bims-gerecp Biomed News
on Gene regulatory networks of epithelial cell plasticity
Issue of 2026–01–25
eighteen papers selected by
Xiao Qin, University of Oxford
  1. Critical role for a high-plasticity cell state in lung cancer.
  2. Pooled single-cell screen in colorectal cancer defines transcriptional modules linked to oncogenes.
  3. SpatialProp: tissue perturbation modeling with spatially resolved single-cell transcriptomics.
  4. The rise of spatial insights into tumour tissue architecture.
  5. Tumour explants as next-generation models of cancer.
  6. Gene regulatory network transitions reveal the central transcription factors in lung adenocarcinoma progression.
  7. Targeting transcriptional plasticity in cancer.
  8. Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer.
  9. Temporal tissue dynamics from a spatial snapshot.
  10. Genomic evolution of pancreatic cancer at single-cell resolution.
  11. Haruka Resolves Perturbation Response Heterogeneity in Spatial Cell Niches.
  12. Emerging technologies and current challenges in intratumoral microbiota research.
  13. It's poster time.
  14. Gut microbiome-driven colorectal cancer via immune, metabolic, neural, and endocrine axes reprogramming.
  15. Bioengineering multicellular tumor spheroids with tunable extracellular matrix deposition.
  16. Decoding 'Wntch': the intertwined Wnt and Notch pathways in development and disease.
  17. From Evidence to Action: Reinforcing FIT as the Cornerstone of Colorectal Cancer Prevention Worldwide.
  18. Morphological evaluation of brain organoids.
  1. Nature. 2026 Jan 21.
    Critical role for a high-plasticity cell state in lung cancer.
    Jason E Chan, Chun-Hao Pan, Jonathan Rub, Gary Guzman, Klavdija Krause, Emma Brown, Zeda Zhang, Hannah Styers, Griffin Hartmann, Zhuxuan Li, Xueqian Zhuang, Scott W Lowe, Doron Betel, Yan Yan, Tuomas Tammela.
      Plasticity-the ability of cells to undergo phenotypic transitions-drives cancer progression and therapy resistance1-3. Recent studies have suggested that plasticity in solid tumours is concentrated in a minority subset of cancer cells4-6, yet functional studies examining this high-plasticity cell state (HPCS) in situ are lacking. Here we develop mouse models enabling the detection, longitudinal lineage tracing and ablation of the HPCS in autochthonous lung tumours in vivo. Lineage tracing reveals that the HPCS cells possess a high capacity for cell state transitions, giving rise to both early neoplastic (differentiated) and progressed lung cancer cell states in situ. Longitudinal lineage tracing using secreted luciferases reveals that HPCS-derived cells have a high capacity for growth compared with bulk cancer cells or another cancer cell state with features of differentiated lung epithelium. Ablation of HPCS cells in early neoplasias abrogates benign-to-malignant transition, whereas ablation in established tumours by suicide gene or chimeric antigen receptor (CAR) T cells robustly reduces tumour burden. We further demonstrate that the HPCS gives rise to therapy-resistant cell states, whereas HPCS ablation suppresses resistance to chemotherapy and oncoprotein-targeted therapy. Notably, an HPCS-like state is ubiquitous in regenerating epithelia and in carcinomas of multiple other tissues, revealing a convergence of plasticity programs. Our work establishes the HPCS as a critical hub enabling reciprocal transitions between cancer cell states. Targeting the HPCS in lung cancer and in other carcinomas may suppress cancer progression and eradicate treatment resistance.
    DOI:  https://doi.org/10.1038/s41586-025-09985-x
  2. Mol Syst Biol. 2026 Jan 19.
    Pooled single-cell screen in colorectal cancer defines transcriptional modules linked to oncogenes.
    Viola Hollek, Francisca Böhning, Catalina Florez Vargas, Anja Sieber, Markus Morkel, Nils Blüthgen.
      Oncogenic mutations shape colorectal cancer (CRC) biology, yet their impact on transcriptional phenotypes remains incompletely understood, and their individual prognostic value is limited. Here, we perform a pooled single-cell transcriptomic screen of over 100,000 CRC cells with a comprehensive barcoded library of oncogenic variants across genetically diverse CRC lines. Using a variational autoencoder-based interpretable factor model, we identify ten conserved oncogene-driven transcriptional modules (TMOs) representing core cancer phenotypes such as cellular plasticity, inflammatory response, replicative stress, and epithelial-to-mesenchymal transition. Engagement of these modules can be context-dependent, reflecting interactions between oncogene-induced driver pathways and background genetics. TMO activity in patient tumors stratifies CRC cohorts into high- and low-risk groups, improving relapse-free survival prediction beyond existing classification systems. Our study systematically links oncogenic signaling to transcriptional states and clinical outcomes, establishing a functional framework for module-based patient stratification in precision oncology.
