British Journal of Cancer最新文献

{"title":"Correction: Differential cellular origins of the extracellular matrix of tumor and normal tissues according to colorectal cancer subtypes","authors":"Hyun Jin Lee, Sang Woo Park, Jun Hyeong Lee, Shin Young Chang, Sang Mi Oh, Siwon Mun, Junho Kang, Jong-Eun Park, Jung Kyoon Choi, Tae Il Kim, Jin Young Kim, Pilnam Kim","doi":"10.1038/s41416-025-02988-5","DOIUrl":"10.1038/s41416-025-02988-5","url":null,"abstract":"","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":"132 9","pages":"862-862"},"PeriodicalIF":6.4,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41416-025-02988-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143884261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Infectious agents and progression from Barrett's oesophagus to oesophageal adenocarcinoma: a nested case-control study.","authors":"Talita H A de Oliveira, Lesley A Anderson, Stephanie G Craig, Helen G Coleman, Tarik Gheit, Sandrine McKay-Chopin, Jacqueline Jamison, Damian T McManus, Christopher R Cardwell, Victoria Bingham, Brian T Johnston, Jacqueline A James, Andrew T Kunzmann","doi":"10.1038/s41416-025-03003-7","DOIUrl":"https://doi.org/10.1038/s41416-025-03003-7","url":null,"abstract":"<p><strong>Background: </strong>A causal role of high-risk HPV in oesophageal adenocarcinoma development has been hypothesised, but longitudinal evidence is limited. This study aims to investigate a potential causal role of infectious agents in the malignant progression of Barrett's oesophagus.</p><p><strong>Methods: </strong>Using a retrospective nested case-control study design, index Barrett's biopsies were retrieved for individuals within the Northern Ireland Barrett's oesophagus register who subsequently progressed to oesophageal adenocarcinoma (n = 150) and matched non-progressors (n = 298). Index Barrett's biopsies were assessed for the presence of 142 infectious agents by multiplex polymerase chain reaction using the Luminex platform. RNA in-situ hybridisation assessed persistent transcriptional activity in subsequent tissue samples, for infectious agents detected more frequently in progressors.</p><p><strong>Results: </strong>High-risk HPV genotypes (HPV16 and HPV18) were only identified in the index biopsies of progressors but not non-progressors (4% [5/150] versus 0% [0/298], P = 0.004), though no signs of persistence or transcriptional activity were observed in subsequent tissue. Prevalence of infections did not differ between progressors and non-progressors for any other infectious agents, including Helicobacter Pylori and Herpes.</p><p><strong>Conclusion: </strong>Despite a higher prevalence of high-risk HPV in progressors than non-progressors, no evidence of transcriptionally active high-risk HPV was observed in subsequent samples, indicating presence in Barrett's is likely non-causal.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810482","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":"Development of radiomics-based models on mammograms with mass lesions to predict prognostically relevant characteristics of invasive breast cancer in a screening cohort.","authors":"Jim Peters, Merle M van Leeuwen, Nikita Moriakov, Jos A A M van Dijck, Ritse M Mann, Jonas Teuwen, Esther H Lips, Alexandra W van den Belt-Dusebout, Jelle Wesseling, Bas B L Penning de Vries, Sarah Verboom, Nico Karssemeijer, Sjoerd G Elias, Mireille J M Broeders","doi":"10.1038/s41416-025-02995-6","DOIUrl":"10.1038/s41416-025-02995-6","url":null,"abstract":"<p><strong>Background: </strong>Optimizing breast-screening performance involves minimizing overdiagnosis of prognostically favorable invasive breast cancer (IBC) that does not need immediate recall and underdiagnosis of prognostically unfavorable IBC that is not recalled timely. We investigated whether mammographic features of masses predict prognostically relevant IBC characteristics.</p><p><strong>Methods: </strong>In a screening cohort, we obtained pathological information of 1587 IBCs presenting as a mass through the nationwide cancer registry and pathology databank. We developed models based on mammographic tumor appearance to predict whether IBC was prognostically favorable (T1N0M0 luminal A-like) or unfavorable. Models were based on 1095 positive screening mammograms (possible overdiagnosis), or on 603 last negative mammograms with in retrospect visible masses (possible underdiagnosis). We calculated performance metrics using cross-validation.