British Journal of Cancer最新文献

{"title":"Identification of increased dedifferentiation along the Prom1+ cancer cells in Müllerian adenosarcoma with sarcomatous overgrowth.","authors":"Xingming Ye, Jianfeng Zheng, Dan Hu, Li Liu, Fukun Chen, Xintong Cai, Yangmei Xu, Lifeng Li, Jie Lin, Qinying Liu, Yang Sun","doi":"10.1038/s41416-025-02943-4","DOIUrl":"https://doi.org/10.1038/s41416-025-02943-4","url":null,"abstract":"<p><strong>Background: </strong>Müllerian adenosarcoma (MA) is a rare tumour accounts for 5-7% of uterine sarcomas. Tumours with sarcomatous overgrowth (MASO) or high-grade tend to be aggressive. However, the tumour aetiology is elusive.</p><p><strong>Methods: </strong>Single-cell RNA sequencing and bioinformatics were used to analyse the MASO and paired normal tissues. Expression and clinical significance of key genes were analysed by TCGA data and immunohistochemistry. In vitro experiment was used to verify the effect of E2F1 in cell dedifferentiation.</p><p><strong>Results: </strong>We prove malignant stromal cells originate from fibrous tissue, Prom1-derived with complex intra-tumoral heterogeneity. Along the developmental trajectory, we discover three phenotypes of Prom1+ cancer cells (differentiation-like, intermediate-like, dedifferentiation-like). A distinct HMGB2/3+ subtype of Prom1+ cluster is predominant dedifferentiation-like cancer cells, with high proliferation and stemness traits at the tail of trajectory. E2F1 is a master transcription factor for Prom1 lineage dedifferentiation, which could occupy the HMGB2/3 promoter to enhance their transcription, facilitating the stemness and self-renewal of cancer cells. Gene signature of Prom1 lineage is associated with poorer prognosis in uterine malignancies. The expression of Prom1 and HMGB3 was verified by immunohistochemistry.</p><p><strong>Conclusions: </strong>Our study reveal the heterogeneity and dynamics of Prom1 lineage cells, which are key to tailor efficient therapies for MASO.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Machine learning-based decision support model for selecting intra-arterial therapies for unresectable hepatocellular carcinoma: A national real-world evidence-based study.","authors":"Chao An, Ran Wei, Wendao Liu, Yan Fu, Xiaolong Gong, Chengzhi Li, Wang Yao, Mengxuan Zuo, Wang Li, Yansheng Li, Fatian Wu, Kejia Liu, Dong Yan, Peihong Wu, Jianjun Han","doi":"10.1038/s41416-025-02940-7","DOIUrl":"https://doi.org/10.1038/s41416-025-02940-7","url":null,"abstract":"","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNA methylation of CD47 mediates tumor immunosuppression in EGFR-TKI resistant NSCLC.","authors":"Wei Zhang, Jiawen Wang, Jialu Liang, Zhanghai He, Kefeng Wang, Huayue Lin","doi":"10.1038/s41416-025-02945-2","DOIUrl":"https://doi.org/10.1038/s41416-025-02945-2","url":null,"abstract":"<p><strong>Background: </strong>Although immune checkpoint inhibitors (ICIs) have been successfully utilized in patients with non-small cell lung cancer (NSCLC), EGFR-mutated patients didn't benefit from ICIs. The underlying mechanisms for the poor efficacy of this subgroup remain unclear.</p><p><strong>Methods: </strong>CD8⁺T cells cytotoxicity, DCs phagocytosis and immunofluorescence assay were applied to examine the immunosuppressive microenvironment of NSCLC. m⁶A RNA immunoprecipitation, luciferase assay and immunohistochemistry were used to explore the relationship between CD47 and ALKBH5 in EGFR-TKI resistant NSCLC. Autochthonous EGFR-driven lung tumor mouse model and PDXs were performed to explore the therapeutic potential of CD47 antibody and EGFR-TKI combination.</p><p><strong>Results: </strong>We found that EGFR-TKI resistance promoted a more immunosuppressive tumor microenvironment and inhibited anti-tumor functions of CD8⁺ T cells. Mechanistically, the m⁶A eraser ALKBH5 was inhibited in EGFR-TKI resistant NSCLC, which subsequently upregulates CD47 by catalyzing m⁶A demethylation and causes immunosuppression. Combined treatment with EGFR-TKI and inhibitors of CD47 enhances antitumor immunity and EGFR-TKI efficacy in vivo.</p><p><strong>Conclusions: </strong>Collectively, our findings reveal the possible underlying mechanism for poor immune response of ICIs in EGFR-TKI resistant NSCLC and provide preclinical evidence that targeted therapy combined with innate immune checkpoint blockade may provide synergistic effects in NSCLC treatment.