Nature genetics最新文献

{"title":"ERG-driven prostate cancer initiation is cell-context dependent and requires KMT2A and DOT1L","authors":"Weiran Feng, Erik Ladewig, Matthew Lange, Nazifa Salsabeel, Huiyong Zhao, Young Sun Lee, Anuradha Gopalan, Hanzhi Luo, Wenfei Kang, Ning Fan, Eric Rosiek, Elisa de Stanchina, Yu Chen, Brett S. Carver, Christina S. Leslie, Charles L. Sawyers","doi":"10.1038/s41588-025-02289-w","DOIUrl":"10.1038/s41588-025-02289-w","url":null,"abstract":"Despite the high prevalence of ERG transcription factor translocations in prostate cancer, the mechanism of tumorigenicity remains poorly understood. Using lineage tracing, we find the tumor-initiating activity of ERG resides in a subpopulation of murine basal cells that coexpress luminal genes (BasalLum) and not in the larger population of ERG+ luminal cells. Upon ERG activation, BasalLum cells give rise to highly proliferative intermediate (IM) cells with stem-like features that coexpress basal, luminal, hillock and club marker genes, before transitioning to Krt8+ luminal cells. Transcriptomic analysis of ERG+ human prostate cancers confirms the presence of rare ERG+ BasalLum cells, as well as IM cells whose presence is associated with a worse prognosis. Single-cell analysis revealed a chromatin state in ERG+ IM cells enriched for STAT3 transcription factor binding sites and elevated expression of the KMT2A/MLL1 and DOT1L, all three of which are essential for ERG-driven tumorigenicity in vivo. In addition to providing translational opportunities, this work illustrates how single-cell approaches combined with lineage tracing can identify cancer vulnerabilities not evident from bulk analysis. Lineage tracing in mice identifies a subpopulation of basal cells that express Tmprss2 and Nkx3 as the origin of ERG-driven prostate cancer. Upon expansion, these cells show an enrichment for STAT3 chromatin binding and elevated expression of KMT2A and DOT1L as dependencies for ERG oncogenicity.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2177-2191"},"PeriodicalIF":29.0,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02289-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144900354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mutational landscape of triple-negative breast cancer in African American women","authors":"Song Yao, Lei Wei, Qiang Hu, Song Liu, Zarko Manojlovic, Peter N. Fiorica, Mark Long, Gary R. Zirpoli, Qiuyin Cai, Jirong Long, Jie Ping, Mollie E. Barnard, Yuxin Jin, Mitsuko Murakami, Jianmin Wang, Qianqian Zhu, Warren Davis, Jianhong Chen, Rochelle P. Ondracek, Thaer Khoury, Shipra Gandhi, Kazuaki Takabe, Naomi Ko, Maureen Sanderson, Chi-Chen Hong, Elisa V. Bandera, David W. Craig, Christine B. Ambrosone, Julie R. Palmer, Wei Zheng, John D. Carpten","doi":"10.1038/s41588-025-02322-y","DOIUrl":"10.1038/s41588-025-02322-y","url":null,"abstract":"African American (AA) women have the highest incidence of triple-negative breast cancer (TNBC) among all racial groups, but are underrepresented in cancer genomic studies. In 462 AA women with TNBC, we characterized the tumor mutational landscape by whole-exome sequencing and RNA sequencing. We unveiled a high-resolution mutational portrait of TNBC in AA women reminiscent of that in Asian and non-Hispanic white women, with no evidence of associations of mutational features with African ancestry. We also made some distinctive discoveries, including an almost complete dominance of TP53 mutations, low frequency of PIK3CA mutations and mutational signature-based subtypes with etiologic and prognostic significance. These findings do not support major racial differences in TNBC biology at the level of somatic mutations. Our study contributes considerably to diversifying the knowledge base of breast cancer genomics and provides insights into the disease etiology, disparities and therapeutic vulnerability of TNBC in AA women. This study explores the genomic and transcriptomic landscapes of triple-negative breast cancer in African American women. The authors show that the mutational profile is broadly similar to that observed in European and East Asian ancestry women while highlighting some interesting differences.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2166-2176"},"PeriodicalIF":29.0,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02322-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144900355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tamoxifen induces PI3K activation in uterine cancer","authors":"Kirsten Kübler, Agostina Nardone, Shankara Anand, Daniel Gurevich, Jianjiong Gao, Marjolein Droog, Francisco Hermida-Prado, Tara Akhshi, Ariel Feiglin, Avery S. Feit, Gabriella Cohen Feit, Gwen Dackus, Matthew Pun, Yanan Kuang, Justin Cha, Mendy Miller, Sebastian Gregoricchio, Mirthe Lanfermeijer, Sten Cornelissen, William J. Gibson, Cloud P. Paweletz, Eliezer M. Van Allen, Flora E. van Leeuwen, Petra M. Nederlof, Quang-Dé Nguyen, Marian J. E. Mourits, Milan Radovich, Ignaty Leshchiner, Chip