bims-enbcad Biomed News
on Engineering biology for causal discovery
Issue of 2026–01–18
eighteen papers selected by
Xiao Qin, University of Oxford
  1. Single-cell exploration in natural language.
  2. Bioprinting a human small intestine.
  3. The dynamics of mutational selection in cutaneous squamous carcinogenesis.
  4. Genetic Context Shapes Selection or Decay of Driver Mutations in Colon Cancer.
  5. Year in review 2025.
  6. Intratumoral microbiome: the double-edged sword in remodeling cancer immunotherapy.
  7. Panorama: a database for the oncogenic evaluation of somatic mutations in pan-cancer.
  8. Mutational Landscape of Colorectal Tumors From Individuals With Unexplained Adenomatous or Serrated Colorectal Polyposis.
  9. Artificial intelligence agents in cancer research and oncology.
  10. HumanBase: an interactive AI platform for human biology.
  11. A Blood-Based Test for Colorectal Cancer Screening.
  12. Five decades of colorectal cancer mortality in the United States: Trends, disparities, and emerging challenges.
  13. Single-cell integration and multi-modal profiling reveals phenotypes and spatial organization of neutrophils in colorectal cancer.
  14. CancerSEA-X: A Single-cell Resource for Tumor Microenvironment Cell States Across over 30 Cancer Types.
  15. Microbiota-induced T cell plasticity enables immune-mediated tumour control.
  16. A Prospective, Cross-Sectional, Multicenter Study Evaluating a Multi-Target Blood Protein in Vitro Diagnostic Test for Colorectal Cancer.
  17. Integration of multi-omics data uncovers novel germline susceptibility candidates in early-onset colorectal cancer.
  18. Cellular neighborhoods in cancer.
  1. Nat Methods. 2026 Jan;23(1): 10
    Single-cell exploration in natural language.
    Lin Tang.
      
    DOI:  https://doi.org/10.1038/s41592-025-03000-x
  2. Nat Methods. 2026 Jan;23(1): 10
    Bioprinting a human small intestine.
    Michelle Korda.
      
    DOI:  https://doi.org/10.1038/s41592-025-02999-3
  3. Commun Biol. 2026 Jan 12.
    The dynamics of mutational selection in cutaneous squamous carcinogenesis.
    Greta Skrupskelyte, Joanna C Fowler, Stefan Dentro, Carine Winkler, Irina Abnizova, Niklaus Beumer, Roshan Sood, Thomas Quarrell, Charlotte King, Jivko Kamarashev, Emmanuella Guenova, Moritz Gerstung, Benjamin A Hall, Liliane Michalik, Philip H Jones.
      Identifying the mutant genes that are selected during carcinogenesis is key to identifying candidates for intervention and understanding the processes that promote transformation. Here we applied two selection metrics to study the dynamics of mutational selection in a mouse model of ultraviolet light driven skin carcinogenesis in which multiple synchronous tumors develop in each animal. Sequencing normal skin and tumors over a time course revealed two genetic routes to squamous carcinoma. Nonsynonymous Trp53 mutants were positively selected in both epidermis and tumors and present in 90% of tumors. The remaining tumors carried other oncogenic mutants, including activating Kras mutations. However, other positively selected mutant genes lost their competitive advantage in heavily mutated epidermis and in tumors. We found ten mutant genes under negative selection in normal skin, one of which was also negatively selected in tumors. In addition one gene was negatively selected in tumors but not normal skin. We conclude that analysing selection in normal tissue alongside tumors may resolve the dynamics of selection in carcinogenesis and refine the identification of cancer drivers.
    DOI:  https://doi.org/10.1038/s42003-025-09406-9
  4. Cancer Discov. 2026 Jan 09. OF1
    Genetic Context Shapes Selection or Decay of Driver Mutations in Colon Cancer.
      
    DOI:  https://doi.org/10.1158/2159-8290.CD-RW2026-003
  5. Nat Methods. 2026 Jan;23(1): 1
    Year in review 2025.
      
    DOI:  https://doi.org/10.1038/s41592-025-02997-5
  6. Mol Cancer. 2026 Jan 13.
    Intratumoral microbiome: the double-edged sword in remodeling cancer immunotherapy.
    Di Yan, Ying Yu, Chengtong Liang, Zixing Cui, Lei Shi, Guiling Li, Chuanli Ren.