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated serum levels of GPX4, NDUFS4, PRDX5, and TXNRD2 as predictive biomarkers for castration resistance in prostate cancer patients: an exploratory study.","authors":"Rong Wang, Shaopeng Wang, Yuanyuan Mi, Tianyi Huang, Jun Wang, Jiang Ni, Jian Wang, Jian Yin, Menglu Li, Xuebin Ran, Shuangyi Fan, Qiaoyang Sun, Soo Yong Tan, H Phillip Koeffler, Lingwen Ding, Yong Q Chen, Ninghan Feng","doi":"10.1038/s41416-025-02947-0","DOIUrl":"https://doi.org/10.1038/s41416-025-02947-0","url":null,"abstract":"<p><strong>Background: </strong>Prostate cancer (PCa) is a heterogeneous disease affecting over 14% of the male population worldwide. Although patients often respond positively to initial treatments within the first 2-3 years, many eventually develop a more lethal form of the disease known as castration-resistant PCa (CRPC). At present, no biomarkers that predict the onset of CRPC are available. This study aims to provide insights into the diagnosis and prediction of CRPC emergence.</p><p><strong>Methods: </strong>Protein expression dynamics were analysed in drug (androgen receptor inhibitor)-tolerant persister (DTP) and drug withdrawal cells using proteomics to identify potential biomarkers. These biomarkers were subsequently validated using a mouse model, 180-paired carcinoma/benign tissues, and 482 serum samples. Five machine learning algorithms were employed to build clinical prediction models, wherein the SHapley Additive exPlanation (SHAP) framework was used to interpret the best-performing model. Moreover, three regression models were developed to determine the Time from initial PCa diagnosis to CRPC development (TPC) in patients.</p><p><strong>Results: </strong>We identified that the protein expression levels of GPX4, NDUFS4, PRDX5, and TXNRD2 were significantly upregulated in PCa patients, particularly in those with CRPC. Among the tested machine learning models, the random forest and extreme gradient boosting models performed best on tissue and serum cohorts, achieving AUCs of 0.958 and 0.988, respectively. In addition, a significant inverse correlation was observed between TPC and serum levels of these four biomarkers. This correlation was formulated in three regression models, which achieved the smallest mean absolute error of 1.903 on independent datasets for predicting CRPC emergence.</p><p><strong>Conclusion: </strong>Our study provides new insights into the role of DTP cells in CRPC development. The quad protein panel identified in our study, along with the post hoc and intrinsically explainable prediction models, may serve as a convenient and real-time prognostic tool, addressing the current lack of clinical biomarkers for CRPC.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of ARID1A accelerates prostate tumourigenesis with a proliferative collagen-poor phenotype through co-operation with AP1 subunit cFos.","authors":"Andrew Hartley, Laura C A Galbraith, Robin Shaw, Amy Tibbo, Rajan Veeratterapillay, Laura Wilson, Rakesh Heer, Karen Blyth, Hing Leung, Imran Ahmad","doi":"10.1038/s41416-025-02944-3","DOIUrl":"https://doi.org/10.1038/s41416-025-02944-3","url":null,"abstract":"<p><strong>Background: </strong>Prostate cancer (PC) is the commonest male visceral cancer, and second leading cause of cancer mortality in men in the Western world.</p><p><strong>Methods: </strong>Using a forward-mutagenesis Sleeping Beauty (SB) transposon-based screen in a Probasin Cre-Recombinase (Pb-Cre) Pten-deficient mouse model of PC, we identified Arid1a loss as a driver in the development of metastatic disease.</p><p><strong>Results: </strong>The insertion of transposon in the Arid1a gene resulted in a 60% reduction of Arid1a expression, and reduced tumour free survival (SB:Pten^fl/fl Arid1a^INT median 226 days vs SB:Pten^fl/fl Arid1a^WT 293 days, p = 0.02),with elevated rates of metastasis (SB:Pten^fl/fl Arid1a^INT 75% lung metastasis rate vs 17% SB:Pten^fl/fl Arid1a^WT, p < 0.001). We further generated a Pb-Cre Pten- and Arid1a-deficient mouse model, in which loss of Arid1a demonstrated a profound acceleration in tumorigenesis in Pten^fl/fl mice compared to Pten loss alone (Pb-Cre Pten^fl/flArid1a^+/+ median survival of 267 days vs Pb-Cre Pten^fl/fl Arid1a^fl/fl 103 days, p < 0.0001).</p><p><strong>Conclusion: </strong>Our data revealed homozygous Arid1a loss is required to dramatically accelerate prostate tumourigenesis. Analysis of RNA and ChIP -Sequencing data suggests Arid1a loss enhanced the function of AP-1 subunit cFos. In clinical PC cohort, ARID1A and cFos levels stratified an aggressive subset of PC with a poor survival outcome with a median of only 30 months.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Semi-mechanistic efficacy model for PARP + ATR inhibitors-application to rucaparib and talazoparib in combination with gartisertib in breast cancer PDXs.","authors":"Claire C Villette, Nathalie Dupuy, Frances A Brightman, Astrid Zimmermann, Floriane Lignet, Frank T Zenke, Nadia Terranova, Jayaprakasam Bolleddula, Samer El Bawab, Christophe Chassagnole","doi":"10.1038/s41416-024-02935-w","DOIUrl":"https://doi.org/10.1038/s41416-024-02935-w","url":null,"abstract":"<p><strong>Background: </strong>Promising cancer treatments, such as DDR inhibitors, are often challenged by the heterogeneity of responses in clinical trials. The present work aimed to build a computational framework to address those challenges.