BJC reports最新文献_第3页

The evolution of non-surgical management in stage III non-small cell lung cancer. 非小细胞肺癌III期非手术治疗的进展。

BJC reports Pub Date : 2026-06-03 DOI: 10.1038/s44276-026-00212-2

Milit S Patel, Alessandro Hammond, Edward Christopher Dee, Puneeth Iyengar

引用次数: 0

Debate: why surgery should remain central in the management of locally advanced (Stage III) non-small-cell lung cancer. 争论：为什么手术仍然是局部晚期（III期）非小细胞肺癌治疗的核心。

BJC reports Pub Date : 2026-06-03 DOI: 10.1038/s44276-026-00226-w

Chris Aboujudom, David B Nelson, Inderpal Sarkaria, Kemp H Kernstine

{"title":"Debate: why surgery should remain central in the management of locally advanced (Stage III) non-small-cell lung cancer.","authors":"Chris Aboujudom, David B Nelson, Inderpal Sarkaria, Kemp H Kernstine","doi":"10.1038/s44276-026-00226-w","DOIUrl":"10.1038/s44276-026-00226-w","url":null,"abstract":"Stage III non-small cell lung cancer (NSCLC) comprises a broadly heterogeneous disease with historically poor survival, and treatment decisions must account for both pathophysiology and resectability. Despite conclusions from older trials that questioned the role of surgery, modern evidence supports surgical resection as an indispensable component of treatment when performed by experienced thoracic surgeons. Advances in neoadjuvant systemic therapy, particularly chemo-immunotherapy, have significantly improved outcomes and reinforced the added value of surgery in appropriately selected Stage III NSCLC patients. In PACIFIC, consolidation durvalumab after concurrent chemoradiation improved progression-free (16.9 vs 5.6 months) and overall survival (47.5 vs 29.1 months). Also, perioperative pembrolizumab reduced progression or death by 42% (*P* < 0.0001) and improved pCR and major pathologic response. Additional trials (NEOTORCH, NADIM 2) showed large reductions in events and higher pCR rates with checkpoint inhibitors plus chemotherapy. Collectively, these data underscore that Stage III NSCLC requires both systemic therapy and durable local control, and neoadjuvant chemo-immunotherapy followed by surgery can significantly improve oncologic outcomes without increasing perioperative mortality in carefully selected patients.","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13233840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148160355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Machine learning and artificial intelligence in liquid biopsy-based early detection of pancreatic cancer: a scoping review. 机器学习和人工智能在基于液体活检的胰腺癌早期检测中的应用：综述。

BJC reports Pub Date : 2026-05-21 DOI: 10.1038/s44276-026-00232-y

Joy Ku, Meenakshi Singhal, Margaret Burnette, Samar A Hegazy

{"title":"Machine learning and artificial intelligence in liquid biopsy-based early detection of pancreatic cancer: a scoping review.","authors":"Joy Ku, Meenakshi Singhal, Margaret Burnette, Samar A Hegazy","doi":"10.1038/s44276-026-00232-y","DOIUrl":"10.1038/s44276-026-00232-y","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) presents as a cancer with an especially poor prognosis, largely due to the challenges surrounding its early diagnosis. Liquid biopsy has emerged as a promising, noninvasive method for screening across a variety of cancers. This approach is limited, however, by the extensive heterogeneity of biological samples, a challenge that teams are looking to address using artificial intelligence (AI) and machine learning (ML) strategies. By harnessing the ability of ML algorithms to extract the most salient features from complex datasets, researchers can identify biomarkers with high predictive value for PDAC. This review explores the current landscape of AI-powered liquid biopsy for early PDAC diagnosis, focusing on specific techniques and their respective degrees of success. Following PRISMA-ScR guidelines, 85 studies were extracted from PubMed and Scopus with a final 18 studies included. The majority of papers utilized blood (n = 15) as the source of liquid biopsy, with the remainder analyzing urine, bile, or cyst fluid. Random forests (n = 9) and support vector machines (n = 7) were the most frequently implemented ML models, while two papers focused on deep learning methods. Limitations include the lack of standardized reporting for model performance metrics and small cohort sizes with non-granular labels.","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13195041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147990787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Beckwith-Wiedemann syndrome multiomic analysis of hepatoblastoma uncovers unique tumour heterogeneity and cellular landscapes, including transition cells leading to tumour formation. 肝母细胞瘤的贝克维斯-魏德曼综合征多组学分析揭示了独特的肿瘤异质性和细胞景观，包括导致肿瘤形成的过渡细胞。

