitabine (GEMCAP) or FOLFIRINOX or chemoradiotherapy (CRT) in patients with borderline resectable pancreatic cancer [abstract]. J. Clin. Oncol. 38, 4505 (2020).

    Conroy, T. et al. FOLFIRINOX or gemcitabine as adjuvant therapy for pancreatic cancer. N. Engl. J. Med. 379, 2395–2406 (2018).

    Sugawara, T. et al. Association of adjuvant chemotherapy in patients with resected pancreatic adenocarcinoma after multiagent neoadjuvant chemotherapy. JAMA Oncol. 9, 316–323 (2022).

    Conroy, T. et al. Five-year outcomes of FOLFIRINOX vs gemcitabine as adjuvant therapy for pancreatic cancer: a randomized clinical trial. JAMA Oncol. 8, 1571–1578 (2022).

    Tempero, M. A. et al. Adjuvant nab-paclitaxel + gemcitabine in resected pancreatic ductal adenocarcinoma: results from a randomized, open-label, phase III trial. J. Clin. Oncol. 41, 2007–2019 (2022).

    Tempero, M. A. et al. NCCN guidelines: pancreatic adenocarcinoma. NCCN www.nccn.org/guidelines/guidelines-detail?category=1&id=1455 (2025).

    Strobel, O., Neoptolemos, J., Jäger, D. & Büchler, M. W. Optimizing the outcomes of pancreatic cancer surgery. Nat. Rev. Clin. Oncol. 16, 11–26 (2019).

    Tung, S. et al. Population-level symptom assessment following pancreaticoduodenectomy for adenocarcinoma. JAMA Surg. 154, e193348 (2019).

    Halloran, C. M. et al. A multicenter, randomized, double-blinded, clinical trial comparing Cattell–Warren and Blumgart anastomoses following partial pancreatoduodenectomy: PANasta trial. Ann. Surg. Open. 3, e198 (2022).

    Dreyer, S. B. et al. Precision oncology in surgery: patient selection for operable pancreatic cancer. Ann. Surg. 272, 366–376 (2020).

    Mackay, T. M. et al. The risk of not receiving adjuvant chemotherapy after resection of pancreatic ductal adenocarcinoma: a nationwide analysis. HPB 22, 233–240 (2020).

    Ghaneh, P. et al. The impact of positive resection margins on survival and recurrence following resection and adjuvant chemotherapy for pancreatic ductal adenocarcinoma. Ann. Surg. 269, 520–529 (2019).

    Jamieson, N. B. et al. Positive mobilization margins alone do not influence survival following pancreatico-duodenectomy for pancreatic ductal adenocarcinoma. Ann. Surg. 251, 1003–1010 (2010).

    Dreyer, S. B. et al. The impact of molecular subtyping on pathological staging of pancreatic cancer. Ann. Surg. 277, e396–e405 (2021).

    Murphy, J. E. et al. Total neoadjuvant therapy with FOLFIRINOX followed by individualized chemoradiotherapy for borderline resectable pancreatic adenocarcinoma: a phase 2 clinical trial. JAMA Oncol. 4, 963–969 (2018).

    Versteijne, E. et al. Neoadjuvant chemoradiotherapy versus upfront surgery for resectable and borderline resectable pancreatic cancer: long-term results of the Dutch randomized PREOPANC trial. J. Clin. Oncol. 40, 1220–1230 (2022).

    Murphy, J. E. et al. Total neoadjuvant therapy with FOLFIRINOX in combination with losartan followed by chemoradiotherapy for locally advanced pancreatic cancer: a phase 2 clinical trial. JAMA Oncol. https://doi.org/10.1001/jamaoncol.2019.0892 (2019).

    Groot Koerkamp, B. et al. Neoadjuvant chemotherapy with FOLFIRINOX versus neoadjuvant gemcitabine-based chemoradiotherapy for borderline resectable and resectable pancreatic cancer (PREOPANC-2): a multicenter randomized controlled trial [abstract LBA83]. Ann. Oncol. 34, S1323 (2023).

    Labori, K. J. et al. Neoadjuvant FOLFIRINOX versus upfront surgery for resectable pancreatic head cancer (NORPACT-1): a multicentre, randomised, phase 2 trial. Lancet Gastroenterol. Hepatol. 9, 205–217 (2024).

    Chawla, A. et al. Alliance A021806: a phase III trial evaluating perioperative versus adjuvant therapy for resectable pancreatic cancer [abstract]. J. Clin. Oncol. 41, TPS4204 (2023).

    van Dam, J. L. et al. Perioperative or adjuvant mFOLFIRINOX for resectable pancreatic cancer (PREOPANC-3): study protocol for a multicenter randomized controlled trial. BMC Cancer 23, 728 (2023).

    Neoptolemos, J. P. et al. A randomized trial of chemoradiotherapy and chemotherapy after resection of pancreatic cancer. N. Engl. J. Med. 350, 1200–1210 (2004).

    Hammel, P. et al. Effect of chemoradiotherapy vs chemotherapy on survival in patients with locally advanced pancreatic cancer controlled after 4 months of gemcitabine with or without erlotinib: the LAP07 randomized clinical trial. JAMA 315, 1844–1853 (2016).

    Fietkau, R. et al. Randomized phase III trial of induction chemotherapy followed by chemoradiotherapy or chemotherapy alone for nonresectable locally advanced pancreatic cancer: first results of the CONKO-007 trial [abstract]. J. Clin. Oncol. 40, 4008 (2022).

    Doleh, Y., Lal, L. S., Blauer-Petersen, C., Antico, G. & Pishvaian, M. Treatment patterns and outcomes in pancreatic cancer: retrospective claims analysis. Cancer Med. 9, 3463–3476 (2020).

    Kordes, M., Larsson, L., Engstrand, L. & Löhr, J.-M. Pancreatic cancer cachexia: three dimensions of a complex syndrome. Br. J. Cancer 124, 1623–1636 (2021).

    Mitsunaga, S., Kasamatsu, E. & Machii, K. Incidence and frequency of cancer cachexia during chemotherapy for advanced pancreatic ductal adenocarcinoma. Support. Care Cancer 28, 5271–5279 (2020).

    Kays, J. K. et al. Three cachexia phenotypes and the impact of fat-only loss on survival in FOLFIRINOX therapy for pancreatic cancer. J. Cachexia Sarcopenia Muscle 9, 673–684 (2018).

    Gerstberger, S., Jiang, Q. & Ganesh, K. Metastasis. Cell 186, 1564–1579 (2023).

    Patel, S. A., Rodrigues, P., Wesolowski, L. & Vanharanta, S. Genomic control of metastasis. Br. J. Cancer 124, 3–12 (2021).

    Bielski, C. M. et al. Genome doubling shapes the evolution and prognosis of advanced cancers. Nat. Genet. 50, 1189–1195 (2018).

    Lee, J. W. et al. Hepatocytes direct the formation of a pro-metastatic niche in the liver. Nature 567, 249–252 (2019).

    Karamitopoulou, E. et al. Spatially restricted tumour-associated and host-associated immune drivers correlate with the recurrence sites of pancreatic cancer. Gut 72, 1523–1533 (2023).

    Dreyer, S. B. et al. Genomic and molecular analyses identify molecular subtypes of pancreatic cancer recurrence. Gastroenterology 162, 320–324.e4 (2021).