</p><p><strong>Methods: </strong>A semi-mechanistic pharmacokinetic-pharmacodynamic model of tumour growth inhibition was developed to investigate the efficacy of PARP and ATR inhibitors as monotherapies, and in combination. Key features of the DNA damage response were incorporated into the model to allow the emergence of synthetic lethality, including redundant DNA repair pathways that may be impaired due to genetic mutations, and due to PARP and ATR inhibition. Model parameters were calibrated using preclinical in vivo data for PARP inhibitors rucaparib and talazoparib and the ATR inhibitor gartisertib.</p><p><strong>Results: </strong>The model successfully captured the monotherapy efficacies of rucaparib and talazoparib, as well as the combination efficacy with gartisertib. The model was evaluated against multiple tumour xenografts with diverse genetic backgrounds and was able to capture the observed heterogeneity of response profiles.</p><p><strong>Conclusions: </strong>By enabling simulation of in vivo tumour growth inhibition with PARP and ATR inhibitors for specific tumour types, the model provides a rational approach to support the optimisation of dosing regimens to stratified populations.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular vesicles from pancreatic cancer and its tumour microenvironment promote increased Schwann cell migration.","authors":"Fang Cheng Wong, Sebastian R Merker, Lisa Bauer, Yi Han, Van Manh Hung Le, Carina Wenzel, Lukas Böthig, Max Heiduk, Pascal Drobisch, Venkatesh Sadananda Rao, Farzaneh Malekian, Ana Mansourkiaei, Christian Sperling, Heike Polster, Mathieu Pecqueux, Rouzanna Istvanffy, Linhan Ye, Bo Kong, Daniela E Aust, Gustavo Baretton, Lena Seifert, Adrian M Seifert, Jürgen Weitz, Ihsan Ekin Demir, Christoph Kahlert","doi":"10.1038/s41416-024-02915-0","DOIUrl":"https://doi.org/10.1038/s41416-024-02915-0","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic ductal adenocarcinoma (PDAC) exhibits a high frequency of neural invasion (NI). Schwann cells (SCs) have been shown to be reprogrammed to facilitate cancer cell migration and invasion into nerves. Since extracellular vesicles (EVs) affect the tumour microenvironment and promote metastasis, the present study analysed the involvement of EVs from pancreatic cancer cells and their microenvironment in altering SC phenotype as part of the early events in the process of NI.</p><p><strong>Methods: </strong>EVs were isolated from human/murine PDAC cells, pancreatic stellate cells (PSCs), human tissues and plasma to perform a novel 3D migration assay, qRT-PCR and western blot. Kaplan-Meier and Cox regression analyses were employed to evaluate the clinical potential of plasma EV-derived candidate from 165 PDAC patients.</p><p><strong>Results: </strong>The EVs from PDAC cells, PSCs derived from human tumour tissues, other cell types in the tumour microenvironment from tumour tissues and circulating plasma act as drivers of a pro-migratory phenotype of SCs by inducing dedifferentiation in SCs. Notably, p75NTR expression was upregulated in the plasma-derived EVs from patients with NI (Pn1) relative to those without NI (Pn0). High expression of plasma-derived EV p75NTR correlated with reduced overall survival and was identified as an independent prognostic factor.</p><p><strong>Conclusions: </strong>These findings suggest that EV-mediated SC migration underlies the interactions contributing to PDAC-associated NI with implications for improved outcome and therapeutic strategy.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143036541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory non-coding somatic mutations as drivers of neuroblastoma.","authors":"Annalaura Montella, Matilde Tirelli, Vito Alessandro Lasorsa, Vincenzo Aievola, Vincenza Cerbone, Rosa Manganiello, Achille Iolascon, Mario Capasso","doi":"10.1038/s41416-025-02939-0","DOIUrl":"https://doi.org/10.1038/s41416-025-02939-0","url":null,"abstract":"<p><strong>Background: </strong>Emerging evidence suggests that non-coding somatic single nucleotide variants (SNVs) in cis-regulatory elements (CREs) contribute to cancer by disrupting gene expression networks. However, the role of non-coding SNVs in cancer, particularly neuroblastoma, remains largely unclear.</p><p><strong>Methods: </strong>SNVs effect on CREs activity was evaluated by luciferase assays. Motif analysis and ChIP-qPCR experiments were employed to reveal the transcription factors (TFs) involved in these processes. We exploited CRISPR-Cas9 experiments to elucidate the role of these SNVs on the CREs target genes expression. Cell proliferation and invasion assays were performed to assess their role in neuroblastoma tumorigenesis.