</p><p><strong>Results: </strong>23.5% of masses were prognostically favorable IBC. Using 1095 positive mammograms, the model's predictions to have prognostically favorable IBC (10th-90th percentile range 8.7-47.0%) yielded AUC 0.75 (SD across repeats 0.01), slope 1.16 (SD 0.07). Performance in 603 last negative screening mammograms with masses was poor: AUC 0.60 (SD 0.02), slope 0.85 (SD 0.28).</p><p><strong>Conclusions: </strong>Mammography-based models from masses representing IBC at time of recall (possible overdiagnosis) predict prognostically relevant characteristics of IBC. Models based on in retrospect visible masses (possible underdiagnosis) performed poorly.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787939","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":"De novo colorectal cancer after kidney transplantation: a systematic review and meta-analysis.","authors":"Bima J Hasjim, Arsha Ostowari, Monique Gandawidjaja, Mohsen D Mohammadi, Linda Suk-Ling Murphy, Matthew D Whealon, Valery Vilchez, Hirohito Ichii, Robert R Redfield, Oliver S Eng","doi":"10.1038/s41416-025-02994-7","DOIUrl":"10.1038/s41416-025-02994-7","url":null,"abstract":"<p><strong>Background: </strong>Kidney transplant (KT) patients have higher risks of developing de novo colorectal cancer (CRC) compared to the general population. However, there is still a knowledge gap in their clinical characteristics, as most single- or multi-center efforts are underpowered and lack generalizability.</p><p><strong>Methods: </strong>PubMed, Web of Science, Cochrane CENTRAL, and Scopus databases were queried for studies published until July 22^nd, 2024. Studies reporting the clinicopathologic characteristics and outcomes of de novo CRC among KT recipients were included.</p><p><strong>Results: </strong>There were 49 articles included involving 1855 KT patients who developed CRC. The mean time from transplantation to CRC diagnosis was 8·7 years (95%CI 7·2, 10·3 years; I² = 98·3%). De novo CRC was most commonly located in the ascending colon (43·6%; 95%CI 29·5%, 58·9%; I² = 55·3%), and 37·1% had advanced CRC at diagnosis (95%CI 22·3%, 54·8%; I² = 64·1%). Although 68·8% underwent curative intent treatment (95%CI 45·4%, 85·4%; I² = 65·4%), pooled 5-year survival rate was 31·8% (95%CI 10·5%, 65·1%; I² = 82·5%).</p><p><strong>Conclusions: </strong>De novo CRC was diagnosed in under 10 years after KT, and nearly 40% of patients already have advanced stage disease at diagnosis. The pooled rate of 5-year survival was 31.8%. However, there was wide heterogeneity between studies and further research is required. PROSPERO Registration: CRD42023415767.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787936","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":"Anti-Inflammatory Diet Index and risk of renal cell carcinoma.","authors":"Tahir Taj, Pernilla Sundqvist, Alicja Wolk, Katja Fall, Henrik Ugge","doi":"10.1038/s41416-025-03000-w","DOIUrl":"10.1038/s41416-025-03000-w","url":null,"abstract":"<p><strong>Introduction: </strong>A diet rich in fruits, vegetables, coffee, and tea, limited red meat, and moderate alcohol intake may reduce the risk of renal cell carcinoma (RCC). The anti-inflammatory potential of diet has been proposed as a mechanism influencing cancer risk. This study assessed the association between an anti-inflammatory diet and RCC risk.</p><p><strong>Methodology: </strong>Data from two Swedish cohorts, the Swedish-Mammography-Cohort and the Cohort-of-Swedish-Men, were analysed. Dietary habits were assessed using a 96-item food frequency questionnaire. The Anti-Inflammatory Diet Index (AIDI), composed of 16 food groups (11 anti-inflammatory and 5 pro-inflammatory), was used to score dietary patterns. RCC cases were identified from the Swedish Cancer Register using ICD-10 codes, and Cox proportional hazards models were used to estimate hazard ratios based on AIDI quartiles.</p><p><strong>Results: </strong>Among 71,421 participants, 431 RCC cases were identified during a 19.7-year follow-up. Higher AIDI scores were associated with a lower RCC risk (HR for Q4 vs. Q1: 0.68, CI: 0.52-0.89). In sex-stratified analyses (p-for heterogeneity = 0.006), the association was stronger in among women (HR: 0.47, CI: 0.30-0.75) but less clear in among men (HR: 0.83, CI: 0.63-1.24).</p><p><strong>Conclusion: </strong>These data suggest that adherence to an anti-inflammatory diet may confer a reduced risk for RCC, especially among women.