    Rhim, A. D. et al. EMT and dissemination precede pancreatic tumor formation. Cell 148, 349–361 (2012).

    Grünwald, B. et al. Pancreatic premalignant lesions secrete tissue inhibitor of metalloproteinases-1, which activates hepatic stellate cells via CD63 signaling to create a premetastatic niche in the liver. Gastroenterology 151, 1011–1024.e7 (2016).

    Costa-Silva, B. et al. Pancreatic cancer exosomes initiate pre-metastatic niche formation in the liver. Nat. Cell Biol. 17, 816–826 (2015).

    Hoshino, A. et al. Tumour exosome integrins determine organotropic metastasis. Nature 527, 329–335 (2015).

    Xu, Z. et al. Role of pancreatic stellate cells in pancreatic cancer metastasis. Am. J. Pathol. 177, 2585–2596 (2010).

    Zhang, S. et al. Single cell transcriptomic analyses implicate an immunosuppressive tumor microenvironment in pancreatic cancer liver metastasis. Nat. Commun. 14, 5123 (2023).

    Bretthauer, M. & Kalager, M. Principles, effectiveness and caveats in screening for cancer. Br. J. Surg. 100, 55–65 (2013).

    Yachida, S. et al. Distant metastasis occurs late during the genetic evolution of pancreatic cancer. Nature 467, 1114–1117 (2010).

    Overbeek, K. A. et al. Timeline of development of pancreatic cancer and implications for successful early detection in high-risk individuals. Gastroenterology 162, 772–785.e4 (2022).

    Yu, J., Blackford, A. L., Dal Molin, M., Wolfgang, C. L. & Goggins, M. Time to progression of pancreatic ductal adenocarcinoma from low-to-high tumour stages. Gut 64, 1783–1789 (2015).

    Notta, F. et al. A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns. Nature 538, 378–382 (2016).

    Crippa, S. et al. Mucin-producing neoplasms of the pancreas: an analysis of distinguishing clinical and epidemiologic characteristics. Clin. Gastroenterol. Hepatol. 8, 213–219 (2010).

    Goh, B. K. P. et al. A review of mucinous cystic neoplasms of the pancreas defined by ovarian-type stroma: clinicopathological features of 344 patients. World J. Surg. 30, 2236–2245 (2006).

    Nilsson, L. N. et al. Nature and management of pancreatic mucinous cystic neoplasm (MCN): a systematic review of the literature. Pancreatology 16, 1028–1036 (2016).

    Park, J. W. et al. Mucinous cystic neoplasm of the pancreas: is surgical resection recommended for all surgically fit patients? Pancreatology 14, 131–136 (2014).

    Springer, S. et al. A combination of molecular markers and clinical features improve the classification of pancreatic cysts. Gastroenterology 149, 1501–1510 (2015).

    Lennon, A. M. & Canto, M. I. Pancreatic cysts – part 2: should we be less cyst centric? Pancreas 46, 745–750 (2017).

    Marchegiani, G. et al. Surveillance for presumed BD-IPMN of the pancreas: stability, size, and age identify targets for discontinuation. Gastroenterology 165, 1016–1024.e5 (2023).

    Pezzilli, R. et al. Epidemiology, clinical features and diagnostic work-up of cystic neoplasms of the pancreas: interim analysis of the prospective PANCY survey. Dig. Liver Dis. 52, 547–554 (2020).

    Marchegiani, G. et al. IPMN involving the main pancreatic duct: biology, epidemiology, and long-term outcomes following resection. Ann. Surg. 261, 976–983 (2015).

    Hata, T. et al. Genome-wide somatic copy number alterations and mutations in high-grade pancreatic intraepithelial neoplasia. Am. J. Pathol. 188, 1723–1733 (2018).

    Braxton, A. M. et al. 3D genomic mapping reveals multifocality of human pancreatic precancers. Nature 629, 679–687 (2024).

    Søreide, K. & Marchegiani, G. Clinical management of pancreatic premalignant lesions. Gastroenterology 162, 379–384 (2022).

    Søreide, K., Ismail, W., Roalsø, M., Ghotbi, J. & Zaharia, C. Early diagnosis of pancreatic cancer: clinical premonitions, timely precursor detection and increased curative-intent surgery. Cancer Control. 30, 10732748231154711 (2023).

    Cao, K. et al. Large-scale pancreatic cancer detection via non-contrast CT and deep learning. Nat. Med 29, 3033–3043 (2023).

    Goggins, M. et al. Management of patients with increased risk for familial pancreatic cancer: updated recommendations from the International Cancer of the Pancreas Screening (CAPS) Consortium. Gut 69, 7–17 (2019).

    Henrikson, N. B. et al. Screening for pancreatic cancer: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA 322, 445–454 (2019).

    Vasen, H. et al. Benefit of surveillance for pancreatic cancer in high-risk individuals: outcome of long-term prospective follow-up studies from three European expert centers. J. Clin. Oncol. 34, 2010–2019 (2016).

    Oldfield, L. et al. United Kingdom Early Detection Initiative (UK-EDI): protocol for establishing a national multicentre cohort of individuals with new-onset diabetes for early detection of pancreatic cancer. BMJ Open. 12, e068010 (2022).

    US Preventive Services Task Force. Screening for pancreatic cancer: US Preventive Services Task Force reaffirmation recommendation statement. JAMA 322, 438–444 (2019).

    Ferrer, M. et al. Cachexia: a systemic consequence of progressive, unresolved disease. Cell 186, 1824–1845 (2023).

    Roberts, K. J., Bannister, C. A. & Schrem, H. Enzyme replacement improves survival among patients with pancreatic cancer: results of a population based study. Pancreatology 19, 114–121 (2019).

    Roberts, K. J. et al. Pancreas exocrine replacement therapy is associated with increased survival following pancreatoduodenectomy for periampullary malignancy. HPB 19, 859–867 (2017).

    Abraham, J. P. et al. Clinical validation of a machine-learning-derived signature predictive of outcomes from first-line oxaliplatin-based chemotherapy in advanced colorectal cancer. Clin. Cancer Res. 27, 1174–1183 (2021).

    Graham, J. S. et al. PRIMUS-001: an adaptive phase II study of FOLFOX-A (FOLFOX and nab-paclitaxel) versus AG (nab-paclitaxel and gemcitabine) in patients with metastatic pancreatic cancer, with integrated biomarker evaluation (ISRCTN75002153) – part of Precision-Panc [abstract]. J. Clin. Oncol. 36, TPS4158 (2018).

    Dreyer, S. B. et al. PRECISION-panc: the next generation therapeutic development platform for pancreatic cancer. Clin. Oncol. 32, 1–4 (2020).

    Dreyer, S. B. et al. Pancreatic cancer: from genome discovery to PRECISION-panc. Clin. Oncol. 32, 5–8 (2020).

    Knox, J. J. et al. PASS-01: pancreatic adenocarcinoma signature stratification for treatment–01 [abstract]. J. Clin. Oncol. 40, TPS635 (2022).

    Dreyer, S. B. et al. Targeting DNA damage response and replication stress in pancreatic cancer. Gastroenterology 160, 362–377.e13 (2021).

    Dreyer, S. B., Chang, D. K., Bailey, P. & Biankin, A. V. Pancreatic cancer genomes: implications for clinical management and therapeutic development. Clin. Cancer Res. 23, 1638–1646 (2017).

