British Journal of Cancer最新文献

{"title":"PD-L1 CPS in gastroesophageal cancer: differences in routine care versus Checkmate 649 and implications for biopsy-site choice and assay standardisation.","authors":"Lucy Flanders, Thomas Savy, Miriam Ficial, Narjis Al-Ghraibawi, Louise Barber, Sarah Slater, Rille Pihlak, David Propper, Sultana Begum, Manuel Rodriguez-Justo, Marco Gerlinger","doi":"10.1038/s41416-026-03404-2","DOIUrl":"https://doi.org/10.1038/s41416-026-03404-2","url":null,"abstract":"<p><strong>Purpose: </strong>To explore why PD-L1 scores in metastatic gastro-esophageal adenocarcinomas (GEAs) were significantly lower in a real-world cohort compared with the CheckMate 649 (CM649) trial.</p><p><strong>Methods: </strong>PD-L1 combined positive scores (CPS) were evaluated using validated assays in 100 consecutive patients with advanced/metastatic GEA at St Bartholomew's Hospital (SBH) and compared with CM649 (n = 1567). Clinicopathological factors and biopsy site were analysed to assess their impact on PD-L1 results.</p><p><strong>Results: </strong>CPS ≥ 5 was substantially less frequent in SBH patients (30%) compared with CM649 (61%). Older age ( ≥ 65 years), non-diffuse histology, and MMR deficiency were associated with CPS ≥ 5 across both cohorts, yet these factors were more common at SBH and therefore did not explain the lower positivity rate. Metastatic biopsies were more frequent in CM649 (21% vs. 9%), but CPS ≥ 5 was lower in metastases (50%) than in primary tumors (60%). Importantly, PD-L1 positivity varied by metastatic site: lymph node metastases showed the highest rate (80%), while liver (50%) and other sites (44%) were significantly lower than primaries (60%).</p><p><strong>Conclusion: </strong>PD-L1 CPS is shaped by clinicopathological context and biopsy site. The persistently lower CPS ≥ 5 prevalence at SBH despite validated testing highlights assay variability and reinforces the urgent need for assay standardisation. Preferential use of primary tumor tissue may help reduce metastasis-specific bias.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716260","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":"Kidney-specific HIF-1α-dependent ARL10/miR-1271-5p overexpression in clear cell renal cell carcinoma.","authors":"Patric M Page, Tania Laperrière, Sonia A Dastous, Sophie E Landry, Patrick O Richard, Michel Pavic, Sandra Turcotte","doi":"10.1038/s41416-026-03399-w","DOIUrl":"https://doi.org/10.1038/s41416-026-03399-w","url":null,"abstract":"<p><strong>Background: </strong>Clear cell renal cell carcinoma (ccRCC) is primarily driven by chromosome 3p loss and inactivation of the von Hippel-Lindau (VHL) gene, which is frequently accompanied by chromosome 5q gain. However, the oncogenic contribution of 5q remains unclear. This study examines how 5q gain affects the expression of microRNAs implicated in ccRCC.</p><p><strong>Methods: </strong>Bioinformatic analyses were conducted to evaluate miRNAs associated with 5q gain and 3p loss. RT-qPCR validation was performed in tumour tissues and patient plasma. Mechanistic investigations integrated open-source ChIP-seq datasets and luciferase reporter assays.</p><p><strong>Results: </strong>miR-1271-5p overexpression was significantly associated with both 5q gain and 3p loss and strongly correlated with its host gene, ARL10. RT-qPCR confirmed elevated levels of miR-1271-5p and ARL10 in ccRCC tumours and increased circulating miR-1271-5p in patient plasma. Mechanistically, these upregulations resulted from VHL loss and subsequent HIFα stabilisation. ChIP-seq datasets and luciferase assays demonstrated that HIF-1α, but not HIF-2α, directly binds within the intragenic region of ARL10. Importantly, this regulatory mechanism was specific to kidney cells.</p><p><strong>Conclusions: </strong>Coordinated upregulation of miR-1271-5p and ARL10 reflects key genomic events in ccRCC and is driven by kidney-specific HIF-1a activity. Our findings suggest their promise for early detection and disease monitoring.