J Steggall, V Rajeeve, N Al-Subaie, A Naeem, A Ikram, A Naeem, A Hayat
{"title":"Integrative proteo-genomic profiling uncovers key biomarkers of lapatinib resistance in HER2-positive breast cancer.","authors":"J Steggall, V Rajeeve, N Al-Subaie, A Naeem, A Ikram, A Naeem, A Hayat","doi":"10.1038/s41416-025-03174-3","DOIUrl":"https://doi.org/10.1038/s41416-025-03174-3","url":null,"abstract":"<p><strong>Introduction: </strong>Drug resistance is a major obstacle to the long-term effectiveness of cancer therapies. Approximately 70% of breast cancer patients relapse after 5 years of treatment, and the lack of biomarkers associated with drug resistance translates to poor prognosis in the clinic. Previous research has utilised omics approaches to uncover biomarkers driving drug resistance, with a strong emphasis on genetic mutations.</p><p><strong>Methods: </strong>Here, we identified a nine-marker signature associated with resistance to lapatinib in a HER2-positive breast cancer model using a target discovery approach by employing an integrative multi-omics strategy, combining ATAC-seq, RNA-seq and proteomics.</p><p><strong>Results: </strong>We found that seven markers in the drug resistance-signature had not been previously found to be implicated in HER2-positive breast cancer, some of which we further validated using an additional lung cancer model. We counterintuitively found that drug-resistant cells have restrictive chromatin accessibility with reduced gene expression associated with limited total proteome changes. However, upon closer look, we identified that the drug resistance-signature had increased chromatin accessibility near the transcriptional start sites of those seven markers and was highly differentially expressed across the three datasets. Our data show that despite the overall transcriptional and proteomic landscape showing limited changes, there are several markers that are highly expressed, which correlate with increased anchorage-independent and invasive phenotype in vitro in lapatinib-resistant cells compared to cancer cells.</p><p><strong>Conclusions: </strong>Our results demonstrate that disease aggressiveness can be related to reduced chromatin and gene expression dynamics. We anticipate that the resistant signature identified here using an integrative target discovery approach can be applied to complex, more representative models and validated before they can be targeted by suitable therapeutic agents.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058336","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}
Matthias Monnereau, Jean-Pierre Delord, Stefan Michiels, Christophe Le Tourneau, Sebastien Marque, Louise Baschet, Thomas Filleron
{"title":"Acceptance of external control arms by HTA agencies: a review of oncology submissions in France, England, Germany and Norway from 2021 to 2023.","authors":"Matthias Monnereau, Jean-Pierre Delord, Stefan Michiels, Christophe Le Tourneau, Sebastien Marque, Louise Baschet, Thomas Filleron","doi":"10.1038/s41416-025-03155-6","DOIUrl":"https://doi.org/10.1038/s41416-025-03155-6","url":null,"abstract":"<p><strong>Purpose: </strong>External control arms (ECAs) are sometimes considered as an alternative to phase III trials, enabling comparisons without head-to-head trials. Deploying ECAs is complex, partially due to varying regulatory guidelines. We aimed to assess their acceptance in oncology by Health Technology Assessment (HTA) bodies across France, England, Germany, and Norway from 2021 to 2023.</p><p><strong>Methods: </strong>We conducted a review of HTA evaluation reports for oncology treatments using ECAs. Reports were extracted from national HTA body websites and systematically reviewed. Data extraction included drug characteristics, ECA methodology, acceptance status, and reported issues. ECAs were categorized by type of data: Individual Patient Data (IPD), Aggregated Data (AgD), or naive comparisons.</p><p><strong>Results: </strong>We analysed 175 ECAs from 123 reviews, none were accepted without restrictions, and only 17% were not rejected. Acceptance rates varied significantly between countries, with England showing the highest non-rejection rate (accepted with restrictions) (41%), followed by France (14%) while Germany and Norway rejected all ECAs. The main methodological issues identified were lack of/unclear data (54%), heterogeneity between studies or risk of bias (51%), study design concerns (29%), and statistical methodology limitations (26%). These challenges were consistent across different types of ECAs, though their relative importance varied by country.