BJC reports Pub Date : 2026-05-20 DOI: 10.1038/s44276-026-00215-z

Snehal Nirgude, Elisia D Tichy, Yuanchao Zhang, Khanh B Trang, Rose D Pradieu, Michael Xie, Kathrin M Bernt, Suzanne P MacFarland, Jennifer M Kalish

{"title":"Beckwith-Wiedemann syndrome multiomic analysis of hepatoblastoma uncovers unique tumour heterogeneity and cellular landscapes, including transition cells leading to tumour formation.","authors":"Snehal Nirgude, Elisia D Tichy, Yuanchao Zhang, Khanh B Trang, Rose D Pradieu, Michael Xie, Kathrin M Bernt, Suzanne P MacFarland, Jennifer M Kalish","doi":"10.1038/s44276-026-00215-z","DOIUrl":"10.1038/s44276-026-00215-z","url":null,"abstract":"Background: Beckwith-Wiedemann syndrome (BWS) is an overgrowth and cancer predisposition syndrome caused by epigenetic alterations on chromosome 11p15 that predisposes children to multiple cancer types, including hepatoblastoma. Hepatoblastoma is heterogenous in nature, and the 11p15 changes that cause BWS can also be found as a somatic alteration in nonBWS hepatoblastomas, further adding complexity to this disease.Methods: To understand the impact of the predisposition molecular cues in BWS hepatoblastoma, we interrogated BWS and nonBWS hepatoblastomas, as well as adjacent normal liver, using a multiomic approach [single nuclei RNA-sequencing (snRNA-seq) + single nuclei assay for transposable-accessible chromatin sequencing (snATAC-seq)].Results: Our approach identified an enrichment of the WNT signaling pathway in BWS hepatoblastoma. Despite similar histology, we found greater tumour heterogeneity and embryonic transcriptional signatures in BWS hepatoblastoma. Furthermore, using pseudotime analysis, we identified a population of transition cells in BWS, with unique molecular profiles, which likely promote the precancer to cancer neoplastic transition in BWS.Conclusions: This study highlights key signaling pathways, particularly WNT, and identifies a unique population of intermediate/transition cells that may drive neoplastic transformation in BWS hepatoblastoma. These findings provide new insights into the molecular events leading to cancer in BWS and suggest potential targets for early intervention and prevention strategies.","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13190687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147984947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

4-weekly avelumab plus axitinib in patients with metastatic renal cell carcinoma. 转移性肾细胞癌患者的4周avelumab加axitinib治疗。

BJC reports Pub Date : 2026-05-08 DOI: 10.1038/s44276-026-00224-y

Naveen S Vasudev, Umair Aleem, Kathryn Humphries, Manon Pillai, Ben Pickwell-Smith, Christy Ralph, Satinder Jagdev, Joanne Simpson, Helen Dearden, Tom Waddell