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787934","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":"PD-L1 imaging with [^99mTc]NM-01 SPECT/CT is associated with metabolic response to pembrolizumab with/without chemotherapy in advanced lung cancer.","authors":"Daniel Johnathan Hughes, Gitasha Chand, Jessica Johnson, Ronan Tegala, Damion Bailey, Kathryn Adamson, Scott Edmonds, Levente K Meszaros, Amelia Elizabeth Broomfield Moore, Thubeena Manickavasagar, Susan Ndagire, Spyridon Gennatas, Alexandros Georgiou, Sharmistha Ghosh, Debra Josephs, Eleni Karapanagiotou, Emma McLean, Hong Hoi Ting, James Spicer, Vicky Goh, Gary J R Cook","doi":"10.1038/s41416-025-02991-w","DOIUrl":"https://doi.org/10.1038/s41416-025-02991-w","url":null,"abstract":"<p><strong>Background: </strong>Programmed death-ligand 1 (PD-L1) immunohistochemistry is a predictive biomarker for anti-PD-(L)1 therapy in non-small cell lung cancer (NSCLC). It is not a reliable predictor of clinical benefit with non-invasive imaging providing a potential solution. We present the PECan study, the aim of which to assess the relationship of [^99mTc]-labeled anti-PD-L1 single-domain antibody (NM-01) single-photon emission computed tomography (SPECT)/CT with metabolic response to anti-PD-(L)1.</p><p><strong>Methods: </strong>PD-L1 tumour proportion score (TPS) measured using SP263 assay. [^99mTc]NM-01 SPECT/CT and [¹⁸F]FDG PET/CT performed before and 9-weeks following pembrolizumab with/without chemotherapy in patients with advanced NSCLC. Tumor (T) to blood pool (BP) maximum region of interest (ROI_max) measurements performed in primary and metastatic lesions using SPECT/CT images.</p><p><strong>Results: </strong>Fifteen patients were included (median age 63 years, 9 male). Intertumoural heterogeneity evident in 10(67%) patients. Mean [^99mTc]NM-01 T:BP demonstrated moderate correlation with PD-L1 TPS (r = 0.45, p < 0.05). Depth of [¹⁸F]FDG PET/CT metabolic response at 9-weeks (n = 13), correlated strongly with baseline [^99mTc]NM-01 T:BP (r = -0.73, p < 0.05), but only moderately with PD-L1 TPS (r = -0.46, p = 0.06).</p><p><strong>Conclusion: </strong>[^99mTc]NM-01 SPECT/CT allows non-invasive quantification of PD-L1 in primary tumour and metastases in NSCLC. [^99mTc]NM-01 uptake moderately correlates with PD-L1 immunohistochemistry, determines heterogeneity, and is associated with early metabolic response to anti-PD-1 pembrolizumab.</p><p><strong>Clinical trials registration: </strong>PD-L1 Expression in Cancer (PECan) study (NCT04436406), registered 18 June 2020 https://clinicaltrials.gov/ct2/show/NCT04436406.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787915","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":"YKL-40 and risk of incident cancer in early type 2 diabetes: a Danish cohort study.","authors":"Alisa D Kjaergaard, Allan A Vaag, Verena H Jensen, Michael H Olsen, Kurt Højlund, Peter Vestergaard, Torben Hansen, Reimar W Thomsen, Niels Jessen","doi":"10.1038/s41416-025-02996-5","DOIUrl":"10.1038/s41416-025-02996-5","url":null,"abstract":"<p><strong>Background: </strong>We examined the association of serum YKL-40, an inflammatory biomarker, with incident cancer risk in early type 2 diabetes.</p><p><strong>Methods: </strong>A cohort of 11,346 individuals newly diagnosed with type 2 diabetes was followed for up to 14 years. YKL-40 levels (n = 9010) were categorised into five percentiles (0-33%, 34-66%, 67-90%, 91-95%, and 96-100%), and baseline YKL-40 and CRP (n = 9644) were analyzed continuously (per 1 SD log increment) for comparison. Cox regression models assessed associations with obesity-related, gastrointestinal, liver, pancreatic, colorectal, bladder and lung cancers, as well as cancers of reproductive organs.</p><p><strong>Results: </strong>Adjusted HRs (95% CIs) for the highest versus lowest YKL-40 category were 2.4 (1.6-3.7) for obesity-related, 2.6 (1.7-4.1) for gastrointestinal, 44.2 (12.8-153.4) for liver, and 4.2 (1.3-14.1) for bladder cancers. No associations were found for other cancers. YKL-40 and CRP had similar prognostic abilities for obesity-related and gastrointestinal cancers, but YKL-40 outperformed CRP for liver and bladder cancers. Conversely, CRP was a stronger predictor for lung, colorectal, and ovarian cancers.</p><p><strong>Discussion: </strong>YKL-40 was associated with the risks of liver and bladder cancers, clearly outperforming CRP for these cancers. This suggests distinct prognostic roles for YKL-40 and CRP, and highlights YKL-40 as a promising biomarker for liver cancer.