Stewart, Ursula A. Matulonis, Wilbert Zwart, Yosef E. Maruvka, Gad Getz, Rinath Jeselsohn","doi":"10.1038/s41588-025-02308-w","DOIUrl":"10.1038/s41588-025-02308-w","url":null,"abstract":"Mutagenic processes and clonal selection contribute to the development of therapy-associated secondary neoplasms, a known complication of cancer treatment. The association between tamoxifen therapy and secondary uterine cancers is uncommon but well established; however, the genetic mechanisms underlying tamoxifen-driven tumorigenesis remain unclear. We find that oncogenic PIK3CA mutations, common in spontaneously arising estrogen-associated de novo uterine cancer, are significantly less frequent in tamoxifen-associated tumors. In vivo, tamoxifen-induced estrogen receptor stimulation activates phosphoinositide 3-kinase (PI3K) signaling in normal mouse uterine tissue, potentially eliminating the selective benefit of PI3K-activating mutations in tamoxifen-associated uterine cancer. Together, we present a unique pathway of therapy-associated carcinogenesis in which tamoxifen-induced activation of the PI3K pathway acts as a non-genetic driver event, contributing to the multistep model of uterine carcinogenesis. While this PI3K mechanism is specific to tamoxifen-associated uterine cancer, the concept of treatment-induced signaling events may have broader applicability to other routes of tumorigenesis. Sequencing analysis of tamoxifen-associated uterine cancers and further in vivo analyses suggest that the drug tamoxifen can activate the PI3K pathway in the absence of oncogenic mutations.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2192-2202"},"PeriodicalIF":29.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02308-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144898390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Precise modulation of BRG1 levels reveals features of mSWI/SNF dosage sensitivity","authors":"Yota Hagihara, Chao Zhang, Yi Zhang","doi":"10.1038/s41588-025-02305-z","DOIUrl":"10.1038/s41588-025-02305-z","url":null,"abstract":"Mammalian switch/sucrose nonfermentable (mSWI/SNF) complex regulates chromatin accessibility and frequently shows alterations due to mutation in cancer and neurological diseases. Inadequate expression of mSWI/SNF in heterozygous mice can lead to developmental defects, indicating dosage-sensitive effects of mSWI/SNF. However, how its dosage affects function has remained unclear. Using a targeted protein degradation system, we investigated its dosage-sensitive effects by precisely controlling protein levels of BRG1, the ATPase subunit of the mSWI/SNF complex. We found that binding of BRG1 to chromatin exhibited a linear response to the BRG1 protein level. Although chromatin accessibility at most promoters and insulators was largely unaffected by BRG1 depletion, 44% of enhancers, including 84% of defined superenhancers, showed reduced accessibility. Notably, half of the BRG1-regulated enhancers, particularly superenhancers, exhibited a buffered response to BRG1 loss. Consistently, transcription exhibited a predominantly buffered response to changes in BRG1 levels. Collectively, our findings demonstrate a genomic feature-specific response to BRG1 dosage, shedding light on the dosage-sensitive effects of mSWI/SNF complex defects in cancer and other diseases. This study investigates the dosage-sensitive effects of BRG1, a core SWI/SNF subunit, on chromatin binding, accessibility and transcriptional regulation by precisely controlling its protein level.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2250-2263"},"PeriodicalIF":29.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02305-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144898392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KidneyGenAfrica, a pan-African partnership to deliver research and training excellence in genomics of kidney disease","authors":"Segun Fatumo, Oyesola Ojewunmi, Rebecca Camenzuli, Christopher Kintu, Abram Kamiza, Jean-Tristan Brandenburg, Allan Kalungi, Robert Kalyesubula, Babatunde Salako, Oyekanmi Nash, Amelia Crampin, Adebowale Adeyemo, Moffat Nyirenda, Michele Ramsay, June Fabian, on behalf of the KidneyGenAfrica Consortium","doi":"10.1038/s41588-025-02299-8","DOIUrl":"10.1038/s41588-025-02299-8","url":null,"abstract":"Despite Africa’s vast genetic diversity, its populations are underrepresented in global genomic datasets. Here we describe the vision of the KidneyGenAfrica, a pan-African initiative launched to address this inequity, and call for more inclusive genomics research that recognizes Africa’s key role in genetic variation and potential to generate insights in chronic kidney disease.