    Waddell, N. et al. Whole genomes redefine the mutational landscape of pancreatic cancer. Nature 518, 495–501 (2015).

    Casolino, R. et al. Homologous recombination deficiency in pancreatic cancer: a systematic review and prevalence meta-analysis. J. Clin. Oncol. 39, 2617–2631 (2021).

    ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium. Pan-cancer analysis of whole genomes. Nature 578, 82–93 (2020).

    Golan, T. et al. Maintenance olaparib for germline BRCA-mutated metastatic pancreatic cancer. N. Engl. J. Med. 381, 317–327 (2019).

    Kindler, H. L. et al. Overall survival results from the POLO trial: a phase III study of active maintenance olaparib versus placebo for germline BRCA-mutated metastatic pancreatic cancer. J. Clin. Oncol. 40, 3929–3939 (2022).

    Batalini, F. et al. Homologous recombination deficiency landscape of breast cancers and real-world effectiveness of poly ADP-ribose polymerase inhibitors in patients with somatic BRCA1/2, germline PALB2, or homologous recombination deficiency signature. JCO Precis. Oncol. 7, e2300091 (2023).

    Moore, K. et al. Maintenance olaparib in patients with newly diagnosed advanced ovarian cancer. N. Engl. J. Med. 379, 2495–2505 (2018).

    Davies, H. et al. HRDetect is a predictor of BRCA1 and BRCA2 deficiency based on mutational signatures. Nat. Med. 23, 517–525 (2017).

    Chopra, N. et al. Homologous recombination DNA repair deficiency and PARP inhibition activity in primary triple negative breast cancer. Nat. Commun. 11, 2662 (2020).

    González-Martín, A. et al. Niraparib in patients with newly diagnosed advanced ovarian cancer. N. Engl. J. Med. 381, 2391–2402 (2019).

    Bailey, P. et al. Genomic analyses identify molecular subtypes of pancreatic cancer. Nature 531, 47–52 (2016).

    Biankin, A. V. et al. Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes. Nature 491, 399–405 (2012).

    Cancer Genome Atlas Research Network. Integrated genomic characterization of pancreatic ductal adenocarcinoma. Cancer Cell 32, 185–203.e13 (2017).

    Clark, C. E. et al. Dynamics of the immune reaction to pancreatic cancer from inception to invasion. Cancer Res. 67, 9518–9527 (2007).

    Cullis, J., Das, S. & Bar-Sagi, D. Kras and tumor immunity: friend or foe? Cold Spring Harb. Perspect. Med. 8, a031849 (2018).

    Chan-Seng-Yue, M. et al. Transcription phenotypes of pancreatic cancer are driven by genomic events during tumor evolution. Nat. Genet. 52, 463 (2020).

    Connor, A. A. et al. Integration of genomic and transcriptional features in pancreatic cancer reveals increased cell cycle progression in metastases. Cancer Cell 35, 267–282.e7 (2019).

    Link, J. M. et al. Ongoing replication stress tolerance and clonal T cell responses distinguish liver and lung recurrence and outcomes in pancreatic cancer. Nat. Cancer 6, 123–144 (2025).

    Moffitt, R. A. et al. Virtual microdissection identifies distinct tumor- and stroma-specific subtypes of pancreatic ductal adenocarcinoma. Nat. Genet. 47, 1168–1178 (2015).

    Collisson, E. A., Bailey, P., Chang, D. K. & Biankin, A. V. Molecular subtypes of pancreatic cancer. Nat. Rev. Gastroenterol. Hepatol. 16, 207–220 (2019).

    Collisson, E. A. et al. Subtypes of pancreatic ductal adenocarcinoma and their differing responses to therapy. Nat. Med. 17, 500–503 (2011).

    Brunton, H. et al. HNF4A and GATA6 loss reveals therapeutically actionable subtypes in pancreatic cancer. Cell Rep. 31, 107625 (2020).

    George, B. et al. Transcriptomic-based microenvironment classification reveals precision medicine strategies for pancreatic ductal adenocarcinoma. Gastroenterology 166, 859–871.e3 (2024).

    Wang, Y. et al. Single-cell analysis of pancreatic ductal adenocarcinoma identifies a novel fibroblast subtype associated with poor prognosis but better immunotherapy response. Cell Discov. 7, 36 (2021).

    Rashid, N. U. et al. Purity independent subtyping of tumors (PurIST), a clinically robust, single-sample classifier for tumor subtyping in pancreatic cancer. Clin. Cancer Res. 26, 82–92 (2019).

    O’Kane, G. M. et al. GATA6 expression distinguishes classical and basal-like subtypes in advanced pancreatic cancer. Clin. Cancer Res. 26, 4901–4910 (2020).

    Grünwald, B. T. et al. Spatially confined sub-tumor microenvironments in pancreatic cancer. Cell 184, 5577–5592 (2021).

    Hingorani, S. R. Epithelial and stromal co-evolution and complicity in pancreatic cancer. Nat. Rev. Cancer 23, 57–77 (2023).

    Topham, J. T. et al. Subtype-discordant pancreatic ductal adenocarcinoma tumors show intermediate clinical and molecular characteristics. Clin. Cancer Res. 27, 150–157 (2021).

    Candido, J. B. et al. CSF1R+ macrophages sustain pancreatic tumor growth through T cell suppression and maintenance of key gene programs that define the squamous subtype. Cell Rep. 23, 1448–1460 (2018).

    Chou, A. et al. Clinical and molecular characterization of HER2 amplified-pancreatic cancer. Genome Med. 5, 78 (2013).

    Strickler, J. H. et al. Sotorasib in KRAS p.G12C-mutated advanced pancreatic cancer. N. Engl. J. Med. 388, 33–43 (2023).

    Sacher, A. et al. Single-agent divarasib (GDC-6036) in solid tumors with a KRAS G12C mutation. N. Engl. J. Med. 389, 710–721 (2023).

    Bekaii-Saab, T. S. et al. Adagrasib in advanced solid tumors harboring a KRASG12C mutation. J. Clin. Oncol. 41, 4097–4106 (2023).

    Lito, P., Solomon, M., Li, L.-S., Hansen, R. & Rosen, N. Allele-specific inhibitors inactivate mutant KRAS G12C by a trapping mechanism. Science 351, 604–608 (2016).

    Kemp, S. B. et al. Efficacy of a small-molecule inhibitor of KrasG12D in immunocompetent models of pancreatic cancer. Cancer Discov. 13, 298–311 (2023).

    Park, W. et al. Preliminary safety and clinical activity of ASP3082, a first-in-class, KRAS G12D selective protein degrader in adults with advanced pancreatic (PC), colorectal (CRC), and non-small cell lung cancer (NSCLC) [abstract 608O]. Ann. Oncol. 35, S486–S487 (2024).

    Hallin, J. et al. Anti-tumor efficacy of a potent and selective non-covalent KRASG12D inhibitor. Nat. Med. 28, 2171–2182 (2022).

    Singhal, A., Li, B. T. & O’Reilly, E. M. Targeting KRAS in cancer. Nat. Med. 30, 969–983 (2024).

    Wasko, U. N. et al. Tumour-selective activity of RAS-GTP inhibition in pancreatic cancer. Nature 629, 927–936 (2024).