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716233","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":"Identification of novel drug-specific PARP inhibitor resistance mechanisms in ovarian cancer-implications for clinical practice.","authors":"Caitlin J Macdonald, Amber McWhirter, Aparajitha Vaidyanathan, Michelle J Ferguson, H Christian Eberl, Euan A Stronach, Lynne Sawers, Gillian Smith","doi":"10.1038/s41416-026-03423-z","DOIUrl":"https://doi.org/10.1038/s41416-026-03423-z","url":null,"abstract":"<p><strong>Background: </strong>Maintenance PARP inhibitor (olaparib or niraparib) treatment is commonly prescribed following carboplatin/paclitaxel chemotherapy in ovarian cancer patients, but response is compromised by adaptive drug resistance [1]. We have shown that P-gp/ABCB1 influences resistance to paclitaxel and olaparib, but similar niraparib resistance mechanisms have not been described [2, 3].</p><p><strong>Methods: </strong>We used qRT-PCR, Western blot, RNASeq and LC-MS/MS proteomics analysis to compare drug transporter expression in sensitive and resistant immortalised and primary patient-derived cell lines. ABCB1 and ABCG2 expression was modified by shRNA-mediated knockdown and heterologous expression, with chemosensitivity changes assessed by MTT and clonogenic assays. Substrate specificity of P-gp and BCRP was assessed by efflux assays in polarised cells.</p><p><strong>Results: </strong>P-gp/ABCB1 expression was not increased in A2780nirapR cells, which alternatively up-regulated BCRP/ABCG2. ABCG2 was consistently induced in niraparib-resistant patients, but ABCB1 only in patients pre-treated with paclitaxel. shABCG2 re-sensitised A2780nirapR cells, while heterologous expression in A2780 cells induced drug resistance. Efflux assays confirmed that olaparib and niraparib are both P-gp and BCRP substrates, suggesting that resistance results from transcriptional regulation of efflux transporters not substrate specificity.</p><p><strong>Conclusions: </strong>Treatment-induced BCRP/ABCG2 induction is a novel clinically relevant niraparib resistance biomarker. Routine inclusion of paclitaxel in first-line chemotherapy regimens may promote efflux transporter-mediated resistance, compromising response to PARPi maintenance treatment.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716251","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":"Boron neutron capture therapy (BNCT) for experimental bladder cancer: systemic or intravesical approach.","authors":"Kerem Teke, Cüneyt Özer, Büşra Yaprak Bayrak, İskender Atilla Reyhancan, Çiğdem Vural, Murat Kasap, Ayşegül Ünal Karabey, Gürler Akpınar, Efe Bosnalı, Neslihan Koyuncu, İbrahim Erkut Avcı, Onur Erbay, Muhammet Sahip Kızıltaş, Fatih Hunç, Zeyneb Camtakan, Önder Kara, Görkem Aksu, Özdal Dillioğlugil","doi":"10.1038/s41416-026-03418-w","DOIUrl":"https://doi.org/10.1038/s41416-026-03418-w","url":null,"abstract":"<p><strong>Background: </strong>To investigate the antitumoral and pro-inflammatory effect of Boron Neutron Capture Therapy (BNCT) following systemic or intravesical borophenilalanine administration, and to compare it with conventional radiotherapy (cRT) in an experimental bladder cancer (BC) model.</p><p><strong>Methods: </strong>Sixty-four Wistar rats were used, of which half were exposed to carcinogen to induce BC. Radiation therapy (RT) was performed both in the MARK TRIGA-II reactor for BNCT and in the Radiation Oncology divison for cRT. After necropsy, bladder and perivesical tissues were collected. Tumour staging, tumour burden, proliferative, and apoptotic indexes were evaluated for bladder samples. Bladder and perivesical tissues (colon, uterus, and anterior abdominal wall) were also assessed for inflammatory changes in H&E-stained sections, and also bladder TNF-α expressions was examined by immunohistochemistry and Western blot.