{"title":"4-weekly avelumab plus axitinib in patients with metastatic renal cell carcinoma.","authors":"Naveen S Vasudev, Umair Aleem, Kathryn Humphries, Manon Pillai, Ben Pickwell-Smith, Christy Ralph, Satinder Jagdev, Joanne Simpson, Helen Dearden, Tom Waddell","doi":"10.1038/s44276-026-00224-y","DOIUrl":"10.1038/s44276-026-00224-y","url":null,"abstract":"Background: 800 mg avelumab, given every 2 weeks, in combination with axitinib, is an approved first-line treatment option for patients with metastatic renal cell carcinoma (mRCC). Less frequent administration of avelumab would be preferable to patients and service providers but has not been previously explored.Methods: We retrospectively analysed the clinical outcomes of patients from two academic centres who received 4-weekly avelumab plus axitinib between Oct 2019 and Oct 2023. Patients in cohort 1 (C1) were treated with 4-weekly avelumab from the start of therapy. Patients in cohort 2 (C2) initially received standard 2-weekly avelumab and were later switched to 4-weekly infusions. Overall response rate (ORR), progression-free survival (PFS), overall survival (OS) and toxicities leading to dose reductions or cessation were evaluated.Results: We identified 94 patients in total, 46 patients in C1 and 48 patients in C2. The majority (56%) of patients in both cohorts had IMDC favourable-risk disease. The ORR in C1 was 53% and the median PFS was 22.1 months. In C2, the median time to switch was 4.9 months (range 1.8-35.6) and median time on 4-weekly avelumab was 16.7 months (range 0.9-39.1). Toxicity was consistent with prior reports. Limitations include retrospective design.Conclusions: These preliminary data support prospective evaluation of modified avelumab scheduling in patients with mRCC. Reducing treatment burden stands to improve patient quality of life and lower associated costs.","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13156266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147857958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular subtypes and the (in vitro) response of glioblastoma to temozolomide. 替莫唑胺对胶质母细胞瘤的分子亚型和体外反应。

BJC reports Pub Date : 2026-05-08 DOI: 10.1038/s44276-026-00228-8

Silvia Rancati, Matilde Campolungo, Gerusa Duarte Dalmolin, Pierre Lau, Federica Furia, Alessandro Coppe, Fabio Landuzzi, Manuela Vecchi, Andrea Cavalli, Stefano Gustincich, Nicola Tirelli

{"title":"Molecular subtypes and the (in vitro) response of glioblastoma to temozolomide.","authors":"Silvia Rancati, Matilde Campolungo, Gerusa Duarte Dalmolin, Pierre Lau, Federica Furia, Alessandro Coppe, Fabio Landuzzi, Manuela Vecchi, Andrea Cavalli, Stefano Gustincich, Nicola Tirelli","doi":"10.1038/s44276-026-00228-8","DOIUrl":"10.1038/s44276-026-00228-8","url":null,"abstract":"Background: We address the therapeutic relevance of glioblastoma (GBM)'s molecular characterization, focusing on whether a proneural-vs-mesenchymal classification may describe GBM heterogeneity, correlate to stemness and CD44 (a marker often, but conflictingly, used in GBM), and have a prognostic value in terms of temozolomide (TMZ) resistance.Methods: We molecularly profiled 4 patient-derived GBM cells (PD-GBM) and a reference cell line (U87), validating the results in public datasets (PD-GBM, TCGA-GBM), then studying the subtype-specific response to TMZ in vitro, both under normoxia and simulated hypoxia.Results: Firstly, the proneural subtype transcriptionally and phenotypically correlates with higher stemness. Secondly, CD44 inversely correlates to stemness, acting as a mesenchymal marker both intra-tumorally (FACS-sorted CD44LOW cells had higher stemness than CD44HIGH) and inter-tumorally (also in larger datasets). Further, mesenchymal PD-GBM cells are also enriched in other hyaluronic acid (HA) surface receptors, proneural in matrix HA receptors. Finally, although TMZ stimulates a general mesenchymal shift in all cells, there are proneural-specific responses: this subtype resists TMZ better under hypoxia (vs. normoxia) in a first treatment, and in a second treatment (vs. single) under normoxia.Conclusion: PD-GBM show clear proneural/stemness and mesenchymal/CD44 correlations, which may bear prognostic significance, as more proneural/stem GBMs appeared more capable to develop TMZ resistance.","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13156310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147857952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Significance and challenges in dissecting cancer-bacteriome interactions. 解剖癌症-细菌组相互作用的意义和挑战。