    Arbour, K. C. et al. Preliminary clinical activity of RMC-6236, a first-in-class, RAS-selective, tri-complex RAS-MULTI(ON) inhibitor in patients with KRAS mutant pancreatic ductal adenocarcinoma (PDAC) and non-small cell lung cancer (NSCLC) [abstract 652O]. Ann. Oncol. 34, S458 (2023).

    Jiang, J. et al. Translational and therapeutic evaluation of RAS-GTP inhibition by RMC-6236 in RAS-driven cancers. Cancer Discov. 14, 994–1017 (2024).

    Gulay, K. C. M. et al. Dual Inhibition of KRASG12D and pan-ERBB is synergistic in pancreatic ductal adenocarcinoma. Cancer Res. 83, 3001–3012 (2023).

    Huynh, M. V. et al. Functional and biological heterogeneity of KRASQ61 mutations. Sci. Signal. 15, eabn2694 (2022).

    Hobbs, G. A. et al. Atypical KRASG12R mutant is impaired in PI3K signaling and macropinocytosis in pancreatic cancer. Cancer Discov. 10, 104–123 (2020).

    Masuishi, T. et al. Sotorasib (Soto) + panitumumab (Pmab) and FOLFIRI in previously treated KRASG12C-mutated metastatic colorectal cancer (mCRC): safety and efficacy for CodeBreaK 101 phase Ib expansion cohort [abstract 92MO]. Ann. Oncol. 34, S1505 (2023).

    Mugarza, E. et al. Therapeutic KRASG12C inhibition drives effective interferon-mediated antitumor immunity in immunogenic lung cancers. Sci. Adv. 8, eabm8780 (2022).

    Simnica, D. & Kobold, S. Neoantigen T-cell receptor gene therapy in pancreatic cancer. N. Engl. J. Med. 387, 573 (2022).

    Sim, M. J. W. et al. High-affinity oligoclonal TCRs define effective adoptive T cell therapy targeting mutant KRAS-G12D. Proc. Natl Acad. Sci. USA 117, 12826–12835 (2020).

    Poole, A. et al. Therapeutic high affinity T cell receptor targeting a KRASG12D cancer neoantigen. Nat. Commun. 13, 5333 (2022).

    Lu, D. et al. KRAS G12V neoantigen specific T cell receptor for adoptive T cell therapy against tumors. Nat. Commun. 14, 6389 (2023).

    Huff, A. L. et al. A pooled mutant KRAS peptide vaccine activates polyfunctional T cell responses in patients with resected pancreatic cancer [abstract]. Cancer Res. 83, LB197 (2023).

    Haldar, S. D. et al. Mutant KRAS peptide-based vaccine in patients at high risk of developing pancreatic cancer: preliminary analysis from a phase I study [abstract]. Cancer Res. 84, CT022 (2024).

    Provenzano, P. P. et al. Enzymatic targeting of the stroma ablates physical barriers to treatment of pancreatic ductal adenocarcinoma. Cancer Cell 21, 418–429 (2012).

    DuFort, C. C. et al. Interstitial pressure in pancreatic ductal adenocarcinoma is dominated by a gel-fluid phase. Biophys. J. 110, 2106–2119 (2016).

    Hingorani, S. R. et al. Phase Ib study of PEGylated recombinant human hyaluronidase and gemcitabine in patients with advanced pancreatic cancer. Clin. Cancer Res. 22, 2848–2854 (2016).

    Hingorani, S. R. et al. HALO 202: randomized phase II study of PEGPH20 plus nab-paclitaxel/gemcitabine versus nab-paclitaxel/gemcitabine in patients with untreated, metastatic pancreatic ductal adenocarcinoma. J. Clin. Oncol. 36, 359–366 (2018).

    Van Cutsem, E. et al. Randomized phase III trial of pegvorhyaluronidase alfa with nab-paclitaxel plus gemcitabine for patients with hyaluronan-high metastatic pancreatic adenocarcinoma. J. Clin. Oncol. 38, 3185–3194 (2020).

    Lander, V. E. et al. Stromal reprogramming by FAK inhibition overcomes radiation resistance to allow for immune priming and response to checkpoint blockade. Cancer Discov. 12, 2774–2799 (2022).

    Biffi, G. et al. IL1-Induced JAK/STAT signaling is antagonized by TGFβ to shape CAF heterogeneity in pancreatic ductal adenocarcinoma. Cancer Discov. 9, 282–301 (2019).

    Öhlund, D. et al. Distinct populations of inflammatory fibroblasts and myofibroblasts in pancreatic cancer. J. Exp. Med. 214, 579–596 (2017).

    Bryce, A. S., Dreyer, S. B., Froeling, F. E. M. & Chang, D. K. Exploring the biology of cancer-associated fibroblasts in pancreatic cancer. Cancers 14, 5302 (2022).

    Lee, B. Y. et al. Heterocellular OSM-OSMR signalling reprograms fibroblasts to promote pancreatic cancer growth and metastasis. Nat. Commun. 12, 7336 (2021).

    Hutton, C. et al. Single-cell analysis defines a pancreatic fibroblast lineage that supports anti-tumor immunity. Cancer Cell 39, 1227–1244.e20 (2021).

    Biffi, G. & Tuveson, D. A. Diversity and biology of cancer-associated fibroblasts. Physiol. Rev. 101, 147–176 (2021).

    Elyada, E. et al. Cross-species single-cell analysis of pancreatic ductal adenocarcinoma reveals antigen-presenting cancer-associated fibroblasts. Cancer Discov. 9, 1102–1123 (2019).

    Chen, K. et al. Single-cell RNA-seq reveals dynamic change in tumor microenvironment during pancreatic ductal adenocarcinoma malignant progression. eBioMedicine 66, 103315 (2021).

    Froeling, F. E. M. et al. Retinoic acid-induced pancreatic stellate cell quiescence reduces paracrine Wnt-β-catenin signaling to slow tumor progression. Gastroenterology 141, 1486–1497.e14 (2011).

    Hingorani, S. R. et al. Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice. Cancer Cell 7, 469–483 (2005).

    Sherman, M. H. et al. Vitamin D receptor-mediated stromal reprogramming suppresses pancreatitis and enhances pancreatic cancer therapy. Cell 159, 80–93 (2014).

    Gorchs, L. et al. The vitamin D analogue calcipotriol promotes an anti-tumorigenic phenotype of human pancreatic CAFs but reduces T cell mediated immunity. Sci. Rep. 10, 17444 (2020).

    Balachandran, V. P., Beatty, G. L. & Dougan, S. K. Broadening the impact of immunotherapy to pancreatic cancer: challenges and opportunities. Gastroenterology 156, 2056–2072 (2019).

    Garcia Garcia, C. J. et al. Stromal HIF2 regulates immune suppression in the pancreatic cancer microenvironment. Gastroenterology 162, 2018–2031 (2022).

    Huang, H. et al. Mesothelial cell-derived antigen-presenting cancer-associated fibroblasts induce expansion of regulatory T cells in pancreatic cancer. Cancer Cell 40, 656–673.e7 (2022).

    Ho, W. J., Jaffee, E. M. & Zheng, L. The tumour microenvironment in pancreatic cancer – clinical challenges and opportunities. Nat. Rev. Clin. Oncol. 17, 527–540 (2020).

    Danilova, L. et al. Programmed cell death ligand-1 (PD-L1) and CD8 expression profiling identify an immunologic subtype of pancreatic ductal adenocarcinomas with favorable survival. Cancer Immunol. Res. 7, 886–895 (2019).