      Emerging evidence reveals that intratumoral microbial (ITM) communities within the tumor immune microenvironment (TIME) critically influence tumor progression and immunotherapy response. Studies have shown that resident bacteria within tumors, such as Sphingobacterium multivorum, regulate the secretion of chemokines like CCL20 and CXCL8, promoting the infiltration of regulatory T cells (Tregs) and inhibiting the function of cytotoxic T cells (CD8+ T cells)-thereby weakening the efficacy of immune checkpoint inhibitors. Additionally, microbial metabolites may serve as potential biomarkers for predicting sensitivity to immunotherapy. Concurrently, engineered bacteria (e.g., oncolytic mineralizing bacteria) demonstrate significant antitumor effects by activating innate immunity and enhancing antitumor-specific immune responses, providing new strategies to overcome immunotherapy resistance. These findings highlight the dual role of ITM in tumor immune evasion and immunotherapy sensitivity, laying an important theoretical foundation for developing novel immunotherapy strategies targeting tumoral microbiota metabolism.
    Keywords:  Cancer immunotherapy; Intratumoral microbiome; Tumor immune microenvironment
    DOI:  https://doi.org/10.1186/s12943-025-02566-6
  7. Database (Oxford). 2026 Jan 15. pii: baaf086. [Epub ahead of print]2026
    Panorama: a database for the oncogenic evaluation of somatic mutations in pan-cancer.
    Seung-Jin Park, Seon-Young Kim.
      Somatic mutations, key alterations in cancer development, exert differential effects across tissues and biological layers, such as transcriptomes, proteomes, and post-translational modifications (PTMs). Although previous pan-cancer studies have characterized the molecular landscape of cancer, the effects of individual somatic mutations across different tissues remain insufficiently explored. Here, we developed Panorama to evaluate the oncogenic potential of single somatic mutations across all cancer types. We collected cancer proteogenomics or multiomics data from over 10 000 individuals across 19 cancer types. Based on five evaluation criteria, we assessed whether a specific mutation affects the abundance of a particular gene's transcriptome, proteome, or phosphoproteome; the tumor microenvironment; specific RNA- or protein-based signaling pathways; and outlier-level overexpression of PTMs, aiding in potential drug target identification. By leveraging five oncogenic metrics, Panorama quantifies the oncogenic potential of individual somatic mutations and provides a framework for identifying driver mutations by incorporating their downstream effects. With Panorama, researchers can integrate cancer proteogenomics data, providing a comprehensive approach that enhances our understanding of single somatic mutations in specific tissues. Finally, Panorama was developed as a web-based database to ensure easy access for researchers and is freely available at http://139.150.65.64:8080/or https://github.com/prosium/panorama.
    DOI:  https://doi.org/10.1093/database/baaf086
  8. Gastroenterology. 2026 Jan 12. pii: S0016-5085(25)06134-7. [Epub ahead of print]
    Mutational Landscape of Colorectal Tumors From Individuals With Unexplained Adenomatous or Serrated Colorectal Polyposis.
    Anna K Sommer, Iris B A W Te Paske, Erik A M Jansen, Axel Gschwind, German Demidov, Verena Steinke-Lange, Isabel Spier, Wouter Steyaert, Burcu Yaldiz, Marloes Steehouwer, Oliver Hommerding, Dimo Dietrich, Sophia Peters, José Garcia-Pelaez, Andreas Laner, Carla Oliveira, Gabriel Capellá, Iris D Nagtegaal, Hendrik Bläker, Kornelia Ellwanger, Alexander Hoischen, Christian Gilissen, Rachel S van der Post, Glen Kristiansen, Nicoline Hoogerbrugge, Stephan Ossowski, Laura Valle, Elke Holinski-Feder, Marjolijn J L Ligtenberg, Stefan Aretz, Richarda M de Voer.
       BACKGROUND & AIMS: Individuals with colorectal polyposis are suspected to be genetically predisposed to tumor development. However, in around half of adenomatous and the vast majority of serrated polyposis patients, no explanatory pathogenic germline variant is found in routine diagnostics. Here, we aimed to improve the characterization of the early steps of polyp formation and provide clues on the tumorigenic processes involved.
    METHODS: We performed whole-exome sequencing of colorectal tumors (n = 299) from 153 individuals with adenomatous or serrated polyposis and 16 individuals with early-onset colorectal cancer in the absence of known pathogenic germline variants. Subsequently, somatic mutations were called and a driver gene analysis for pathogenicity was performed. In addition, CpG island methylator phenotypes, tumor mutational burden, microsatellite instability, and mutational signatures were analyzed and compared with publicly available datasets of molecularly profiled colorectal cancers and polyps.
