American Society of Clinical Oncology educational book / ASCO. American Society of Clinical Oncology. Meeting最新文献

{"title":"Reinventing the <i>ASCO Educational Book</i> to Capture the Advances in Oncology Year-Round.","authors":"Gerald Hsu","doi":"10.1200/EDBK-26-00001","DOIUrl":"https://doi.org/10.1200/EDBK-26-00001","url":null,"abstract":"","PeriodicalId":37969,"journal":{"name":"American Society of Clinical Oncology educational book / ASCO. American Society of Clinical Oncology. Meeting","volume":"46 4","pages":"e00001"},"PeriodicalIF":0.0,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148686111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Finding Hope, One Breath at a Time.","authors":"Inemesit Akpan, Kimberly Staley, Amany Keruakous","doi":"10.1200/EDBK-26-00005","DOIUrl":"https://doi.org/10.1200/EDBK-26-00005","url":null,"abstract":"","PeriodicalId":37969,"journal":{"name":"American Society of Clinical Oncology educational book / ASCO. American Society of Clinical Oncology. Meeting","volume":"46 4","pages":"e00005"},"PeriodicalIF":0.0,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148913407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Equipping Clinicians for Cancer Clinical Trial Conversations: Developing and Applying Smart Phrases.","authors":"Naomi D Parker, Susan Eggly, Leah Szumita, Daphne R Friedman, Danny Trotier, Tithi B Amin, Martina C Murphy, Andrea Sitlinger, Stephanie A S Staras, Samuel F Sestito, Subhash Edupuganti, Elisa S Weiss, Carma L Bylund","doi":"10.1200/EDBK-26-00004","DOIUrl":"https://doi.org/10.1200/EDBK-26-00004","url":null,"abstract":"","PeriodicalId":37969,"journal":{"name":"American Society of Clinical Oncology educational book / ASCO. American Society of Clinical Oncology. Meeting","volume":"46 4","pages":"e00004"},"PeriodicalIF":0.0,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149274424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New Tractor.","authors":"Rohit Singh, Kevin Zhu, Elsy Rivera","doi":"10.1200/EDBK-26-00009","DOIUrl":"https://doi.org/10.1200/EDBK-26-00009","url":null,"abstract":"","PeriodicalId":37969,"journal":{"name":"American Society of Clinical Oncology educational book / ASCO. American Society of Clinical Oncology. Meeting","volume":"46 4","pages":"e00009"},"PeriodicalIF":0.0,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148913491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Routine Surveillance Imaging for Melanoma: Emerging Technologies for Detecting Early Recurrence and Guiding Clinical Management.","authors":"Giselle de Souza Carvalho, Cicero Luiz Cunha de Sousa Martins, Kevin Wang, Michael D Farwell, April K S Salama","doi":"10.1200/EDBK-26-520544","DOIUrl":"10.1200/EDBK-26-520544","url":null,"abstract":"<p><p>Melanoma recurrence risk is highest within the first 2 years after diagnosis and progressively declines thereafter. Current surveillance strategies remain largely guided by clinicopathologic risk stratification, with the comprehensive medical history, physical examination, and complete skin assessment forming the cornerstone of follow-up. Although cross-sectional imaging and lymph node ultrasound are used in selected higher-risk patients, routine intensive imaging has not consistently demonstrated survival benefit and may increase costs and false-positive findings. Emerging technologies are reshaping melanoma surveillance and clinical management. Circulating tumor DNA (ctDNA) has shown promise as a minimally invasive biomarker capable of detecting molecular residual disease and anticipating clinical recurrence. Persistent or newly positive ctDNA after surgery is consistently associated with inferior recurrence-free survival. However, ctDNA does not reliably detect all recurrence patterns and its sensitivity varies according to disease burden and metastatic site. Prospective validation and clarification of how ctDNA should guide adjuvant therapy or imaging strategies remain necessary. In parallel, CD8-targeted positron emission tomography (CD8 PET) has emerged as a novel functional imaging modality capable of noninvasively visualizing whole-body T-cell dynamics. By differentiating tumor burden from immune infiltration and capturing early T-cell recruitment, CD8 PET offers predictive insights into immunotherapy response. Nevertheless, limitations of this technique include dependence on optimal imaging timing, limited tracer availability, cost, and an inability to directly assess T-cell functionality. Together, ctDNA and immune-focused imaging approaches represent promising steps toward precision surveillance and management of melanoma. Further robust prospective studies are required to define their integration into clinical decision making and optimize patient outcomes.