</p><p><strong>Conclusions: </strong>Despite the increasing use of ECAs in oncology trials, their acceptance by HTA bodies remains limited. Our findings highlight significant disparities in assessment approaches between countries and persistent challenges in data quality and methodological consistency. Future efforts should focus on improving transparency, robustness, and residual bias assessment of ECA methodologies.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051841","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}
Abderaouf Hamza, Pierre Gestraud, Maryam Karimi, Alicia Tran-Dien, Laurène Syx, Sophie Vacher, Quentin Peretti, Ludovic Lacroix, Valery Attignon, Isabelle Soubeyran, Pascal Jézéquel, David Planchard, Samia Melaabi, Trenton Dailey-Chwalibóg, Marta Jimenez, Stefan Michiels, Nicolas Servant, Christophe Le Tourneau, Nicolas Girard, Fabrice André, Benjamin Besse, Maud Kamal, Fabrice Barlesi, Ivan Bièche
{"title":"Molecular analysis of lung adenocarcinomas from the SAFIR02-Lung cohort reveals new metastasis-associated copy-number alterations including frequent mutant-specific KRAS-allelic imbalance and identifies CDKN2A homozygous deletions as an independent biomarker of poor prognosis.","authors":"Abderaouf Hamza, Pierre Gestraud, Maryam Karimi, Alicia Tran-Dien, Laurène Syx, Sophie Vacher, Quentin Peretti, Ludovic Lacroix, Valery Attignon, Isabelle Soubeyran, Pascal Jézéquel, David Planchard, Samia Melaabi, Trenton Dailey-Chwalibóg, Marta Jimenez, Stefan Michiels, Nicolas Servant, Christophe Le Tourneau, Nicolas Girard, Fabrice André, Benjamin Besse, Maud Kamal, Fabrice Barlesi, Ivan Bièche","doi":"10.1038/s41416-025-03183-2","DOIUrl":"https://doi.org/10.1038/s41416-025-03183-2","url":null,"abstract":"<p><strong>Background: </strong>Identifying molecular alterations specific to advanced lung adenocarcinomas could provide insights into tumour progression and dissemination mechanisms.</p><p><strong>Method: </strong>We analysed tumour samples, either from locoregional lesions or distant metastases, from patients with advanced lung adenocarcinoma from the SAFIR02-Lung trial by targeted sequencing of 45 cancer genes and comparative genomic hybridisation array and compared them to early tumours samples from The Cancer Genome Atlas.</p><p><strong>Results: </strong>Differences in copy-number alterations frequencies suggest the involvement in tumour progression of LAMB3, TNN/KIAA0040/TNR, KRAS, DAB2, MYC, EPHA3 and VIPR2, and in metastatic dissemination of AREG, ZNF503, PAX8, MMP13, JAM3, and MTURN. Conversely, no meaningful difference was found in pathogenic single-nucleotide variant frequencies, reinforcing the notion that they are early events in tumorigenesis. CDKN2A homozygous deletion was linked to poor clinical outcome in patients with early tumours (overall survival hazard ratio 2.17, 95% CI: 1.43-3.28, corrected p-value = 0.01). Furthermore, we found that KRAS mutant allele specific imbalance, i.e. focal amplification of the mutant allele, is more prevalent in locoregional or distant samples of metastatic patients than in early lesions (8.4%, 13% and 2.8% respectively). This observation was replicated in three public cohorts. Tumours with KRAS mutant allele specific imbalance show specific patterns of co-occurrence and mutual exclusion with alterations in key cancer genes like CDKN2A, TP53, STK11 and NKX2-1, often in a tumour type dependent manner.</p><p><strong>Conclusion: </strong>Advanced LUAD tumours exhibit higher copy-number alteration burden, with distinct alterations associated with tumour progression and metastasis. CDKN2A homozygous deletions predict poor prognosis in early disease, while KRAS mutant allele-specific imbalance is enriched in advanced tumours.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032670","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":"Insulin signalling-associated cell fate promotes neoplastic invasiveness in non-functioning pituitary gonadotroph adenoma via cis-regulatory elements activation.","authors":"Hongwei Liu, Zhouyang Pan, Qi Yang, Luohuan Dai, Wei Zhang, Yihao Zhang, Hongyi Liu, Yueshuo Li, Kexuan Zhong, Jia Gu, Kang Peng, Nian Jiang, Siyi Wanggou, Xuejun Li","doi":"10.1038/s41416-025-03122-1","DOIUrl":"https://doi.org/10.1038/s41416-025-03122-1","url":null,"abstract":"<p><strong>Background: </strong>Non-functioning pituitary gonadotroph adenoma (NFGA) is the most prevalent subtype of pituitary adenomas with a tendency to develop into a refractory invasive type. Currently, effective pharmacotherapy for NFGA remains to be developed due to limited understanding of exact mechanisms of its invasiveness.