</p><p><strong>Results: </strong>The animals with cancer had a 15-30% decrease in tumour burden after RT. The incidence of persistent papillary urothelial carcinoma was 100% in the Cancer-cRT group and 87.5% in the Cancer-BNCT-Sys group, whereas a lower incidence was observed in the Cancer-BNCT-IV group (71.4%). A lower proliferative and a higher apoptotic indexes were observed in  Cancer-BNCT-IV group compared to Cancer-cRT. Immunohistochemistry and Western blot for TNF-α expression showed that pro-inflammatory response in bladder was lower in BNCT-IV group among cancer treated groups. Moreover, there were lower proinflammatory adverse findings in perivesical tissues, including colon and uterus, in animals receiving BNCT-IV.</p><p><strong>Conclusion: </strong>Similar to cRT, systemic or intravesical BNCT resulted in a partial decrease in tumour burden, but fewer adverse findings by intravesical borophenilalanine.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716268","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":"Hepatic metastasis surveillance in uveal melanoma: a retrospective cohort study from a UK tertiary centre (2006-2022).","authors":"Benjamin Rea, Mahan Salehi, Ahmed Maiter, Lorraine Ochieng, Sarah Lanham, Joe Kang, Sharabh Sinha, Jenna Hawthorn, Amarit Gill, Christopher Johns, Michael J Campbell, Umiya Harley, Hibba Quhill, Sachin Salvi","doi":"10.1038/s41416-026-03445-7","DOIUrl":"https://doi.org/10.1038/s41416-026-03445-7","url":null,"abstract":"<p><strong>Background: </strong>Liver surveillance imaging is essential for detecting early asymptomatic metastases in uveal melanoma, which predominantly involves the liver. Early detection may improve treatment opportunities, but variability in imaging protocols and a lack of consensus on surveillance duration present challenges. This study aimed to evaluate our systemic surveillance protocol, optimise pathways, and assess risk factors for metastasis.</p><p><strong>Methods: </strong>We retrospectively analysed patients diagnosed with uveal melanoma between 2006 and 2021 who underwent hepatic imaging surveillance at Sheffield Teaching Hospitals NHS Foundation Trust. Demographics, tumour characteristics, treatments, disease status, and survival outcomes were collected.</p><p><strong>Results: </strong>Among 1086 patients (45% female, 79% White; median age 68 years), 315 (29%) developed metastases, with 293 (93%) detected within five years of ocular treatment. The number needed to scan (NNS) increased substantially after five years, indicating reduced detection efficiency. Higher T stage and ciliary body involvement were significantly associated with increased metastatic risk (P < 0.01).</p><p><strong>Conclusions: </strong>Most metastases from uveal melanoma occur within five years of treatment. Personalised, risk-based surveillance strategies considering tumour stage and location may improve efficiency and optimise healthcare resource use.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697705","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":"TLR7 signature of tumour innervation reveals two distinct pathways of triple-negative breast cancer progression.","authors":"Dong-Yu Wang, Zhe Jiang, Yaacov Ben-David, Susan J Done, Eldad Zacksenhaus","doi":"10.1038/s41416-026-03419-9","DOIUrl":"https://doi.org/10.1038/s41416-026-03419-9","url":null,"abstract":"<p><strong>Background: </strong>Emerging evidence indicates that tumour innervation promotes cancer progression via a non-canonical TLR7 signalling pathway. However, its impact across breast cancer subtypes, patient populations, associated molecular pathways, and oncogenic drivers remains poorly defined.</p><p><strong>Methods: </strong>We analysed TLR7 signature scores in human breast cancer across multiple datasets and evaluated their associations with prognosis, clinical outcomes, TNBC subtypes, metastasis, molecular signatures, oncogenic signalling, and pathological complete response.</p><p><strong>Results: </strong>We demonstrate that the TLR7score signature is significantly elevated in triple-negative breast cancer (TNBC) - the most aggressive breast cancer subtype-compared with ER⁺ disease. Within TNBC, high TLR7 signalling characterises basal- and mesenchymal-like tumours relative to the luminal androgen receptor (LAR) subtype. Across multiple breast cancer cohorts, including TNBC, TLR7score alone does not uniformly predict prognosis, as both high- and low-scoring tumours are associated with reduced survival. Using sequential cut-off analysis in seven independent clinical cohorts, we show that both TLR7score-high (e.g.