</p>","PeriodicalId":37969,"journal":{"name":"American Society of Clinical Oncology educational book / ASCO. American Society of Clinical Oncology. Meeting","volume":"46 3","pages":"e520544"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147821529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Performance Status: Optimize Cancer Care in Older Adults.","authors":"Stuart M Lichtman","doi":"10.1200/EDBK-26-100055","DOIUrl":"10.1200/EDBK-26-100055","url":null,"abstract":"<p><p>Older adults account for approximately 60% of new cancer diagnoses and 70% of cancer-related deaths, yet they remain consistently under-represented in clinical trials and are routinely assessed using performance status (PS) tools developed over seven decades ago. The Karnofsky Performance Status and Eastern Cooperative Oncology Group (ECOG) PS scales, while simple and widely adopted, fail to capture the multidimensional vulnerabilities that define physiologic aging. Studies show that 43%-69% of patients with good PS have geriatric assessment (GA)-identified deficits that independently predict treatment toxicity and survival. Comprehensive GA evaluates functional status, cognition, nutrition, comorbidity burden, polypharmacy, and social support-domains that PS entirely misses. Landmark randomized controlled trials, including GAP70+, GAIN, INTEGERATE, COACH, and PERI-OP, provide level 1 evidence that GA-guided interventions reduce grade 3-5 treatment toxicities by 10%-20% without affecting survival. These trials demonstrate two complementary mechanisms of benefit: treatment modification (dose attenuation and regimen selection) and intensive supportive care. Disease-specific evidence further supports GA integration, including colon, pancreatic, and lung cancers, hematologic malignancies, and surgical oncology. Practical screening tools, including the CARG score, CRASH score, Geriatric 8, and VES-13, can be completed in under 30 minutes and are feasible in routine practice. A proposed clinical algorithm integrates GA findings into treatment decision making alongside standard National Comprehensive Cancer Network, ASCO, and ECOG guidelines. Moving beyond chronologic age and PS toward an understanding of functional reserve is both an evidence-based imperative and an ethical obligation to the fastest growing and most vulnerable segment of the cancer population.</p>","PeriodicalId":37969,"journal":{"name":"American Society of Clinical Oncology educational book / ASCO. American Society of Clinical Oncology. Meeting","volume":"46 3","pages":"e100055"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147934197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Before the Race Even Starts: Early Intervention to Prevent Long-Term Late Effects From Childhood Cancer Therapies.","authors":"Etan Orgel, Karen C Burns, Joshua Gorlick, Lisa S Kahalley","doi":"10.1200/EDBK-26-517242","DOIUrl":"https://doi.org/10.1200/EDBK-26-517242","url":null,"abstract":"<p><p>Increasing treatment intensity has improved survival rates for children with cancer, resulting in an increasing population burdened with late effects from treatment. The Children's Oncology Group Survivorship Guidelines provide a compendium of late effects with recommendations for risk-adapted surveillance based on treatment components and intensity. However, many late effects from therapy are permanent; alternative strategies are therefore necessary to prevent their debilitating impact on the quality of life for childhood cancer survivors. Prevention of late effects via early intervention is an increasingly vital component of pediatric cancer therapy. In this review, we highlight three common and debilitating late effects amenable to this strategy: oncofertility and fertility preservation, cisplatin-induced ototoxicity (hearing loss) and otoprotection, and radiation-induced neurocognitive deficits and cognitive-sparing approaches. For each toxicity, current practice, knowledge gaps, and future directions are discussed.</p>","PeriodicalId":37969,"journal":{"name":"American Society of Clinical Oncology educational book / ASCO. American Society of Clinical Oncology. Meeting","volume":"46 3","pages":"e517242"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148279146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Smoldering Multiple Myeloma: From Clinical to Immunogenomic Risk Stratification and Therapeutic Implications of Early Intervention.","authors":"Nizar J Bahlis, María V Mateos, Ajay K Nooka","doi":"10.1200/EDBK-26-517488","DOIUrl":"10.1200/EDBK-26-517488","url":null,"abstract":"<p><p>Smoldering multiple myeloma (SMM) is an asymptomatic precursor state that precedes the development of symptomatic active MM. Newer immunogenomic data highlight the monoclonal gammopathy of undetermined significance-SMM-MM spectrum as a continuous genomic gradient rather than a series of discrete clinical categories. Current risk stratifications to define high-risk SMM use a progression rate of ≥50% within 2 years. The International Myeloma Working Group uses the 20/2/20 model that identifies serum M-protein >2 g/dL, bone marrow plasma cells >20%, and involved/uninvolved free light chain ratio >20 as independent predictors for risk of progression to MM. Having ≥2 risk factors increases the 2-year risk of SMM progression to 40%-50%. This risk is further increased by the presence of adverse cytogenetics [del13, t(4;14), t(14;16), +1q]. The model is purely based on tumor burden and cytogenetics and could be further refined by using genomics that predict tumor evolution. Key genomic features identified as independent risk factors for SMM progression include mutations