</p><p><strong>Results: </strong>Our findings demonstrate that non-coding SNVs modify the transcriptional activity of two CREs altering the binding of STAT3 and SIN3A. Therefore, these SNVs reduce the expression of CTTNBP2 and MCF2L. We demonstrate that these two genes act as tumor suppressor in neuroblastoma. These pathogenetic SNVs may serve as oncogenic drivers by impairing the transcriptional programs essential for neuronal development and differentiation in which both the investigated TFs and target genes are involved.</p><p><strong>Conclusion: </strong>Overall, the understanding of the functional role of non-coding variants elucidates their impact on tumorigenesis and can uncover new potential targets of cancer therapeutic strategies.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patterns of incident Burkitt lymphoma during the HIV epidemic among the Black African and White population in South Africa.","authors":"Carole Metekoua, Yann Ruffieux, Judith Mwansa-Kambafwile, Patricia Kellett, Matthias Egger, Mazvita Muchengeti, Eliane Rohner, Tracey Wiggill","doi":"10.1038/s41416-024-02937-8","DOIUrl":"10.1038/s41416-024-02937-8","url":null,"abstract":"<p><strong>Background: </strong>Burkitt lymphoma (BL) may be HIV-associated but data on BL trends in South Africa (SA), where HIV is highly prevalent, are scarce. We compared BL incidence trends over 36 years among Black African and White individuals.</p><p><strong>Methods: </strong>We included histologically diagnosed BL from the National Cancer Registry in SA between 1986-2021. We computed yearly age-standardised incidence rates (ASIR) by race, and annual percentage changes in ASIR using Joinpoint regression.</p><p><strong>Results: </strong>Between 1986-2021, 2205 Black African (ASIR: 1.68/1,000,000; 95% confidence interval [CI] 1.63-1.73) and 366 White individuals (ASIR: 2.34/1,000,000; 95% CI 2.15-2.53) had incident BL. Median age at diagnosis increased over time, while the male proportion among those diagnosed declined. The ASIR among Black Africans increased from 1986-2012 and declined thereafter with BL incidence peaks shifting from children and elderly to middle-aged adults. Among White individuals, BL rates rose among all age groups over time.</p><p><strong>Conclusions: </strong>The BL epidemiology among Black Africans, with decreasing rates since 2012, may reflect SA's evolving HIV epidemic. In contrast, BL rates among White individuals in SA and many high-income countries continue to increase over time. Further studies are needed to better understand the differences in BL epidemiology across geographic regions and population groups.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A UK population-based case-control study of blood tests before cancer diagnosis in patients with non-specific abdominal symptoms.","authors":"Meena Rafiq, Becky White, Matthew Barclay, Gary Abel, Cristina Renzi, Georgios Lyratzopoulos","doi":"10.1038/s41416-024-02936-9","DOIUrl":"https://doi.org/10.1038/s41416-024-02936-9","url":null,"abstract":"<p><strong>Background: </strong>Abnormal results in commonly used primary care blood tests could be early markers of cancer in patients presenting with non-specific abdominal symptoms.</p><p><strong>Methods: </strong>Using linked data from the UK Clinical Practice Research Datalink (CPRD) and national cancer registry we compared blood test use and abnormal results from the 24-months pre-diagnosis in 10,575 cancer patients (any site), and 52,875 matched-controls aged ≥30 presenting, with abdominal pain or bloating to primary care.</p><p><strong>Results: </strong>Cancer patients had two-fold increased odds of having a blood test (odds ratio(OR):1.51-2.29) and 2-3-fold increased odds of having an abnormal blood test result (OR:2.42-3.30) in the year pre-diagnosis compared to controls. Raised inflammatory markers were the most common abnormality (74-79% of tested cases). Rates of blood test use and abnormal results progressively increased from 7 months pre-diagnosis in cancer patients, with relatively small corresponding increases in symptomatic controls. In cancer patients, the largest increases from baseline were raised platelets in males with abdominal pain (increased 33-fold), raised white blood cell count in males with abdominal bloating (increased 37-fold) and low albumin in females with either symptom (increased 22-41 fold).</p><p><strong>Conclusions: </strong>Common blood test abnormalities are early signals of cancer in some individuals with non-specific abdominal symptoms and could support expedited cancer diagnosis.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}