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Italian guidelines for cervical cancer screening. Multisocietal recommendations on the use of biomarkers in HPV screening with risk-based approach and GRADE methodology. 意大利子宫颈癌筛查指南。在基于风险的方法和GRADE方法的HPV筛查中使用生物标志物的多社会建议。
IF 6.8 1区 医学
British Journal of Cancer Pub Date : 2025-09-11 DOI: 10.1038/s41416-025-03161-8
Silvia Gori, Francesco Venturelli, Francesca Carozzi, Paolo Giorgi Rossi, Annarosa Del Mistro
{"title":"Italian guidelines for cervical cancer screening. Multisocietal recommendations on the use of biomarkers in HPV screening with risk-based approach and GRADE methodology.","authors":"Silvia Gori, Francesco Venturelli, Francesca Carozzi, Paolo Giorgi Rossi, Annarosa Del Mistro","doi":"10.1038/s41416-025-03161-8","DOIUrl":"https://doi.org/10.1038/s41416-025-03161-8","url":null,"abstract":"<p><p>The European Council recommends adopting risk-based screening when relevant. In triaging HPV-positive women, it can be an effective strategy to reduce overtreatment and referral to colposcopy. HPV genotyping and p16/ki67 expression may allow a better risk stratification than cytology. In Italy, recommendations on their use (alone or combined) in screening were developed by a multi-professional (nine scientific societies) and multidisciplinary working group (including patients and decision makers). Grading of Recommendations Assessment, Development and Evaluation (GRADE) Evidence to Decision frameworks were used. Data from large clinical trials on screening populations with long follow-up instructed the biomarkers' evaluation. The working group defined the CIN3+ risk thresholds (a surrogate marker of cancer risk) to guide decisions on management: immediate colposcopy, referral to 1-year and 3-year retesting. The risk-based approach allowed to reduce the number of possible strategies to be compared to five specific healthcare questions framed as PICOs. The prioritised outcomes were risk of cancer and of CIN3+ in HPV+/triage-negative women, number of colposcopies, number of samples to be taken, and number of unneeded treatments. The combination of morphological markers (cytology or p16/ki67) and extended HPV genotyping was the only strategy with a conditional recommendation in favour when compared with cytology.</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":"145032708","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}
引用次数: 0
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. 来自SAFIR02-Lung队列的肺腺癌分子分析揭示了新的转移相关拷贝数改变,包括频繁的突变特异性kras等位基因失衡,并将CDKN2A纯合缺失确定为预后不良的独立生物标志物。
IF 6.8 1区 医学
British Journal of Cancer Pub Date : 2025-09-11 DOI: 10.1038/s41416-025-03183-2
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}
引用次数: 0
Insulin signalling-associated cell fate promotes neoplastic invasiveness in non-functioning pituitary gonadotroph adenoma via cis-regulatory elements activation. 胰岛素信号相关的细胞命运通过顺式调节元件激活促进无功能垂体促性腺腺瘤的肿瘤侵袭性。
IF 6.8 1区 医学
British Journal of Cancer Pub Date : 2025-09-11 DOI: 10.1038/s41416-025-03122-1
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
{"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}
引用次数: 0
A call for action: closing the gap on ethnic disparities in oral cavity cancer care 呼吁采取行动:消除口腔癌治疗中的种族差异。
IF 6.8 1区 医学
British Journal of Cancer Pub Date : 2025-09-10 DOI: 10.1038/s41416-025-03186-z
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,&nbsp;Zainab Lal,&nbsp;Thiagarajan Sridhar,&nbsp;Manish Pareek,&nbsp;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}
引用次数: 0
NEK9-mediated Wnt signalling repressor TLE3 rewires Docetaxel resistance in cancer cells by inducing pyroptosis. nek9介导的Wnt信号抑制因子TLE3通过诱导焦亡重新介导癌细胞对多西他赛的耐药。
IF 6.8 1区 医学
British Journal of Cancer Pub Date : 2025-09-09 DOI: 10.1038/s41416-025-03148-5
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}
引用次数: 0
SLC7A11-AS1 contributes to prolonged activation of activin A/Smad signaling by suppressing PPM1A myristoylation in pancreatic cancer. SLC7A11-AS1通过抑制胰腺癌中PPM1A肉豆肉酰化而延长激活素A/Smad信号的激活。
IF 6.8 1区 医学
British Journal of Cancer Pub Date : 2025-09-09 DOI: 10.1038/s41416-025-03149-4