    RESULTS: Somatic mutations in APC/CTNNB1 and BRAF were significantly more frequent in adenomatous and serrated polyps, respectively. APC mosaicism was identified in 19% of individuals with adenomatous polyposis. In 9% of serrated polyps, a CpG island methylator phenotypes high methylation status was detected. Almost all polyps presented with a low tumor mutational burden and the majority were microsatellite stable. In APC/CTNNB1- and BRAF-mutated polyps, we identified a significantly lower contribution of the clock-like signature SBS1 and a significantly higher contribution of the normal colon tissue signature SBS89, respectively, compared with sporadic colorectal tumors.
    CONCLUSIONS: Our results indicate that BRAF-mutated serrated polyps are molecularly more similar to normal colon tissue than APC- and/or CTNNB1-mutated tumors. Overall, molecular tumor profiling of individuals with polyposis contributes to understanding the genetic disease etiology.
    Keywords:  APC Mutational Mosaicism; Colorectal Polyposis; Molecular Tumor Profiling; Mutational Signatures; Solve-RD; Somatic Mutations
    DOI:  https://doi.org/10.1053/j.gastro.2025.10.011
  9. Nat Rev Cancer. 2026 Jan 12.
    Artificial intelligence agents in cancer research and oncology.
    Daniel Truhn, Shekoofeh Azizi, James Zou, Leonor Cerda-Alberich, Faisal Mahmood, Jakob Nikolas Kather.
      Since 2022, artificial intelligence (AI) methods have progressed far beyond their established capabilities of data classification and prediction. Large language models (LLMs) can perform logical reasoning, enabling them to plan and orchestrate complex workflows. By using this planning ability and equipped with the ability to act upon their environment, LLMs can function as agents. Agents are (semi-)autonomous systems capable of sensing, learning and acting upon their environments. As such, they can interact with external knowledge or external software and can execute sequences of tasks with minimal or no human input. In cancer research and oncology, evidence for the capability of AI agents is rapidly emerging. From autonomously optimizing drug design and development to proposing therapeutic strategies for clinical cases, AI agents can handle complex, multistep problems that were not addressable by previous generations of AI systems. Despite rapid developments, many translational and clinical cancer researchers still lack clarity regarding the precise capabilities, limitations, and ethical or regulatory frameworks associated with AI agents. Here we provide a primer on AI agents for cancer researchers and oncologists. We illustrate how this technology is set apart from and goes beyond traditional AI systems. We discuss existing and emerging applications in cancer research and address real-world challenges from the perspective of academic, clinical and industrial research.
    DOI:  https://doi.org/10.1038/s41568-025-00900-0
  10. Nat Methods. 2026 Jan 14.
    HumanBase: an interactive AI platform for human biology.
    Rachel S G Sealfon, Chandra L Theesfeld, Julien Funk, Natalie Sauerwald, Aaron K Wong, Olga G Troyanskaya.
      
    DOI:  https://doi.org/10.1038/s41592-025-02994-8
  11. HCA Healthc J Med. 2025 ;6(6): 571-573
    A Blood-Based Test for Colorectal Cancer Screening.
    Joshua Cullison.
      Description Within the United States (US), colorectal cancer (CRC) remains the fourth most common malignancy and is responsible for over 50 000 deaths annually, second only to lung cancer in cancer mortality. Despite increased public awareness and increasing screening rates, the US remains far below the 80% screening mark set by the National Colorectal Cancer Roundtable at 59%. The addition of non-invasive blood-based tests for CRC screening could potentially increase screening rates and lower CRC deaths. I performed a PubMed search using the search term "blood-based colorectal cancer screening." I was particularly interested in articles that looked at Shield, which is the first and (currently) only blood-based DNA test that is approved by the US Food and Drug Administration (FDA) to screen for CRC. The FDA approval for Shield was based on 1 large cohort trial (ECLIPSE), the results of which were published in Gastroenterology in March 2024. This brief synopsis will detail the major parts of that study and layout the potential benefits, risks, and cost analysis of implementing this test into routine practice.