BJC reports Pub Date : 2026-05-04 DOI: 10.1038/s44276-026-00229-7

Ibraheem Alshareedah, James D Brunner, Patrick S G Chain, Anand Kumar

{"title":"Significance and challenges in dissecting cancer-bacteriome interactions.","authors":"Ibraheem Alshareedah, James D Brunner, Patrick S G Chain, Anand Kumar","doi":"10.1038/s44276-026-00229-7","DOIUrl":"10.1038/s44276-026-00229-7","url":null,"abstract":"Cancer is the leading cause of death around the world. While some types of cancer have become manageable due to advancements in medicine, most cancers still lack available cures and treatments. Recent studies have shown that changes in the human microbiome, especially in the bacteriome, are associated with some cancers. Certain bacterial strains have been reported to promote the initiation and progression of cancer in humans. Other studies have used sequencing to observe changes in the bacteriome of healthy and cancer patients. However, studies that investigate the interactions between cancer cells and the complex bacteriome as a whole remain scarce. This is due to the absence of experimental methods to study the interactions between cancer cells and complex bacterial populations, which has delayed the progress in identifying cancer-causing and cancer-inhibiting bacteria, and in understanding the bacterial interactions and their influence on host cells. Here, we review approaches to studying cancer cell interactions with complex bacteriomes and suggest possible routes to overcome this problem, highlighting the need for interdisciplinary studies that may help advance this field. We speculate that a good understanding of cancer-bacteriome interactions may open the door to new lines of holistic bacteriotherapy for cancer that is otherwise unavailable.","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139594/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Precision oncology in the age of AI: lessons from AI-driven drug discovery and clinical translation. 人工智能时代的精准肿瘤学：人工智能驱动的药物发现和临床转化的经验教训。

BJC reports Pub Date : 2026-04-15 DOI: 10.1038/s44276-026-00221-1

Wonbeak Yoo

{"title":"Precision oncology in the age of AI: lessons from AI-driven drug discovery and clinical translation.","authors":"Wonbeak Yoo","doi":"10.1038/s44276-026-00221-1","DOIUrl":"10.1038/s44276-026-00221-1","url":null,"abstract":"Drug discovery has been constrained by extended timelines and high costs, as the cumulative requirements of preclinical validation, multi-phase clinical trials, and regulatory approval have been imposed. Recently, computational modeling has been explored as a supportive approach to accelerate the identification and refinement of therapeutic candidates. Proof-of-concept was provided in a phase 2a trial of a de novo-designed TNIK inhibitor in idiopathic pulmonary fibrosis, in which safety, tolerability, and pharmacodynamic target engagement were demonstrated, with a trend toward reduced functional decline. This study showed that AI-derived molecules can advance into human testing, but broader validation, mechanistic understanding, and regulatory alignment remain essential. In oncology, where tumor heterogeneity, clonal evolution, and therapeutic resistance continue to constrain durable clinical benefit, there is an increasing need for adaptive and data-informed drug discovery strategies. This Perspective reviews recent progress and limitations in AI-driven drug discovery and early clinical translation. It emphasizes how the clinical evaluation of an AI-generated TNIK inhibitor serves as an early translational reference and outlines practical strategies for integrating multi-omics data, federated model validation, and adaptive trial design to advance precision oncology-oriented therapeutics.","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13083990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147694666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular targeting of the meningioma cell signaling circuit reveals drug vulnerabilities including synergy between sulforaphane and focal adhesion kinase inhibition. 脑膜瘤细胞信号通路的分子靶向揭示了药物脆弱性，包括萝卜硫素和局灶黏附激酶抑制之间的协同作用。

BJC reports Pub Date : 2026-04-15 DOI: 10.1038/s44276-026-00204-2

Michelle C Schwab, Yasmin Kocas, Sarah Gendreizig, Eric Goulin Lippi Fernandes, Tunc F Ersoy, Roland Coras, Lars Uwe Scholtz, Holger Sudhoff, Ingo Todt, Matthias Simon, Matthias Schürmann, Felix Oppel