</p><p><strong>Methods: </strong>Here, we integrated scRNA-seq and scATAC-seq data from three NFGA patients to investigate the cellular heterogeneity underlying tumour invasion. An independent cohort with 210 patients and three primary cell lines was used to evaluate the association between insulin signalling and NFGA invasiveness.</p><p><strong>Results: </strong>We suggested that neoplastic cells exhibited five cellular states with epigenetic heterogeneity along three distinct cell fates. Notably, we identified an insulin signalling-associated cell fate as the driver for tumour invasiveness and invasive NFGAs exhibited elevated insulin resistance-related indices. In vitro assays on primary cell lines showed insulin signalling promoted tumour invasion of NFGA. Additionally, based on cis-co-accessible network analysis, we observed that invasive NFGA reconstructed chromatin-chromatin interactions at insulin signalling-associated-SREBF1-linked cis-regulatory elements (CREs) and IGF2BP2-linked CREs, which recruited active transcriptional factors (TFs) for gene expression activation. We further validated the role of IGF2BP2-linked CREs in regulating IGF2BP2 expression and tumour cell invasion.</p><p><strong>Conclusions: </strong>Our data revealed that cis-regulatory elements activated insulin signalling on invasive cell fate of NFGA and novel therapeutic strategies targeting insulin signalling could be utilised for improving patient outcomes.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039046","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}
Nikila Patil, Zainab Lal, Thiagarajan Sridhar, Manish Pareek, Harriet S. Walter
{"title":"A call for action: closing the gap on ethnic disparities in oral cavity cancer care","authors":"Nikila Patil, Zainab Lal, Thiagarajan Sridhar, Manish Pareek, Harriet S. Walter","doi":"10.1038/s41416-025-03186-z","DOIUrl":"10.1038/s41416-025-03186-z","url":null,"abstract":"The incidence of oral cavity cancers in the UK is rising. Asian/Asian British ethnic groups and socioeconomically deprived groups are at highest risk with some evidence of worse disease outcomes in South Asian individuals receiving radiotherapy. This variation in incidence and outcomes underscores the urgent need for action.","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":"133 7","pages":"917-918"},"PeriodicalIF":6.8,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41416-025-03186-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032680","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}
Shamima Azma Ansari, Sibasish Mohanty, Pallavi Mohapatra, Sudeshna Datta, Mamuni Swain, Rachna Rath, Dillip K Muduly, Saroj K D Majumdar, Rajeeb K Swain, Sunil K Raghav, Rupesh Dash
{"title":"NEK9-mediated Wnt signalling repressor TLE3 rewires Docetaxel resistance in cancer cells by inducing pyroptosis.","authors":"Shamima Azma Ansari, Sibasish Mohanty, Pallavi Mohapatra, Sudeshna Datta, Mamuni Swain, Rachna Rath, Dillip K Muduly, Saroj K D Majumdar, Rajeeb K Swain, Sunil K Raghav, Rupesh Dash","doi":"10.1038/s41416-025-03148-5","DOIUrl":"https://doi.org/10.1038/s41416-025-03148-5","url":null,"abstract":"<p><strong>Background: </strong>Docetaxel is the most common chemotherapy regimen for several neoplasms, including advanced OSCC (Oral Squamous Cell Carcinoma). Unfortunately, chemoresistance leads to relapse and adverse disease outcomes.</p><p><strong>Methods: </strong>We performed CRISPR-based kinome screening to identify potential players of Docetaxel resistance. Immunohistochemistry was performed to examine the expression profile of the target gene across tumour tissues. Global transcriptome analysis was performed to determine the molecular mechanism underlying Docetaxel resistance. NEK9 kinase assay was performed to identify a putative kinase inhibitor.