    Hiraoka, N., Onozato, K., Kosuge, T. & Hirohashi, S. Prevalence of FOXP3+ regulatory T cells increases during the progression of pancreatic ductal adenocarcinoma and its premalignant lesions. Clin. Cancer Res. 12, 5423–5434 (2006).

    Kobayashi, N. et al. FOXP3+ regulatory T cells and tumoral indoleamine 2,3-dioxygenase expression predicts the carcinogenesis of intraductal papillary mucinous neoplasms of the pancreas. Pancreatology 10, 631–640 (2010).

    Mota Reyes, C. et al. Regulatory T cells in pancreatic cancer: of mice and men. Cancers 14, 4582 (2022).

    Dawod, B. et al. Myeloid-derived suppressor cell depletion therapy targets IL-17A-expressing mammary carcinomas. Sci. Rep. 10, 13343 (2020).

    Joshi, N. S. et al. Regulatory T cells in tumor-associated tertiary lymphoid structures suppress anti-tumor T cell responses. Immunity 43, 579–590 (2015).

    Jang, J.-E. et al. Crosstalk between regulatory T cells and tumor-associated dendritic cells negates anti-tumor immunity in pancreatic cancer. Cell Rep. 20, 558–571 (2017).

    Lee, J. W., Komar, C. A., Bengsch, F., Graham, K. & Beatty, G. L. Genetically engineered mouse models of pancreatic cancer: the KPC model (LSL-KrasG12D/+;LSL-Trp53R172H/+;Pdx-1-cre), its variants, and their application in immuno-oncology drug discovery. Curr. Protoc. Pharmacol. 73, 14.39.1–14.39.20 (2016).

    Stromnes, I. M. et al. Targeted depletion of an MDSC subset unmasks pancreatic ductal adenocarcinoma to adaptive immunity. Gut 63, 1769–1781 (2014).

    Steele, C. W. et al. CXCR2 inhibition profoundly suppresses metastases and augments immunotherapy in pancreatic ductal adenocarcinoma. Cancer Cell 29, 832–845 (2016).

    US National Library of Medicine. ClinicalTrials.gov clinicaltrials.gov/study/NCT02583477?tab=results (2019).

    Väyrynen, S. A. et al. Composition, spatial characteristics, and prognostic significance of myeloid cell infiltration in pancreatic cancer. Clin. Cancer Res. 27, 1069–1081 (2021).

    Kersten, K. et al. Spatiotemporal co-dependency between macrophages and exhausted CD8+ T cells in cancer. Cancer Cell 40, 624–638.e9 (2022).

    Caronni, N. et al. IL-1β+ macrophages fuel pathogenic inflammation in pancreatic cancer. Nature 623, 415–422 (2023).

    Zhu, Y. et al. CSF1/CSF1R blockade reprograms tumor-infiltrating macrophages and improves response to T-cell checkpoint immunotherapy in pancreatic cancer models. Cancer Res. 74, 5057–5069 (2014).

    Alonso-Nocelo, M. et al. Macrophages direct cancer cells through a LOXL2-mediated metastatic cascade in pancreatic ductal adenocarcinoma. Gut 72, 345–359 (2022).

    Bellomo, G. et al. Chemotherapy-induced infiltration of neutrophils promotes pancreatic cancer metastasis via Gas6/AXL signalling axis. Gut 71, 2284–2299 (2022).

    Sun, X. et al. Inflammatory cell-derived CXCL3 promotes pancreatic cancer metastasis through a novel myofibroblast-hijacked cancer escape mechanism. Gut 71, 129–147 (2021).

    van Eijck, C. W. F. et al. Enhanced antitumour immunity following neoadjuvant chemoradiotherapy mediates a favourable prognosis in women with resected pancreatic cancer. Gut 73, 311–324 (2023).

    Halbrook, C. J. et al. Macrophage-released pyrimidines inhibit gemcitabine therapy in pancreatic cancer. Cell Metab. 29, 1390–1399.e6 (2019).

    Dixit, A. et al. Targeting TNF-α-producing macrophages activates antitumor immunity in pancreatic cancer via IL-33 signaling. JCI Insight 7, e153242 (2022).

    Datta, J. et al. Combined MEK and STAT3 inhibition uncovers stromal plasticity by enriching for cancer-associated fibroblasts with mesenchymal stem cell-like features to overcome immunotherapy resistance in pancreatic cancer. Gastroenterology 163, 1593–1612 (2022).

    Beatty, G. L. et al. CD40 agonists alter tumor stroma and show efficacy against pancreatic carcinoma in mice and humans. Science 331, 1612–1616 (2011).

    Hallett, R. M. et al. Therapeutic targeting of LIF overcomes macrophage-mediated immunosuppression of the local tumor microenvironment. Clin. Cancer Res. 29, 791–804 (2023).

    Ho, W. J. et al. Multi-omic profiling of lung and liver tumor microenvironments of metastatic pancreatic cancer reveals site-specific immune regulatory pathways. Genome Biol. 22, 154 (2021).

    Yang, J. et al. Integrated genomic and transcriptomic analysis reveals unique characteristics of hepatic metastases and pro-metastatic role of complement C1q in pancreatic ductal adenocarcinoma. Genome Biol. 22, 4 (2021).

    Zhang, Y. et al. PD-L1 and PD-L2 expression in pancreatic ductal adenocarcinoma and their correlation with immune infiltrates and DNA damage response molecules. J. Pathol. Clin. Res. 8, 257–267 (2022).

    Ott, P. A. et al. T-cell-inflamed gene-expression profile, programmed death ligand 1 expression, and tumor mutational burden predict efficacy in patients treated with pembrolizumab across 20 cancers: KEYNOTE-028. J. Clin. Oncol. 37, 318–327 (2019).

    Coston, T. et al. Efficacy of immune checkpoint inhibition and cytotoxic chemotherapy in mismatch repair-deficient and microsatellite instability-high pancreatic cancer: Mayo Clinic experience. JCO Precis. Oncol. 7, e2200706 (2023).

    Taïeb, J. et al. Efficacy of immune checkpoint inhibitors in microsatellite unstable/mismatch repair-deficient advanced pancreatic adenocarcinoma: an AGEO European Cohort. Eur. J. Cancer 188, 90–97 (2023).

    O’Connor, C. A. et al. Lynch syndrome and somatic mismatch repair variants in pancreas cancer. JAMA Oncol. 10, 1511–1518 (2024).

    Humphris, J. L. et al. Hypermutation in pancreatic cancer. Gastroenterology 152, 68–74.e2 (2017).

    Balachandran, V. P. et al. Identification of unique neoantigen qualities in long-term survivors of pancreatic cancer. Nature 551, 512–516 (2017).

    Łuksza, M. et al. Neoantigen quality predicts immunoediting in survivors of pancreatic cancer. Nature 606, 389–395 (2022).

    Quintanilha, J. C. F. et al. Tumor mutational burden in real-world patients with pancreatic cancer: genomic alterations and predictive value for immune checkpoint inhibitor effectiveness. JCO Precis. Oncol. 7, e2300092 (2023).

    Marabelle, A. et al. Efficacy of pembrolizumab in patients with noncolorectal high microsatellite instability/mismatch repair-deficient cancer: results from the phase II KEYNOTE-158 study. J. Clin. Oncol. 38, 1–10 (2020).