in the MAPK pathway (KRAS and NRAS single nucleotide variants [SNVs]), alterations of the DNA repair pathway (TP53, ATM SNVs, and deletion 17p), MYC alterations (translocations or copy number variations), and APOBEC-associated mutational signatures. Integrating the molecular and clinical determinants to define high-risk SMM is described as the holy grail of risk stratification in SMM. Three large, randomized phase III studies demonstrated the benefit of early intervention by meeting their primary end points, one demonstrating an overall survival (OS) benefit (QuiRedex) and another showing a trend toward OS benefit (AQUILA) favoring early intervention. In this context, identifying the patients with high-risk SMM is crucial as the optimal patient might benefit from a therapeutic intervention aimed at preventing progression to MM and prolonging OS.</p>","PeriodicalId":37969,"journal":{"name":"American Society of Clinical Oncology educational book / ASCO. American Society of Clinical Oncology. Meeting","volume":"46 3","pages":"e517488"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148006895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Climate Change and Environmental Exposures Across the Cancer Continuum: Implications for Oncology.","authors":"Robert A Hiatt, Jefferey L Burgess, Prashant Mathur, Leticia M Nogueira","doi":"10.1200/EDBK-26-521654","DOIUrl":"10.1200/EDBK-26-521654","url":null,"abstract":"<p><p>Climate change is here and having a major impact on health, including cancer. Climate change is altering environmental exposures and modifying the frequency, intensity, and behavior of extreme weather events, introducing new challenges to cancer control and oncology. Climate-driven events, such as wildfires, can increase exposure to pollutants that influence cancer risk and mortality. Additionally, climate-driven extreme weather events, such as hurricanes, can disrupt health care services essential for quality cancer care. Therefore, climate change is increasingly recognized as a determinant of cancer risk and outcomes. Through its influence on environmental and occupational exposures, social conditions, and health system functioning, climate change is an important part of the exposome, which encompasses all environmental exposures that influence human health. As leaders in cancer health care, oncologists are uniquely positioned to characterize the downstream consequences of climate change on cancer care and outcomes and act on modifiable factors to improve patient care and health care system resilience.</p>","PeriodicalId":37969,"journal":{"name":"American Society of Clinical Oncology educational book / ASCO. American Society of Clinical Oncology. Meeting","volume":"46 3","pages":"e521654"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148057321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Synthetic Lethal Therapeutic Strategies in Precision Oncology.","authors":"Timothy A Yap, Fiona Simpkins, Marie Porte, Sophie Postel-Vinay","doi":"10.1200/EDBK-26-517160","DOIUrl":"10.1200/EDBK-26-517160","url":null,"abstract":"<p><p>Synthetic lethality is a genetic phenomenon in which the simultaneous presence of two different genetic alterations impairs cellular viability, whereas a single gene defect is compatible with cellular survival. Importantly, targeting such synthetic lethal interactions offers potential therapeutic strategies for cancers with alterations in pathways that might otherwise be previously considered undruggable. Various hallmarks of cancer have proven to be targetable using a synthetic lethal approach, including the DNA damage response (DDR), epigenetic alterations, and changes in cellular metabolism and proliferation. The development of high-throughput drug and CRISPR-Cas9 screening technologies has led to the discovery of new druggable synthetic lethal vulnerabilities in cell lines and to the development of novel drugs designed to target these interactions, together with associated predictive biomarkers of response capable of guiding patient selection in the clinic. Clinically approved PARP inhibitors have provided proof of concept for the synthetic lethality approach by achieving successful outcomes in patients with <i>BRCA</i>-mutant cancers. This has led to the discovery and development of novel synthetic lethal strategies, including novel agents targeting multiple DDR pathways and epigenetic alterations. These approaches are currently in late preclinical and/or early clinical testing. In this article, we detail emerging therapeutic strategies for synthetic lethal drug development and discuss promising therapeutic strategies targeting such interactions. These include MTA-cooperative PRMT5 inhibitors and MAT2A inhibitors in MTAP-deficient cancers, WRN inhibitors in microsatellite instablility-high tumors, as well as PKMYT1 inhibitors and WEE1 inhibitors in <i>CCNE1</i>-amplified tumors.</p>","PeriodicalId":37969,"journal":{"name":"American Society of Clinical Oncology educational book / ASCO. American Society of Clinical Oncology. Meeting","volume":"46 3","pages":"e517160"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148057328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}