</p><p><strong>, scan-b: </strong>HR = 4.7, P = 0.01) and TLR7score-low (HR = 3.37, P = 0.038) tumours are associated with unfavourable outcomes relative to intermediate-score tumours. TLR7score-high lesions are enriched for cell proliferation, neuronal, and mast cell-related pathways, as well as RB1 and TP53 loss and elevated E2F, PI3K, MET, and MYC signalling. In contrast, TLR7score-low tumours show increased ER signalling and are enriched for T cell-associated but not neuronal pathways, delineating innervated versus non-innervated TNBC phenotypes. Moreover, TLR7score correlates with pathological complete response (pCR) in a treatment-dependent manner.</p><p><strong>Conclusions: </strong>Collectively, these findings suggest that TNBC progression involves both TLR7-dependent and TLR7-independent mechanisms and that TLR7score may enable patient stratification for distinct therapeutic strategies.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688669","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":"Alterations in NK cell subsets and the regulatory role of JAB1 in nasopharyngeal carcinoma with implications for tumor immunity and biomarker development.","authors":"Guangzheng Zhuo, Shuang Li, Gui Yang, Shengbao Hu, Huiqing Wu, Kexin Qin, Junhao Wei, Hui Wang, Guohong Liu, Yunbao Pan","doi":"10.1038/s41416-026-03397-y","DOIUrl":"https://doi.org/10.1038/s41416-026-03397-y","url":null,"abstract":"<p><strong>Objective: </strong>This study investigates changes in NK cell subsets in the blood of NPC patients and explores JAB1's role in shaping the tumor immune environment.</p><p><strong>Methods: </strong>We performed RNA sequencing analyses on NPC PBMCs and tissue samples to identify genes associated with JAB1. Dimensionality reduction and clustering analyses were conducted on paired single-cell RNA sequencing data to explore differences in NK cell subsets. Functional assays assessed the roles of these subsets in various immune environments. Flow cytometry characterised NK cell subsets and cytokine profiles. A humanised immune system mouse model with NPC xenografts supported our findings.</p><p><strong>Results: </strong>Higher levels of CD16 + CD57 + NK cells in blood correlated with better patient outcomes, while increased CD16- NK cells indicated worse prognoses. JAB1 enhanced NK cell cytotoxicity, indicating its role in immune regulation. NK subsets showed distinct distributions: CD16hiCD57- and CD16hiCD57+ cells were mainly in blood, while CD16loCD57- cells accumulated in tumors. Functional tests revealed some subsets promoted tumor growth while others suppressed it. Expression of JAB1 and CD107a in NK cells demonstrated superior diagnostic and prognostic value compared to traditional tumor markers like SCC and CEA.</p><p><strong>Conclusion: </strong>This study identifies key roles of NK cell subsets and JAB1 in NPC immunity, offering insights for biomarker and immunotherapy target development.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697720","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":"ATR inhibition potentiates the antitumor efficacy of HER3-DXd in HER3-positive/HR-positive breast cancer by increasing DNA damage.","authors":"Xuemei Xie, Jangsoon Lee, Young Jin Gi, Thanasis Poullikkas, Jon A Fuson, Pang-Dian Fan, Jami A Fukui, Debu Tripathy, Naoto T Ueno","doi":"10.1038/s41416-026-03413-1","DOIUrl":"https://doi.org/10.1038/s41416-026-03413-1","url":null,"abstract":"<p><strong>Background: </strong>Endocrine resistance remains a major challenge in hormone receptor-positive (HR+) breast cancer (BC), where up to 70% of tumours overexpress HER3, a receptor associated with poor prognosis and therapeutic resistance. HER3-DXd (patritumab deruxtecan) is currently under clinical investigation for HER3-expressing metastatic BC. However, strategies to further enhance its efficacy, particularly in endocrine therapy-resistant settings, are urgently needed. We hypothesised that targeting ATR, a key regulator of DNA damage repair (DDR), potentiates HER3-DXd in HER3+/HR+ BC, including tamoxifen-resistant (TMR) disease.