    Keywords:  blood-based screening test; cell-free DNA; colorectal cancer screening; non-invasive screening
    DOI:  https://doi.org/10.36518/2689-0216.2259
  12. Am J Med Sci. 2026 Jan 09. pii: S0002-9629(26)00023-6. [Epub ahead of print]
    Five decades of colorectal cancer mortality in the United States: Trends, disparities, and emerging challenges.
    Rahul Balach, Shahtaj Tariq, Muhammad Taha Nizami, Muhammad Khalid Afridi.
      
    Keywords:  Age-adjusted mortality rate (AAMR); Annual percentage change (APC); Average annual percentage change (AAPC); CDC WONDER; Colorectal cancer (CRC); Early-onset CRC; Epidemiology; Mortality trends; Racial disparities; United States
    DOI:  https://doi.org/10.1016/j.amjms.2026.01.005
  13. Cancer Cell. 2026 Jan 12. pii: S1535-6108(25)00537-9. [Epub ahead of print]44(1): 146-165.e14
    Single-cell integration and multi-modal profiling reveals phenotypes and spatial organization of neutrophils in colorectal cancer.
    Valentin Marteau, Niloofar Nemati, Kristina Handler, Deeksha Raju, Alexander Kirchmair, Dietmar Rieder, Erika Kvalem Soto, Georgios Fotakis, Glenn De Lange, Sandro Carollo, Nina Boeck, Alessia Rossi, Sophia Daum, Alexandra Scheiber, Arno Amann, Andreas Seeber, Elisabeth Gasser, Steffen Ormanns, Michael Günther, Agnieszka Martowicz, Zuzana Loncova, Giorgia Lamberti, Anne Krogsdam, Michela Carlet, Lena Horvath, Marie Theres Eling, Hassan Fazilaty, Tomas Valenta, Gregor Sturm, Sieghart Sopper, Andreas Pircher, Patrizia Stoitzner, Peter J Wild, Patrick Welker, Pascal J May, Paul Ziegler, Markus Tschurtschenthaler, Daniel Neureiter, Florian Huemer, Richard Greil, Lukas Weiss, Marieke Ijsselsteijn, Noel F C C de Miranda, Dominik Wolf, Isabelle C Arnold, Stefan Salcher, Zlatko Trajanoski.
      The immune composition of the tumor microenvironment has a major impact on the therapy response in patients with colorectal cancer. Here, we built an atlas with 4.27 million single cells from 1,670 patient samples and complemented it with single-cell profiles from 266 patients, including cells with low mRNA content, spatial transcriptomics from 3.7 million cells, and protein profiles from 0.7 million cells. The analysis of the atlas allows tumor classification into immune desert, B cell enriched, T cell enriched, and myeloid cell enriched immune phenotypes. Within the myeloid compartment, we identify consensus myeloid gene expression programs with four immunomodulatory programs, and uncover a subpopulation of neutrophils with antigen-presenting properties. Moreover, functional experiments using patient-derived organoids show KRAS-dependent pro-tumorigenic polarization of neutrophils. Further, spatial multimodal single-cell profiling reveals niches with IL-1 signaling-based neutrophil-fibroblast interaction. Finally, using an orthotopic mouse model, we show that cancer-derived signals modify neutrophil production in the bone marrow.
    Keywords:  cellular niches; colorectal cancer; gut-bone marrow axis; single-cell atlas; single-cell sequencing; spatial single-cell profiling; spatial transcriptomics
    DOI:  https://doi.org/10.1016/j.ccell.2025.12.003
  14. Genomics Proteomics Bioinformatics. 2026 Jan 16. pii: qzaf134. [Epub ahead of print]
    CancerSEA-X: A Single-cell Resource for Tumor Microenvironment Cell States Across over 30 Cancer Types.
    Lantian Deng, Wei Liu, Jinyuan Xu, Bo Zhang, Shengyuan He, Kun Liu, Xinxin Zhang, Huating Yuan, Fei Quan, Yun Xiao.