    Maio, M. et al. Pembrolizumab in microsatellite instability high or mismatch repair deficient cancers: updated analysis from the phase II KEYNOTE-158 study. Ann. Oncol. 33, 929–938 (2022).

    Grant, R. C. et al. Clinical and genomic characterisation of mismatch repair deficient pancreatic adenocarcinoma. Gut 70, 1894–1903 (2021).

    Terrero, G. et al. Ipilimumab/nivolumab therapy in patients with metastatic pancreatic or biliary cancer with homologous recombination deficiency pathogenic germline variants. JAMA Oncol. 8, 1–3 (2022).

    Chung, V. et al. Randomized phase II trial of olaparib + pembrolizumab vs olaparib alone as maintenance therapy in metastatic pancreatic cancer patients with germline BRCA1 or BRCA2 (gBRCA1/2+) pathogenic variants: SWOG S2001 [abstract]. J. Clin. Oncol. 41, TPS4198 (2023).

    Macarulla, T. et al. Olaparib and durvalumab (MEDI4736) phase II study in patients with metastatic pancreatic cancer and DNA damage repair genes alterations [abstract 1686TiP]. Ann. Oncol. 34, S923 (2023).

    Wainberg, Z. A. et al. Open-label, phase I study of nivolumab combined with nab-paclitaxel plus gemcitabine in advanced pancreatic cancer. Clin. Cancer Res. 26, 4814–4822 (2020).

    Wang-Gillam, A. et al. A randomized phase II study of cabiralizumab (cabira) + nivolumab (nivo) ± chemotherapy (chemo) in advanced pancreatic ductal adenocarcinoma (PDAC) [abstract]. J. Clin. Oncol. 37, TPS465 (2019).

    O’Hara, M. H. et al. CD40 agonistic monoclonal antibody APX005M (sotigalimab) and chemotherapy, with or without nivolumab, for the treatment of metastatic pancreatic adenocarcinoma: an open-label, multicentre, phase 1b study. Lancet Oncol. 22, 118–131 (2021).

    Padrón, L. J. et al. Sotigalimab and/or nivolumab with chemotherapy in first-line metastatic pancreatic cancer: clinical and immunologic analyses from the randomized phase 2 PRINCE trial. Nat. Med. 28, 1167–1177 (2022).

    Borazanci, E. et al. Phase I, first-in-human study of MSC-1 (AZD0171), a humanized anti-leukemia inhibitory factor monoclonal antibody, for advanced solid tumors. ESMO Open. 7, 100530 (2022).

    Davelaar, J. et al. Trial in progress: a randomized phase II study of pembrolizumab with or without defactinib, a focal adhesion kinase inhibitor, following chemotherapy as a neoadjuvant and adjuvant treatment for resectable pancreatic ductal adenocarcinoma (PDAC) [abstract]. J. Clin. Oncol. 40, TPS4192 (2022).

    Kocher, H. M. et al. Phase I clinical trial repurposing all-trans retinoic acid as a stromal targeting agent for pancreatic cancer. Nat. Commun. 11, 4841 (2020).

    Perez, K. et al. Vitamin D receptor agonist paricalcitol plus gemcitabine and nab-paclitaxel in patients with metastatic pancreatic cancer [abstract]. J. Clin. Oncol. 38, TPS784 (2020).

    Rojas, L. A. et al. Personalized RNA neoantigen vaccines stimulate T cells in pancreatic cancer. Nature 618, 144–150 (2023).

    Sethna, Z. et al. RNA neoantigen vaccines prime long-lived CD8+ T cells in pancreatic cancer. Nature 639, 1042–1051 (2025).

    Brown, T. J., Reiss, K. A. & O’Hara, M. H. Advancements in systemic therapy for pancreatic cancer. Am. Soc. Clin. Oncol. Educ. Book. 43, e397082 (2023).

    Bazan-Peregrino, M. et al. VCN-01 disrupts pancreatic cancer stroma and exerts antitumor effects. J. Immunother. Cancer 9, e003254 (2021).

    da Costa, A. A. B. A., Chowdhury, D., Shapiro, G. I., D’Andrea, A. D. & Konstantinopoulos, P. A. Targeting replication stress in cancer therapy. Nat. Rev. Drug. Discov. 22, 38–58 (2022).

    Philip, P. A. et al. Phase III study comparing gemcitabine plus cetuximab versus gemcitabine in patients with advanced pancreatic adenocarcinoma: Southwest Oncology Group-directed intergroup trial S0205. J. Clin. Oncol. 28, 3605–3610 (2010).

    Qin, S. et al. Nimotuzumab plus gemcitabine for K-Ras wild-type locally advanced or metastatic pancreatic cancer. J. Clin. Oncol. 41, 5163–5173 (2023).

    Singhi, A. D. et al. Real-time targeted genome profile analysis of pancreatic ductal adenocarcinomas identifies genetic alterations that might be targeted with existing drugs or used as biomarkers. Gastroenterology 156, 2242–2253.e4 (2019).

    Luchini, C. et al. KRAS wild-type pancreatic ductal adenocarcinoma: molecular pathology and therapeutic opportunities. J. Exp. Clin. Cancer Res. 39, 227 (2020).

    Subbiah, V. et al. Tumour-agnostic efficacy and safety of selpercatinib in patients with RET fusion-positive solid tumours other than lung or thyroid tumours (LIBRETTO-001): a phase 1/2, open-label, basket trial. Lancet Oncol. 23, 1261–1273 (2022).

    Doebele, R. C. et al. Entrectinib in patients with advanced or metastatic NTRK fusion-positive solid tumours: integrated analysis of three phase 1-2 trials. Lancet Oncol. 21, 271–282 (2020).

    O’Reilly, E. M. & Hechtman, J. F. Tumour response to TRK inhibition in a patient with pancreatic adenocarcinoma harbouring an NTRK gene fusion. Ann. Oncol. 30, viii36–viii40 (2019).

    Heining, C. et al. NRG1 fusions in KRAS wild-type pancreatic cancer. Cancer Discov. 8, 1087–1095 (2018).

    Patil, T. et al. CRESTONE: a phase 2 study of seribantumab in adult patients with neuregulin-1 (NRG1) fusion positive locally advanced or metastatic solid tumors [abstract CT229]. Cancer Res. 83, CT229 (2023).

    Schram, A. M. et al. Zenocutuzumab, a HER2xHER3 bispecific antibody, is effective therapy for tumors driven by NRG1 gene rearrangements. Cancer Discov. 12, 1233–1247 (2022).

    Katayama, E. S. et al. A comprehensive analysis of clinical trials in pancreatic cancer: what is coming down the pike? Oncotarget 11, 3489–3501 (2020).

    Pryce, B. R., Wang, D. J., Zimmers, T. A., Ostrowski, M. C. & Guttridge, D. C. Cancer cachexia: involvement of an expanding macroenvironment. Cancer Cell 41, 581–584 (2023).

    Ouimet, C., Fodor, B., Del Paggio, J. C. & Kimmelman, J. Proportion of patients in phase 2 oncology trials receiving treatments that are ultimately approved. J. Natl Cancer Inst. https://doi.org/10.1093/jnci/djaf013 (2025).