</p><p><strong>Methods: </strong>Synergistic partners for HER3-DXd were identified by whole-genome RNAi screening. Treatments' effects on cell cycle, DNA damage, and protein expression were analysed using flow cytometry, comet assay, and Western blotting, respectively. Treatments' antitumor efficacy was assessed using xenograft mouse models. TCGA and CPTAC databases were analysed for clinical relevance.</p><p><strong>Results: </strong>HER3-DXd inhibited growth in both parental and TMR MCF7 and T47D cells. Compared to monotherapies, combining HER3-DXd with an ATR inhibitor enhanced DNA damage, sub-G1 arrest, apoptosis, downregulation of DDR and cell cycle regulatory proteins, and tumour growth inhibition. TCGA and CPTAC analyses confirmed high HER3 expression and correlation of ATR, CHEK1, and TOP1 gene expression with poor prognosis in HR+ BC.</p><p><strong>Conclusion: </strong>Combining HER3-DXd with an ATR inhibitor could benefit HER3+/HR+ BC patients with both endocrine-sensitive and -resistant diseases.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688576","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":"SUMOylation of EphB4 enhances its stability in prostate cancer.","authors":"Mohanan Sada Nand Maharaj, Inga Mertens-Walker, Jessica E Lisle, Adrian Herington, Carson Stephens, Melissa Chai, Wim Meutermans, Sally-Anne Stephenson","doi":"10.1038/s41416-026-03442-w","DOIUrl":"https://doi.org/10.1038/s41416-026-03442-w","url":null,"abstract":"<p><strong>Background: </strong>The receptor tyrosine kinase EphB4 is frequently overexpressed in epithelial cancers, including prostate cancer (PCa). SUMOylation is a post-translational modification that influences protein interactions, localisation and stability. This study investigated how SUMOylation regulates EphB4 localisation, stability and function in PCa.</p><p><strong>Methods: </strong>EphB4 SUMOylation was analysed in PCa cell lines and its contribution to stability assessed using siRNA or chemical inhibition of SUMOylation. An EphB4 mutant protein (K616R) was expressed in PCa cells and proteasomal inhibition was used to assess its stability. Cell migration was measured using a scratch wound assay. Immunoprecipitation was used to determine if mutant EphB4 could be SUMOylated on other residues.</p><p><strong>Results: </strong>EphB4 in PCa cells is constitutively modified by SUMO2/3 and acquires SUMO1 modification when stimulated with ephrin-B2 ligand. SUMOylation of K616 is critical for EphB4 stability. K616R EphB4 protein is degraded by the proteasome, and this is associated with reduced MYC protein and slower migration. Immunoprecipitation revealed that additional SUMOylated lysines may also contribute to EphB4 function.</p><p><strong>Conclusions: </strong>SUMOylation at K616 stabilises EphB4, promotes MYC signalling and PCa cell migration. These findings identify a novel mechanism regulating EphB4 and highlight SUMOylation as a potential target in EphB4-driven cancers.</p>","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688643","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: Prospective study on 18F-FDG PET-CT for staging locally advanced invasive lobular breast carcinoma","authors":"Ur Metser,&nbsp;Ian S. Dayes,&nbsp;Sameer Parpia,&nbsp;Andrea F. Eisen,&nbsp;Nicole Hodgson,&nbsp;Tulin D. Cil,&nbsp;Ralph George,&nbsp;Phillip Blanchette,&nbsp;Angel Arnaout,&nbsp;Adrien Chan,&nbsp;Mark N. Levine","doi":"10.1038/s41416-026-03435-9","DOIUrl":"10.1038/s41416-026-03435-9","url":null,"abstract":"","PeriodicalId":9243,"journal":{"name":"British Journal of Cancer","volume":"134 10","pages":"1498-1498"},"PeriodicalIF":6.8,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41416-026-03435-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688560","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}