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}
引用次数: 0
The impact of cancer expectations on psychological responses following a cancer signal detected result in asymptomatic multi-cancer detection (MCED) testing. 癌症预期对无症状多癌检测(MCED)检测结果中癌症信号检测后心理反应的影响。
IF 6.8 1区 医学
British Journal of Cancer Pub Date : 2025-09-09 DOI: 10.1038/s41416-025-03180-5
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}
引用次数: 0
Chronic kidney disease and incident cancer risk: an individual participant data meta-analysis. 慢性肾脏疾病和癌症风险:个体参与者数据荟萃分析
IF 6.8 1区 医学
British Journal of Cancer Pub Date : 2025-09-06 DOI: 10.1038/s41416-025-03140-z
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}
引用次数: 0
Correction to: Prostate cancer cell malignancy via modulation of HIF-1α pathway with isoflurane and propofol alone and in combination 更正:异氟醚和异丙酚单独或联合使用对HIF-1α通路的调节可导致前列腺癌细胞恶性。
IF 6.8 1区 医学
British Journal of Cancer Pub Date : 2025-09-05 DOI: 10.1038/s41416-025-03175-2
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,&nbsp;L. L. Benzonana,&nbsp;H. Zhao,&nbsp;H. R. Watts,&nbsp;N. J. S. Perry,&nbsp;C. Bevan,&nbsp;R. Brown,&nbsp;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}
引用次数: 0
Recommendations for studying the association of the cancer diagnosis to treatment interval with overall survival: a modified Delphi process. 研究癌症诊断与治疗间隔与总生存期之间关系的建议:一种改进的德尔菲过程。
IF 6.8 1区 医学
British Journal of Cancer Pub Date : 2025-09-05 DOI: 10.1038/s41416-025-03158-3
Matthew Jalink, Will D King, Benjamin O Anderson, Rinku Sutradhar, Marie Louise Tørring, Michael D Brundage, Patti A Groome, Kelvin K W Chan, Robin Urquhart, Yingwei Peng, Antoine Eskander, Surbhi Grover, Michael J Raphael, Richard Grieve, Cassidy Laub, Christopher M Booth, Timothy P Hanna
{"title":"Recommendations for studying the association of the cancer diagnosis to treatment interval with overall survival: a modified Delphi process.","authors":"Matthew Jalink, Will D King, Benjamin O Anderson, Rinku Sutradhar, Marie Louise Tørring, Michael D Brundage, Patti A Groome, Kelvin K W Chan, Robin Urquhart, Yingwei Peng, Antoine Eskander, Surbhi Grover, Michael J Raphael, Richard Grieve, Cassidy Laub, Christopher M Booth, Timothy P Hanna","doi":"10.1038/s41416-025-03158-3","DOIUrl":"https://doi.org/10.1038/s41416-025-03158-3","url":null,"abstract":"<p><strong>Background: </strong>The duration from diagnosis to primary treatment initiation (DTI) is an important interval for patients with cancer, as delayed treatment has been found to be associated with heightened recurrence rates and worsened survival. Studying the association between DTI duration and overall survival (OS) is biased and confounded by clinical triaging, heterogeneous definitions, and variation in analytic approaches.</p><p><strong>Objective: </strong>To develop consensus-based guidance for conducting studies investigating the association of DTI duration and OS.</p><p><strong>Methods: </strong>A multidisciplinary panel was recruited to participate in a three-round modified Delphi approach to develop consensus recommendations on the best methodological practices when studying the association between DTI duration and OS.</p><p><strong>Results: </strong>The Delphi panel consisted of 15 experts in the fields of epidemiology, biostatistics, health services research, oncology, and health policy. A list of 24 recommendations with accompanying elaborations was generated including variable definition and measurement, cohort creation, confounder control, pertinent biases, analytic techniques, and balanced interpretation of results.</p><p><strong>Conclusion: </strong>Providing valid evidence of the DTI effect on OS requires careful approaches. This paper offers recommendations on how to improve methodological quality. This will ensure that future studies effectively contribute to evidence-informed practice decisions on appropriate waiting times for patients with cancer.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144999730","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}
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