</p><p><strong>Results: </strong>Upon conducting CRISPR-based kinome screening, Never In Mitosis Gene-A Related Kinase-9 (NEK9) was identified as a major player of Docetaxel resistance in OSCC, prostate, and pancreatic cancer lines. NEK9 expression was found to be upregulated in chemotherapy non-responder OSCC patients as compared to responders. NEK9 ablation restores Docetaxel-induced cell death in chemoresistant cells. Mechanistically, we found that NEK9 deletion upregulates Transducin-like enhancer protein 3 (TLE3), which in turn represses Wnt signalling. Fostamatinib was identified as a potent NEK9 inhibitor that overcomes Docetaxel resistance.</p><p><strong>Conclusions: </strong>Our study demonstrated that NEK9 plays an important role in Docetaxel resistance. The novel combination of NEK9 inhibitor Fostamatinib and Docetaxel needs further clinical investigation in advanced OSCC.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145028986","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}
Mengmeng Li, Zhicheng Zhang, Qingzhu Yang, Fei Wang, Xuemei Huang, Huan Nie, Kai Li, Huanjie Yang
{"title":"SLC7A11-AS1 contributes to prolonged activation of activin A/Smad signaling by suppressing PPM1A myristoylation in pancreatic cancer.","authors":"Mengmeng Li, Zhicheng Zhang, Qingzhu Yang, Fei Wang, Xuemei Huang, Huan Nie, Kai Li, Huanjie Yang","doi":"10.1038/s41416-025-03149-4","DOIUrl":"https://doi.org/10.1038/s41416-025-03149-4","url":null,"abstract":"<p><strong>Background: </strong>Activin A/Smad signaling plays an important role in promoting cancer stemness and chemoresistance in pancreatic ductal adenocarcinoma (PDAC), however the precise regulation on the termination of this pathway has not been fully understood.</p><p><strong>Methods: </strong>LncRNA SLC7A11-AS1 interacting proteins were identified through RNA pull-down followed by LC-MS/MS. The protein interaction was analyzed by co-immunoprecipitation. The expressions of SLC7A11-AS1 and activin A in tissue microarray were analyzed by FISH and immunofluerescence. Tumor xenograft mice models were established for in vivo experiments.</p><p><strong>Results: </strong>Overexpression of SLC7A11-AS1 enhanced the activin A-induced Smad2/3 phosphorylation and promoted cancer stemness properties in PDAC cells. Mechanically, SLC7A11-AS1 interacts with scaffold protein RSL1D1. This interaction disrupts PPM1A myristoylation by suppressing the recruitment of PPM1A and myristoyltransferase NMT1 to RSL1D1, leading to prolonged activation of activin A/Smad signaling through the delay of Smad2/3 dephosphorylation. Co-overexpression of SLC7A11-AS1 and activin A were found in pancreatic patients, and related with the extremely short survival periods. Knockdown of SLC7A11-AS1 and blockade of activin A signaling significantly reduced gemcitabine resistance in PDAC in vitro and in vivo.</p><p><strong>Conclusions: </strong>SLC7A11-AS1 contributes to prolonged activation of activin A/Smad signaling by suppressing PPM1A myristoylation. Targeting both SLC7A11-AS1 and activin A may offer a potential therapeutic strategy for overcoming gemcitabine resistance in PDAC.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145028910","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}
Laura A V Marlow, Ninian Schmeising-Barnes, Jo Waller
{"title":"The impact of cancer expectations on psychological responses following a cancer signal detected result in asymptomatic multi-cancer detection (MCED) testing.","authors":"Laura A V Marlow, Ninian Schmeising-Barnes, Jo Waller","doi":"10.1038/s41416-025-03180-5","DOIUrl":"https://doi.org/10.1038/s41416-025-03180-5","url":null,"abstract":"<p><strong>Background: </strong>Multi-cancer detection (MCED) blood tests have the potential to screen for early-stage cancers. Understanding how people experience an MCED cancer signal result is vital prior to any future implementation. We explored experiences in a trial context.</p><p><strong>Methods: </strong>A subset of 41 participants in the NHS-Galleri trial (NCT05611632), with a cancer signal detected result, were interviewed. We selected: 20 participants with cancer found (self-reported) and 21 without cancer (following tests). Transcripts were analysed thematically.</p><p><strong>Results: </strong>Expectations of cancer played a pivotal role in emotional, cognitive and social responses, and were influenced by participants' experiences of health and symptoms. While the cancer signal was often unexpected, the predicted cancer signal origin made sense when consistent with family history or health issues. During the period of diagnostic uncertainty, views of healthiness or lack of family history were sometimes used to self-reassure. For some, a cancer diagnosis was unexpected; for others, expectations of cancer had gradually increased. For those without cancer, believing that it could be present affected their sense of reassurance.</p><p><strong>Discussion: </strong>Information about the meaning of a cancer signal will be needed if MCED screening is implemented. Patient support could be designed around their expectations of cancer at each stage.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145028965","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}