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787919","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":"Unveiling the origin and functions of diagnostic circulating microRNAs in lung cancer.","authors":"Tommaso Colangelo, Francesco Mazzarelli, Roberto Cuttano, Elisa Dama, Valentina Melocchi, Miriam Kuku Afanga, Rosa Maria Perrone, Paolo Graziano, Fabrizio Bianchi","doi":"10.1038/s41416-025-02982-x","DOIUrl":"https://doi.org/10.1038/s41416-025-02982-x","url":null,"abstract":"<p><strong>Background: </strong>Circulating microRNAs (c-miRs) were shown to be effective biomarkers for lung cancer early detection. However, the understanding of c-miRs origin and their biological functions still remains elusive.</p><p><strong>Methods: </strong>We analysed miRNA expression in a large panel of lung cancer (LC) and hematopoietic cell lines (N = 252; CCLE database) coupled with c-miR profile of a large cohort of serum samples (N = 975), from high-risk subjects underwent annual LD-CT for 5 years. Furthermore, we examined intracellular and extracellular miR-29a-3p/223-3p expression profile in lung adenocarcinoma (LUAD) tissues, in matched serum samples and in LC and stromal cell lines. Lastly, through the modulation of expression of selected c-miRs by using mimic (OE) or antisense microRNA (KD), we explored their impact on lung cancer transcriptome and cancer and immune phenotypes.</p><p><strong>Results: </strong>Here, we investigated the origin of an extensively validated 13 c-miRs signature diagnostics for asymptomatic lung cancer (LC) in high-risk subjects (smokers, >20 packs/y; >50 y old). Overall, we found a mixed origin of these c-miRs, originating both from tumour cells and the tumour microenvironment (TME). Intriguingly, we revealed that circulating miR-29a-3p and miR-223-3p are abundantly released from LC epithelial cells and immune cells, respectively. In particular, we found that miR-223-3p triggered several lung cancer related phenotypes such as invasion, migration and tumour-promoting inflammation.</p><p><strong>Conclusions: </strong>Our study highlights a mixed tumour epithelial and stroma-associated origin of LC c-miRs with new evidences on the multifaceted role of miR-223-3p in LC pathogenesis and immune modulation.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787917","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":"Particulate matter air pollution as a cause of lung cancer: epidemiological and experimental evidence.","authors":"Meng Wang, Richard Y Kim, Maija R J Kohonen-Corish, Hui Chen, Chantal Donovan, Brian G Oliver","doi":"10.1038/s41416-025-02999-2","DOIUrl":"https://doi.org/10.1038/s41416-025-02999-2","url":null,"abstract":"<p><p>Air pollution has a significant global impact on human health. Epidemiological evidence strongly suggests that airborne particulate matter (PM), the dust components of polluted air, is associated with increased incidence and mortality of lung cancer. PM2.5 (PM less than 2.5 µm) from various sources carries different toxic substances, such as sulfates, organic compounds, polycyclic aromatic hydrocarbons, and heavy metals, which are considered major carcinogens that increase lung cancer risk. The incidence and mortality of lung cancer caused by PM2.5 exposure may be due to significant geographical differences, and can be influenced by various factors, including local sources of air pollution, socioeconomic conditions, and public health measures. This review aims to provide comprehensive insights into the health implications of air pollution and to inform strategies for lung cancer prevention, by summarising the relationship between exposure to PM2.5 and lung cancer development. We explore the different sources of PM2.5 and relevant carcinogenic mechanisms in the context of epidemiological studies on the development of lung cancer from various geographical regions worldwide.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787913","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":"Expanding the horizon of prognostic markers in oral epithelial dysplasia: a critical appraisal of the novel AI-based IEL score","authors":"Carlos M. Ardila,&nbsp;Pradeep Kumar Yadalam","doi":"10.1038/s41416-025-03010-8","DOIUrl":"10.1038/s41416-025-03010-8","url":null,"abstract":"","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":"132 9","pages":"755-756"},"PeriodicalIF":6.4,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779033","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}