      Single-cell studies have significantly advanced our understanding of the transcriptional and functional heterogeneity in cancers. Recent studies have identified distinct states of cancer, immune, and stromal cells in the tumor microenvironment (TME), with growing evidence highlighting their clinical significance and therapeutic potential. Here, we present CancerSEA-X, an expanded version of CancerSEA that offers a comprehensive atlas of TME cell states. CancerSEA-X integrates 25 cancer cell states, 105 immune cell states, and 26 stromal cell states from systematically curated publications. Combining 239 single-cell datasets across 32 cancer types, encompassing over 9 million cells from 2120 patients, CancerSEA-X provides functional activity spectra and cancer-specific gene associations for these 156 cell states. These cell state-gene relationships were mapped onto networks, providing a systematic view of the TME. To improve usability, we redesigned the user interface to feature cell state characterization, state-gene correlation analysis, and interactive visualization of cell state-gene networks, enabling researchers to comprehensively explore these states and their functional relevance. Overall, CancerSEA-X serves as a valuable platform for investigating TME cell states, deepening our understanding of cancer heterogeneity, and potentially advancing the design of more effective clinical therapies. CancerSEA-X is freely available at http://biocc.hrbmu.edu.cn/CancerState.
    Keywords:  Biological database; Cancer cell state; Single-cell RNA sequencing; Transcriptional heterogeneity; Tumor microenvironment
    DOI:  https://doi.org/10.1093/gpbjnl/qzaf134
  15. Nature. 2026 Jan 14.
    Microbiota-induced T cell plasticity enables immune-mediated tumour control.
    Tariq A Najar, Yuan Hao, Yuhan Hao, Gabriela Romero-Meza, Alexandra Dolynuk, Emma Almo, Dan R Littman.
      Therapies that harness the immune system to target and eliminate tumour cells have revolutionized cancer care. Immune checkpoint blockade (ICB), which boosts the anti-tumour immune response by inhibiting negative regulators of T cell activation1-3, is remarkably successful in a subset of cancer patients. Yet a significant proportion do not respond to treatment, emphasizing the need to understand factors influencing the therapeutic efficacy of ICB4-9. The gut microbiota, consisting of trillions of microorganisms residing in the gastrointestinal tract, has emerged as a critical determinant of immune function and response to cancer immunotherapy, with several studies demonstrating association of microbiota composition with clinical response10-16. However, a mechanistic understanding of how gut commensal bacteria influence the efficacy of ICB remains elusive. Here we use a gut commensal microorganism, segmented filamentous bacteria (SFB), which induces an antigen-specific T helper 17 (TH17) cell effector program in the small intestine lamina propria (SILP)17, to investigate how colonization with this microbe affects the efficacy of ICB in restraining distal growth of tumours sharing antigen with SFB. We find that anti-programmed cell death protein 1 (PD-1) treatment effectively inhibits the growth of implanted SFB antigen-expressing melanoma only if mice are colonized with SFB. Through T cell receptor (TCR) clonal lineage tracing, fate mapping and peptide-major histocompatability complex (MHC) tetramer staining, we identify tumour-associated SFB-specific T helper 1 (TH1)-like cells derived from the homeostatic TH17 cells induced by SFB colonization in the SILP. These gut-educated ex-TH17 cells produce high levels of the pro-inflammatory cytokines interferon (IFN)-γ and tumour necrosis factor (TNF) within the tumour microenvironment (TME), enhancing antigen presentation and promoting recruitment, expansion and effector functions of CD8+ tumour-infiltrating cytotoxic lymphocytes and thereby enabling anti-PD-1-mediated tumour control. Conditional ablation of SFB-induced IL-17A+CD4+ T cells, precursors of tumour-associated TH1-like cells, abolishes anti-PD-1-mediated tumour control and markedly impairs tumour-specific CD8+ T cell recruitment and effector function within the TME. Our data, as a proof of principle, define a cellular pathway by which a single, defined intestinal commensal imprints T cell plasticity that potentiates PD-1 blockade, and indicate targeted modulation of the microbiota as a strategy to broaden ICB efficacy.
    DOI:  https://doi.org/10.1038/s41586-025-09913-z
  16. J Gastrointest Cancer. 2026 Jan 16. 57(1): 19
    A Prospective, Cross-Sectional, Multicenter Study Evaluating a Multi-Target Blood Protein in Vitro Diagnostic Test for Colorectal Cancer.
    Emily Y He, Guy A van Hazel, Andrew M Sloss, Stephen Pianko, Gregor J Brown, Philip R Clingan, Rajvinder Singh, Ann C Solterbeck, Robert Traficante, Louise Formby-Miller, Trevor Lockett, Finlay Macrae.
       PURPOSE: Earlier detection of colorectal cancer (CRC) can improve survival rates. A simple, effective blood test may help improve screening participation. The multi-target blood protein (MTBP; ColoSTAT®) test and algorithm uses concentrations of five protein biomarkers of CRC and patient's sex and age to generate a CRC likelihood score. We compared the performance of the MTBP test in detecting CRC to colonoscopy, the 'gold standard'.