Yejin Mok, Aditya Surapaneni, Yingying Sang, Josef Coresh, Morgan E Grams, Kunihiro Matsushita, Shoshana H Ballew, Natalia Alencar de Pinho, Johan Ärnlöv, Sandhi M Barreto, Samira Bell, Hermann Brenner, Juan-Jesus Carrero, Rajkumar Chinnadurai, Elizabeth Ciemins, Ron T Gansevoort, Simerjot K Jassal, Keum Ji Jung, H Lester Kirchner, Tsuneo Konta, Csaba P Kovesdy, Li Luo, Krutika Pandit, Mahboob Rahman, Cassianne Robinson-Cohen, Charumathi Sabanayagam, Ulla T Schultheiss, Michael Shlipak, Natalie Staplin, Marcello Tonelli, Angela Yee-Moon Wang, Chi-Pang Wen, Mark Woodward, Jennifer S Lees
{"title":"Chronic kidney disease and incident cancer risk: an individual participant data meta-analysis.","authors":"Yejin Mok, Aditya Surapaneni, Yingying Sang, Josef Coresh, Morgan E Grams, Kunihiro Matsushita, Shoshana H Ballew, Natalia Alencar de Pinho, Johan Ärnlöv, Sandhi M Barreto, Samira Bell, Hermann Brenner, Juan-Jesus Carrero, Rajkumar Chinnadurai, Elizabeth Ciemins, Ron T Gansevoort, Simerjot K Jassal, Keum Ji Jung, H Lester Kirchner, Tsuneo Konta, Csaba P Kovesdy, Li Luo, Krutika Pandit, Mahboob Rahman, Cassianne Robinson-Cohen, Charumathi Sabanayagam, Ulla T Schultheiss, Michael Shlipak, Natalie Staplin, Marcello Tonelli, Angela Yee-Moon Wang, Chi-Pang Wen, Mark Woodward, Jennifer S Lees","doi":"10.1038/s41416-025-03140-z","DOIUrl":"https://doi.org/10.1038/s41416-025-03140-z","url":null,"abstract":"<p><strong>Background: </strong>Studies examining the association of chronic kidney disease (CKD) with cancer risk have demonstrated conflicting results.</p><p><strong>Methods: </strong>This was an individual participant data meta-analysis including 54 international cohorts contributing to the CKD Prognosis Consortium. Included cohorts had data on albuminuria [urine albumin-to-creatinine ratio (ACR)], estimated glomerular filtration rate (eGFR), overall and site-specific cancer incidence, and established risk factors for cancer. Included participants were aged 18 years or older, without previous cancer or kidney failure.</p><p><strong>Results: </strong>Among 1,319,308 individuals, the incidence rate of overall cancer was 17.3 per 1000 person-years. Higher ACR was positively associated with cancer risk [adjusted hazard ratio 1.08 (95% CI 1.06-1.10) per 8-fold increase in ACR]. No association of eGFR with overall cancer risk was seen. For site-specific cancers, lower eGFR was associated with urological cancer and multiple myeloma, whereas higher ACR was associated with many cancer types (kidney, head/neck, colorectal, liver, pancreas, bile duct, stomach, larynx, lung, hemolymphatic, leukaemia, and multiple myeloma). Results were similar in a 1-year landmark analysis.</p><p><strong>Discussion: </strong>Albuminuria, but not necessarily eGFR, was independently associated with the subsequent risk of cancer. Our results warrant an investigation into mechanisms that explain the link between albuminuria and cancer.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008121","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}
H. Huang, L. L. Benzonana, H. Zhao, H. R. Watts, N. J. S. Perry, C. Bevan, R. Brown, D. Ma
{"title":"Correction to: Prostate cancer cell malignancy via modulation of HIF-1α pathway with isoflurane and propofol alone and in combination","authors":"H. Huang, L. L. Benzonana, H. Zhao, H. R. Watts, N. J. S. Perry, C. Bevan, R. Brown, D. Ma","doi":"10.1038/s41416-025-03175-2","DOIUrl":"10.1038/s41416-025-03175-2","url":null,"abstract":"","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":"133 7","pages":"1067-1068"},"PeriodicalIF":6.8,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41416-025-03175-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145005976","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}