    Marron, T. U. et al. Neoadjuvant clinical trials provide a window of opportunity for cancer drug discovery. Nat. Med. 28, 626–629 (2022).

    Mills, E. J. et al. Design, analysis, and presentation of crossover trials. Trials 10, 27 (2009).

    Wainberg, Z. A. et al. NALIRIFOX versus nab-paclitaxel and gemcitabine in treatment-naive patients with metastatic pancreatic ductal adenocarcinoma (NAPOLI 3): a randomised, open-label, phase 3 trial. Lancet 402, 1272–1281 (2023).

    Versteijne, E. et al. Preoperative chemoradiotherapy versus immediate surgery for resectable and borderline resectable pancreatic cancer: results of the Dutch randomized phase III PREOPANC trial. J. Clin. Oncol. 38, 1763–1773 (2020).

    Beer, P. A., Cooke, S. L., Chang, D. K. & Biankin, A. V. Defining the clinical genomic landscape for real-world precision oncology. Genomics 112, 5324–5330 (2020).

  • cancer without fear

    Cancer continues to be a formidable global health challenge, ranking as one of the leading causes of death worldwide. The good news is that early detection and preventive care significantly boost survival rates, often making the difference between life and death. Enter OncoPreventer, an innovative AI-powered assistant designed to revolutionize cancer prevention and early detection. By harnessing the power of artificial intelligence, OncoPreventer empowers individuals to take control of their health proactively, offering a personalized and interactive approach that adapts to each user's unique needs and lifestyles. This cutting-edge technology embodies the future of personalized medicine—where health strategies are not one-size-fits-all but tailored, dynamic, and user-friendly.

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    Source

  • ALX Oncology Reports First Quarter 2025 Financial Results and Provides Corporate Update

    Following announcement of prioritized development strategy for evorpacept in combination with anti-cancer antibodies at R&D Day in March, Company is on track to initiate Phase 2 ASPEN-Breast and Phase 1 ASPEN-CRC studies in mid-2025

    IND clearance received from U.S. FDA for novel EGFR-targeted antibody-drug conjugate (ADC), ALX2004, paving way for mid-year clinical program initiation; Company to host webcast focused on ALX2004 research program on May 20

    Company will not pursue U.S. registrational path in gastric cancer following receipt of FDA feedback that accelerated approval pathway is not feasible based on ASPEN-06 due to standard-of-care evolving to ENHERTU®

    Data milestones expected across Company’s three clinical programs in 2026

    Cash runway has been extended into Q4 2026

    SOUTH SAN FRANCISCO, Calif., May 08, 2025 (GLOBE NEWSWIRE) — ALX Oncology Holdings Inc., (“ALX Oncology” or “the Company”) (Nasdaq: ALXO), a clinical-stage biotechnology company advancing a pipeline of novel therapies designed to treat cancer and extend patients’ lives, today reported financial results for the first quarter ended March 31, 2025, and provided a corporate update.

    “In the first quarter of the year, we focused our development strategy for evorpacept on the anti-cancer antibody combinations, as we now have proof-of-concept for this mechanism in gastric cancer, breast cancer and NHL,” said Jason Lettmann, Chief Executive Officer of ALX Oncology. “In addition to the evorpacept program, we diversified our pipeline by moving our in-house ADC candidate, ALX2004, through IND clearance and look forward to beginning clinical trial enrollment by mid-year for this potentially first- and best-in-class EGFR ADC. We also made the difficult but critical decision to streamline the company and, by doing so, extended cash runway into Q4 2026. We are now hyper-focused on pursuing the validated mechanism of action for evorpacept in combination with anti-cancer antibodies and delivering data in breast cancer in combination with HERCEPTIN®, in colorectal cancer in combination with ERBITUX®, as well as from ALX2004, in 2026.”

    ALX Oncology Q1 2025 Highlights and Recent Developments

    Received Investigational New Drug (IND) clearance for ALX2004 from the U.S. Food and Drug Administration (FDA). ALX2004 is a potential best- and first-in-class ADC for the treatment of epidermal growth factor receptor (EGFR)-expressing solid tumors that was fully designed and developed in-house by ALX Oncology scientists utilizing the Company’s proprietary linker-payload platform. Phase 1 clinical trials of ALX2004 are expected to initiate in mid-2025, with initial safety data available in 1H 2026. ALX Oncology will host a webcast highlighting the research program, clinical progress and novel mechanism of action for ALX2004 on May 20, 2025.

    Continued progress with the Phase 2 ASPEN-Breast and Phase 1 ASPEN-CRC clinical studies evaluating evorpacept in combination with anti-cancer antibodies and chemotherapy in breast and colorectal cancers based on strong supporting data that, when combined with an anti-cancer antibody, evorpacept generates durable responses and a consistent safety profile. First patient dosing for both trials is anticipated mid-year 2025.

    The randomized Phase 2 ASPEN-Breast clinical trial will evaluate evorpacept with HERCEPTIN® (trastuzumab) and single-agent chemotherapy in patients with HER2-positive metastatic breast cancer after prior treatment with ENHERTU® (fam-trastuzumab deruxtecan-nxki).

    The Phase 1 ASPEN-CRC clinical trial will evaluate evorpacept with ERBITUX® (cetuximab) and FOLFIRI in patients with second-line metastatic colorectal cancer.

    Announced encouraging final results from the Phase 1 trial evaluating evorpacept with standard-of-care RITUXAN® (rituximab) and lenalidomide (R2) treatment in patients with B-cell non-Hodgkin Lymphoma (B-NHL) presented at the American Association for Cancer Research (AACR) Annual Meeting 2025. The trial was conducted by Paolo Strati, M.D., Associate Professor of Lymphoma-Myeloma at The University of Texas MD Anderson Cancer Center, and colleagues at MD Anderson.

    As previously published, the combination of evorpacept plus R2 was well tolerated and demonstrated promising anti-tumor activity, generating complete responses (CR) in 83% of patients with indolent relapsed or refractory B-NHL comparing favorably to the 34% historical CR rate with R2 alone.

    The Phase 2 portion of the trial in patients with previously untreated indolent NHL is ongoing and has completed enrollment.

    Reported topline results from the ASPEN-03 and ASPEN-04 Phase 2 trials evaluating evorpacept with a checkpoint inhibitor, which did not meet their primary endpoints. In the trials, efficacy data did not support advancing evorpacept in combination with Merck’s anti-PD-1 therapy, KEYTRUDA® (pembrolizumab), into a registrational study. The combination of evorpacept and pembrolizumab with or without chemotherapy in ASPEN-03 and ASPEN-04 demonstrated a manageable safety profile and was consistent with what has been previously reported for pembrolizumab and chemotherapy in this setting.

    Received guidance from the U.S. FDA that the ASPEN-06 Phase 2 trial data evaluating evorpacept in combination with trastuzumab, ramucirumab and paclitaxel was not eligible for submission for accelerated approval given the availability of ENHERTU®. A Phase 3 versus ENHERTU® trial would be needed to pursue a regulatory approval of evorpacept in the second-line setting for HER2-positive gastric and gastroesophageal cancers. Given the Company’s disciplined focus and the allocation of its resources, ALX Oncology will not pursue a U.S. registrational path with a Phase 3 trial in gastric cancer and will consider exploring development partnerships to advance this program in gastric cancer.