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2079-2082"},"PeriodicalIF":29.0,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144898185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Super-pangenome analyses across 35 accessions of 23 Avena species highlight their complex evolutionary history and extensive genomic diversity","authors":"Hongyu Zhang, Ningkun Liu, Yaru Wang, Xinyuan Zheng, Wei Li, Ze Liu, Jianan Liu, Yu Wang, Longsheng Xing, Tao Li, Yange Yun, Qinghong Zhou, Meijia Wang, Yujie Qin, Jinjiang Yan, Zhizhong Gong, Qiang He, Huilong Du","doi":"10.1038/s41588-025-02294-z","DOIUrl":"10.1038/s41588-025-02294-z","url":null,"abstract":"Common oat, belonging to the genus Avena with 30 recognized species, is a nutritionally important cereal crop and high-quality forage worldwide. Here, we construct a genus-level super-pangenome of Avena comprising 35 high-quality genomes from 14 cultivated oat accessions and 21 wild species. The fully resolved phylogenomic analysis unveils the origin and evolutionary scenario of Avena species, and the super-pangenome analysis identifies 26.62% and 59.93% specific genes and haplotypes in wild species. We delineate the landscape of structural variations (SVs) and the transcriptome profile based 1,401 RNA-sequencing (RNA-seq) samples from diverse abiotic stress treatments in oat. We highlight the crucial role of SVs in modulating gene expression and shaping adaptation to diverse stresses. Further combining SV-based genome-wide association studies (GWASs), we characterize 13 candidate genes associated with drought resistance such as AsARF7, validated by transgenic oat lines. Our study provides unprecedented genomic resources to facilitate genomic, evolution and molecular breeding research in oat. A genus-level super-pangenome of Avena comprising 35 high-quality genomes from 23 cultivated or wild oat species highlights the evolution of Avena and the landscape of structural variations related to abiotic stress resistance.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2276-2288"},"PeriodicalIF":29.0,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144898190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell DNA methylome and 3D genome atlas of human subcutaneous adipose tissue","authors":"Zeyuan Johnson Chen, Sankha Subhra Das, Asha Kar, Seung Hyuk T. Lee, Kevin D. Abuhanna, Marcus Alvarez, Mihir G. Sukhatme, Zitian Wang, Kyla Z. Gelev, Matthew G. Heffel, Yi Zhang, Oren Avram, Elior Rahmani, Sriram Sankararaman, Markku Laakso, Sini Heinonen, Hilkka Peltoniemi, Eran Halperin, Kirsi H. Pietiläinen, Chongyuan Luo, Päivi Pajukanta","doi":"10.1038/s41588-025-02300-4","DOIUrl":"10.1038/s41588-025-02300-4","url":null,"abstract":"The cell-type-level epigenomic landscape of human subcutaneous adipose tissue (SAT) is not well characterized. Here, we elucidate the epigenomic landscape across SAT cell types using snm3C-seq. We find that SAT CG methylation (mCG) displays pronounced hypermethylation in myeloid cells and hypomethylation in adipocytes and adipose stem and progenitor cells, driving nearly half of the 705,063 differentially methylated regions (DMRs). Moreover, TET1 and DNMT3A are identified as plausible regulators of the cell-type-level mCG profiles. Both global mCG profiles and chromosomal compartmentalization reflect SAT cell-type lineage. Notably, adipocytes display more short-range chromosomal interactions, forming complex local 3D genomic structures that regulate transcriptional functions, including adipogenesis. Furthermore, adipocyte DMRs and A compartments are enriched for abdominal obesity genome-wide association study (GWAS) variants and polygenic risk, while myeloid A compartments are enriched for inflammation. Together, we characterize the SAT single-cell-level epigenomic landscape and link GWAS variants and partitioned polygenic risk of abdominal obesity and inflammation to the SAT epigenome. This multiomic study, including single-nucleus DNA methylation and chromatin conformation matched with single-nuclei RNA sequencing, provides insights into the epigenomic landscape of human subcutaneous adipose tissue.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2238-2249"},"PeriodicalIF":29.0,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02300-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144898186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporal genomic dynamics shape clinical trajectory in multiple myeloma","authors":"Francesco Maura, Marcella Kaddoura, Alexandra M. Poos, Linda B. Baughn, Bachisio Ziccheddu, Marc-Andrea Bärtsch, Anthony Cirrincione, Kylee Maclachlan, Monika Chojnacka, Benjamin Diamond, Marios Papadimitriou, Patrick Blaney, Lukas John, Philipp Reichert, Stefanie Huhn, Dylan Gagler, Yanming Zhang, Ahmet Dogan, Alexander M. Lesokhin, Faith Davies, Hartmut Goldschmidt, Roland Fenk, Katja C. Weisel, Elias K. Mai, Neha Korde, Gareth J. Morgan, S. Vincent Rajkumar, Shaji Kumar, Saad Usmani, Ola Landgren, Marc S. Raab, Niels Weinhold","doi":"10.1038/s41588-025-02292-1","DOIUrl":"10.1038/s41588-025-02292-1","url":null,"abstract":"Multiple myeloma evolution is characterized by the accumulation of genomic drivers over time. To unravel this timeline and its impact on clinical outcomes, we analyzed 421 whole-genome sequences from 382 patients. Using