{"title":"Molecular targeting of the meningioma cell signaling circuit reveals drug vulnerabilities including synergy between sulforaphane and focal adhesion kinase inhibition.","authors":"Michelle C Schwab, Yasmin Kocas, Sarah Gendreizig, Eric Goulin Lippi Fernandes, Tunc F Ersoy, Roland Coras, Lars Uwe Scholtz, Holger Sudhoff, Ingo Todt, Matthias Simon, Matthias Schürmann, Felix Oppel","doi":"10.1038/s44276-026-00204-2","DOIUrl":"10.1038/s44276-026-00204-2","url":null,"abstract":"Background: Meningiomas represent a common type of brain tumours and arise from the arachnoid cap cells which line the dural coverings of the brain. These predominantly benign tumours cause strong morbidity due to their intracranial location. Due to a lack of established pharmacological treatment approaches, surgery and radiotherapy remain the standard in clinical management of these tumours.Methods: Here, we created a primary meningioma cell culture model and tested molecular compounds targeting key tumour-driving signalling pathways using cell viability assays and isobologram analysis.Results: We found significant drug vulnerabilities within the meningioma-driving cell signalling network. Effective drugs included metformin, inhibitors of STAT3 and focal adhesion kinase (FAK), and the anti-inflammatory phytochemical sulforaphane, known as NRF2 pathway inducer and NFκB pathway inhibitor. Interestingly, FAK inhibitor Y15 and sulforaphane showed synergistic activity across cells of distinct meningioma patients, indicating this combination as a potential therapy approach.Conclusions: Overall, we present a molecular targeting strategy for meningiomas that could pave the way for less invasive clinical management of these tumours and, as a result, help reduce patient mortality and morbidity. Metformin and sulforaphane both have FDA and EU pharmaceutical approval and thus could be repurposed promptly to establish a new meningioma therapy regimen.","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13083847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147694643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Disparities in blood cancer survival in the UK 2009-2019: national cohort studies. 2009-2019年英国血癌生存差异：国家队列研究

BJC reports Pub Date : 2026-04-15 DOI: 10.1038/s44276-026-00222-0

Janice Hoang, Joshua Allen, Rebecca Capel, Rebecca Thomas, Stephanie Smits, Rubina Ahmed, Hilary Webb, Aziz Sheikh, Sally Cox, Ceri Bygrave, Julia Hippisley-Cox

{"title":"Disparities in blood cancer survival in the UK 2009-2019: national cohort studies.","authors":"Janice Hoang, Joshua Allen, Rebecca Capel, Rebecca Thomas, Stephanie Smits, Rubina Ahmed, Hilary Webb, Aziz Sheikh, Sally Cox, Ceri Bygrave, Julia Hippisley-Cox","doi":"10.1038/s44276-026-00222-0","DOIUrl":"10.1038/s44276-026-00222-0","url":null,"abstract":"Abstarct: BACKGROUND: Blood cancers are among the most common and deadliest in the UK, affecting over 40,000 people annually. Survival varies by subtype, but this is not routinely reported for the UK. This study estimated survival for haematological malignancies in the UK stratified by time period, age, sex, ethnicity, deprivation, and rurality.Methods: Four retrospective cohorts of patients aged 15-99 diagnosed with haematological malignancies (2009-2019) across UK cancer registries were used to estimate 1-, 5-, and 10-year net survival by subtype.Results: We identified 413,286 blood cancer cases. Survival in all blood cancer combined significantly improved in England (3.8%), Northern Ireland (5.1%), and Wales (3%), but not Scotland. Men had ≥3% lower survival than women in many subtypes. Older age and higher deprivation were significantly linked to lower survival. In England, white ethnic groups had ≥3% lower survival than non-white groups for myelodysplastic syndrome, myeloid malignancies, plasma cell neoplasms, myeloproliferative neoplasms. In Wales, rural areas showed ≥3% higher survival than urban and mixed regions for lymphoid malignancies, myeloid malignancies, plasma cell neoplasms, Hodgkin lymphoma, mature B-cell neoplasms, acute myeloid leukaemia.Conclusion: Net survival varied markedly by subtype and demographic factors across the UK. Given possible differences in case ascertainment, findings are descriptive and hypothesis‑generating.","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13083837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147694705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0