    The Company made the decision to discontinue its evaluation of evorpacept in combination with PADCEV® (enfortumab vedotin-ejfv) in urothelial cancer based on the final data analysis showing that, in the ASPEN-07 trial, the addition of evorpacept to treatment with PADCEV® did not meet the bar for improved efficacy. Aligned to these data and consistent with recent guidance, ALX Oncology maintains its focus on continuing to progress its trials of evorpacept with anti-cancer antibodies, where there is demonstrated proof-of-concept across multiple clinical settings.

    Through previously announced strategic reprioritization efforts, the Company extended its cash runway into Q4 2026. Data milestones that are expected across the three studies evaluating evorpacept and ALX2004 are included in cash runway.

    Upcoming Clinical Milestones

    Breast Cancer: Patient dosing anticipated to initiate for ASPEN-BREAST Phase 2 clinical trial in mid-year 2025. Interim results from this trial are anticipated in 2H 2026.

    Colorectal Cancer: Patient dosing anticipated to initiate for ASPEN-CRC Phase 1b clinical trial in mid-year 2025. Safety and early efficacy data are anticipated in 1H 2026.

    ALX2004: Patient dosing anticipated to initiate in mid-2025, following IND clearance from the FDA in April 2025. Safety data are anticipated in 1H 2026.

    Breast Cancer: Topline results from Phase 1b I-SPY clinical trial of evorpacept with ENHERTU® are anticipated in 2H 2025.

    First Quarter 2025 Financial Results

    Cash, Cash Equivalents and Investments: Cash, cash equivalents and investments as of March 31, 2025, were $107.0 million. The Company believes its cash, cash equivalents and investments are sufficient to fund planned operations into Q4 of 2026.

    Research and Development (“R&D”) Expenses: R&D expenses consist primarily of preclinical, clinical and development costs related to the development of the Company’s current lead product candidate, evorpacept, and R&D personnel-related expenses including stock-based compensation. R&D expenses for the three months ended March 31, 2025, were $23.9 million compared to $31.7 million for the prior-year period or a decrease of $7.8 million. This decrease was primarily attributable to a decrease of $7.0 million in clinical and development costs primarily due to less manufacturing of clinical trial materials to support active clinical trials for our lead product candidate, evorpacept, and a decrease in stock-based compensation expense slightly offset by increased personnel and related costs.

    General and Administrative (“G&A”) Expenses: G&A expenses consist primarily of administrative personnel-related expenses, including stock-based compensation and other costs such as legal and other professional fees, patent filing and maintenance fees, and insurance. G&A expenses for the three months ended March 31, 2025, were $7.9 million compared to $6.0 million for the prior year period or an increase of $1.9 million. This increase was primarily attributable to an increase in personnel and related costs.

    Net loss: GAAP net loss was ($30.8) million for the three months ended March 31, 2025, or ($0.58) per basic and diluted share, as compared to a GAAP net loss of ($35.6) million for the three months ended March 31, 2024, or ($0.71) per basic and diluted share. The lower net loss is primarily attributed to lower R&D expenses. Non-GAAP net loss was ($25.5) million for the three months ended March 31, 2025, as compared to a non-GAAP net loss of ($28.5) million for the three months ended March 31, 2024. A reconciliation of GAAP to non-GAAP financial results can be found at the end of this news release.

    About ALX Oncology

    ALX Oncology (Nasdaq: ALXO) is a clinical-stage biotechnology company advancing a pipeline of novel therapies designed to treat cancer and extend patients’ lives. ALX Oncology’s lead therapeutic candidate, evorpacept, has demonstrated potential to serve as a cornerstone therapy upon which the future of immuno-oncology can be built. Evorpacept is currently being evaluated across multiple ongoing clinical trials in a wide range of cancer indications. ALX Oncology’s second pipeline candidate, ALX2004, is a novel EGFR-targeted antibody-drug conjugate with a differentiated mechanism of action and is anticipated to enter Phase 1 trials mid-2025. More information is available at www.alxoncology.com and on LinkedIn @ALX Oncology.

    Cautionary Note Regarding Forward-Looking Statements

    This press release contains forward-looking statements that involve substantial risks and uncertainties. Forward-looking statements include statements regarding future results of operations and financial position, business strategy, product candidates, planned preclinical studies and clinical trials, results of clinical trials, research and development costs, regulatory approvals, timing and likelihood of success, plans and objectives of management for future operations, as well as statements regarding industry trends. Such forward-looking statements are based on ALX Oncology’s beliefs and assumptions and on information currently available to it on the date of this press release. Forward-looking statements may involve known and unknown risks, uncertainties and other factors that may cause ALX Oncology’s actual results, performance or achievements to be materially different from those expressed or implied by the forward-looking statements. These and other risks are described more fully in ALX Oncology’s filings with the Securities and Exchange Commission (“SEC”), including ALX Oncology’s Annual Reports on Form 10-K, Quarterly Reports on Form 10-Q and other documents ALX Oncology files with the SEC from time to time. Except to the extent required by law, ALX Oncology undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made.

    ALX ONCOLOGY HOLDINGS INC.

    Condensed Consolidated Statements of Operations

    (unaudited)

    (in thousands, except share and per share amounts)

    Three Months EndedMarch 31,20252024Operating expenses:Research and development$23,888$31,717General and administrative7,9326,045Total operating expenses31,82037,762Loss from operations(31,820)(37,762)Interest income1,4832,622Interest expense(406)(427)Other (expense) income, net(11)(14)Net loss$(30,754)$(35,581)Net loss per share, basic and diluted$(0.58)$(0.71)Weighted-average shares of common stock used to

    compute net loss per shares, basic and diluted53,359,33850,120,758

    Condensed Consolidated Balance Sheet Data

    (unaudited)

    (in thousands)March 31,December 31,20252024Cash, cash equivalents and investments$106,992$131,281Total assets$120,900$147,775Total liabilities$32,605$34,157Accumulated deficit$(651,876)$(621,122)Total stockholders’ equity$88,295$113,618

    GAAP to Non-GAAP Reconciliation

    (unaudited)

    (in thousands)Three Months EndedMarch 31,20252024GAAP net loss, as reported$(30,754)$(35,581)Adjustments:Stock-based compensation expense5,2167,031Accretion of term loan discount and issuance costs6764Total adjustments5,2837,095Non-GAAP net loss$(25,471)$(28,486)

    Use of Non-GAAP Financial Measures

    We supplement our consolidated financial statements presented on a GAAP basis by providing additional measures which may be considered “non-GAAP” financial measures under applicable SEC rules. We believe that the disclosure of these non-GAAP financial measures provides our investors with additional information that reflects the amounts and financial basis upon which our management assesses and operates our business. These non-GAAP financial measures are not in accordance with generally accepted accounting principles and should not be viewed in isolation or as a substitute for reported, or GAAP, net loss, and are not a substitute for, or superior to, measures of financial performance performed in conformity with GAAP.

    “Non-GAAP net loss” is not based on any standardized methodology prescribed by GAAP and represents GAAP net loss adjusted to exclude stock-based compensation expense and accretion of term loan discount and issuance costs. Non-GAAP financial measures used by ALX Oncology may be calculated differently from, and therefore may not be comparable to, non-GAAP measures used by other companies.

    Investor Relations Contact:

    Elhan Webb, CFA, IR Consultant

    [email protected]

    Media Contact:

    Audra Friis, Sam Brown LLC

    [email protected]

    (917) 519-9577