    METHODS: This cross-sectional, multicenter study enrolled participants into two cohorts: participants recently colonoscopically diagnosed with CRC and progressing to surgery or neoadjuvant treatment (Cohort 1), and participants with no CRC history who were scheduled for colonoscopy (Cohort 2). Due to COVID-19 pandemic-related recruitment delays, Cohort 1 was supplemented with bio-banked blood samples (BBS) from patients with clinically confirmed CRC. Performance goals for sensitivity and specificity of the MTBP test compared to colonoscopy were ≥ 73% (lower 95% confidence limit [LCL] > 60%) and ≥ 90% (LCL > 80%), respectively.
    RESULTS: Cohort 1 included 29 patients, Cohort 2 enrolled 768 patients and 192 BBS were included. Median age when providing samples was 64 years (range, 40-85 years); 53.4% were female. Definitive MTBP test results were obtained from 657 samples. 112 and 389 samples met the criteria for inclusion in the primary sensitivity and specificity analyses, respectively. The sensitivity of ColoSTAT® for detection of all-stage CRC compared to colonoscopy was 81.3% (95%CL 73.0%-87.4%) and the specificity, 91.0% (95%CL 87.7%-93.5%).
    CONCLUSIONS: The MTBP test met pre-specified primary performance endpoints and warrants further evaluation in clinical populations at elevated risk of CRC.
    Keywords:  Biomarkers; Colonoscopy; Colorectal cancer; Early detection of cancer; Mass screening
    DOI:  https://doi.org/10.1007/s12029-025-01373-y
  17. Eur J Hum Genet. 2026 Jan 15.
    Integration of multi-omics data uncovers novel germline susceptibility candidates in early-onset colorectal cancer.
    Anael López-Novo, Jorge Amigo, Andrés Dacal, David Remedios-Espino, Joaquín Cubiella, María Victoria Álvarez-Sánchez, María Jesús Ladra-González, Fernando Fernández-López, Ana Álvarez-Castro, Silvia Carlés, José Manuel Cameselle-Teijeiro, Miriam Cuatrecasas, Francesc Balaguer, Sergi Castellví-Bel, Ceres Fernández-Rozadilla, Ángel Carracedo, Clara Ruiz-Ponte.
      Colorectal cancer (CRC) is increasingly diagnosed in individuals under 50 years of age, yet the underlying genetic predisposition remains largely unexplained, particularly in mismatch repair (MMR)-proficient cases. This study aimed to identify novel hereditary CRC susceptibility genes by integrating germline and tumour whole-exome sequencing (WES) with transcriptomic profiling across a cohort of early-onset CRC (EOCRC) patients. Tumours were categorised using Consensus Molecular Subtypes (CMS) classification and analysed for mutational signature and burden. We used a novel 'All vs One' multi-omic integration approach to identify loss-of-function rare germline variants with concordant gene expression alterations in tumour tissue. Five candidate genes (ADCY4, NOXO1, CDHR2, ARHGAP10, EEF2K) were prioritised based on this approach and potential biological relevance in CRC. These findings highlight the molecular heterogeneity of EOCRC and demonstrate the utility of multi-omic approaches in refining germline variant interpretation. Integrating tumour transcriptomics enhances gene discovery efforts and supports a more comprehensive understanding of CRC heritability in younger individuals.
    DOI:  https://doi.org/10.1038/s41431-025-02004-7
  18. Nat Cancer. 2026 Jan 16.
    Cellular neighborhoods in cancer.
    Lichun Ma, Barbara Xiong, Meng Liu, Kai Tan.
      The concept of cellular neighborhoods, defined as recurring structures within the tissue with characteristic cell compositions and interactions, has transformed our understanding of the complexity and dynamics of tumor ecosystems. Recent advances in spatial omics and computational modeling have enabled high-resolution mapping of these neighborhoods, providing unprecedented insights into their roles in shaping tumor heterogeneity, evolution and therapeutic responses. Despite these advances, a unified framework for interpreting cellular neighborhoods remains lacking. This Perspective synthesizes emerging concepts and insights, focusing on the definition and classification of cellular neighborhoods in cancer, computational methods for identifying and comparing them, and their clinical relevance.
    DOI:  https://doi.org/10.1038/s43018-025-01107-w
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