clock-like mutational signatures, we estimated a time lag of two to four decades between the initiation of events and diagnosis. We demonstrate that odd-numbered chromosome trisomies in patients with hyperdiploidy can be acquired simultaneously with other chromosomal gains (for example, 1q gain). We show that hyperdiploidy is acquired after immunoglobulin heavy chain translocation when both events co-occur. Finally, patients with early 1q gain had adverse outcomes similar to those with 1q amplification (>1 extra copy), but fared worse than those with late 1q gain. This finding underscores that the 1q gain prognostic impact depends more on the timing of acquisition than on the number of copies gained. Overall, this study contributes to a better understanding of the life history of myeloma and may have prognostic implications. This analysis of whole-genome sequencing data from 421 multiple myeloma samples elucidates the timing of key genomic events and shows associations between the timing of 1q gain and clinical outcome.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2203-2214"},"PeriodicalIF":29.0,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144898187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comparison of 27 Arabidopsis thaliana genomes and the path toward an unbiased characterization of genetic polymorphism","authors":"Anna A. Igolkina, Sebastian Vorbrugg, Fernando A. Rabanal, Hai-Jun Liu, Haim Ashkenazy, Aleksandra E. Kornienko, Joffrey Fitz, Max Collenberg, Christian Kubica, Almudena Mollá Morales, Benjamin Jaegle, Travis Wrightsman, Vitaly Voloshin, Alexander D. Bezlepsky, Victor Llaca, Viktoria Nizhynska, Ilka Reichardt, Ilja Bezrukov, Christa Lanz, Felix Bemm, Pádraic J. Flood, Sileshi Nemomissa, Angela Hancock, Ya-Long Guo, Paul Kersey, Detlef Weigel, Magnus Nordborg","doi":"10.1038/s41588-025-02293-0","DOIUrl":"10.1038/s41588-025-02293-0","url":null,"abstract":"Making sense of whole-genome polymorphism data is challenging, but it is essential for overcoming the biases in SNP data. Here we analyze 27 genomes of Arabidopsis thaliana to illustrate these issues. Genome size variation is mostly due to tandem repeat regions that are difficult to assemble. However, while the rest of the genome varies little in length, it is full of structural variants, mostly due to transposon insertions. Because of this, the pangenome coordinate system grows rapidly with sample size and ultimately becomes 70% larger than the size of any single genome, even for n = 27. Finally, we show how short-read data are biased by read mapping. SNP calling is biased by the choice of reference genome, and both transcriptome and methylome profiling results are affected by mapping reads to a reference genome rather than to the genome of the assayed individual. New concepts for comparing the genomes of 27 naturally inbred Arabidopsis thaliana accessions provide essential insights into obtaining a less biased view of whole-genome polymorphism.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2289-2301"},"PeriodicalIF":29.0,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02293-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144883236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tracing the evolution of single-cell 3D genomes in Kras-driven cancers.","authors":"Miao Liu, Shengyan Jin, Sherry S Agabiti, Tyler B Jensen, Tianqi Yang, Jonathan S D Radda, Christian F Ruiz, Gabriel Baldissera, Moein Rajaei, Fang-Yong Li, Jeffrey P Townsend, Mandar Deepak Muzumdar, Siyuan Wang","doi":"10.1038/s41588-025-02297-w","DOIUrl":"10.1038/s41588-025-02297-w","url":null,"abstract":"<p><p>Although three-dimensional (3D) genome structures are altered in cancer, it remains unclear how these changes evolve and diversify during cancer progression. Leveraging genome-wide chromatin tracing to visualize 3D genome folding directly in tissues, we generated 3D genome cancer atlases of oncogenic Kras-driven mouse lung adenocarcinoma (LUAD) and pancreatic ductal adenocarcinoma. Here we define nonmonotonic, stage-specific alterations in 3D genome compaction, heterogeneity and compartmentalization as cancers progress from normal to preinvasive and ultimately to invasive tumors, discovering a potential structural bottleneck in early tumor progression. Remarkably, 3D genome architectures distinguish morphologic cancer states in single cells, despite considerable cell-to-cell heterogeneity. Analyses of genome compartmentalization changes not only showed that compartment-associated genes are more homogeneously regulated but also elucidated prognostic and dependency genes in LUAD, as well as an unexpected role for Rnf2 in 3D genome regulation. Our results highlight the power of single-cell 3D genome mapping to identify diagnostic, prognostic and therapeutic biomarkers in cancer.</p>","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":" ","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144874143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}