    Keywords:  Colorectal Cancer; Oncogenes; Signatures; Single Cell Screening; Transcriptional Modules
    DOI:  https://doi.org/10.1038/s44320-025-00186-2
  3. bioRxiv. 2025 Dec 02. pii: 2025.11.30.691355. [Epub ahead of print]
    SpatialProp: tissue perturbation modeling with spatially resolved single-cell transcriptomics.
    Eric D Sun, Alejandro Buendia, Anne Brunet, James Zou.
      Perturbational studies are the gold standard for identifying causal relationships between components of biological systems. Recent technological advances, including Perturb-seq and related assays, have enabled high-throughput screening of genetic perturbation effects on single cells. Several machine learning tools have also been developed to infer the effect of single-cell perturbations. However, both approaches are generally limited to dissociated cells, and the effect of genetic perturbations on neighboring cells within intact tissue has not yet been explored. Here we introduce a computational framework using graph neural networks for predicting the effect of multi-gene, multi-cell type perturbations on cells in whole tissue sections. We leverage the natural heterogeneity in tissue microenvironments across spatially resolved single-cell transcriptomics datasets to train SpatialProp (Spatial Propagation of Single-cell Perturbations). We show that SpatialProp can predict gene expression from the tissue microenvironment and map fine-grained steering of tissue microenvironments to new target states. To assess for causal enrichment in spatial perturbation predictions, we propose CausalInteractionBench, a bidirectional benchmarking approach using curated cell-cell interactions. Under this benchmark, we evaluate the causal utility of SpatialProp in predicting the spatial effects of different perturbations. SpatialProp provides a framework towards rapid hypothesis generation and in silico perturbation experiments, particularly in the study of spatially patterned tissue biology.
    DOI:  https://doi.org/10.64898/2025.11.30.691355
  4. Nat Rev Cancer. 2026 Jan 19.
    The rise of spatial insights into tumour tissue architecture.
    Pablo Siliceo, Alfredo Rodríguez.
      
    DOI:  https://doi.org/10.1038/s41568-026-00906-2
  5. Nat Rev Cancer. 2026 Jan 20.
    Tumour explants as next-generation models of cancer.
    Kenny Zhuoran Wu, N Gopalakrishna Iyer, Chin-Ann Johnny Ong, Eliza Li Shan Fong.
      
    DOI:  https://doi.org/10.1038/s41568-026-00907-1
  6. NPJ Syst Biol Appl. 2026 Jan 20.
    Gene regulatory network transitions reveal the central transcription factors in lung adenocarcinoma progression.
    Upasana Ray, Adarsh Singh, Debabrata Samanta, Riddhiman Dhar.
      Transcription factors play a central role in cancer growth, progression, and metastasis, and contribute to intratumor phenotypic plasticity that enable drug tolerance and cancer relapse. Changes in the regulatory activities of transcription factors in cancer may not always be detected from mutational signatures or differential expression of the transcription factors, as done in traditional analysis. In addition, past studies have focused on the activities of transcription factors in tumor as a whole and thus, have not fully captured the heterogeneity in gene regulation among different cell types within the tumor microenvironment. In this work, through an analysis of the transitions in regulatory network architecture and gene regulation dynamics, we identify the central transcription factors associated with lung adenocarcinoma progression. The gene NR2F1, associated with neurodevelopment and cancer dormancy, emerge as a key transcription factor in the progression of lung adenocarcinoma. We further identify transcription factors that are active in only cancer samples and uncover how changes in gene regulation dynamics influence intratumor heterogeneity. Taken together, our work elucidates the transitions in gene regulatory network during cancer progression, identifies central transcription factors in this process, and reveals the complex regulatory changes cooccurring in different cell types within the tumor microenvironment.
    DOI:  https://doi.org/10.1038/s41540-025-00640-9
  7. Nat Chem Biol. 2026 Jan 22.
    Targeting transcriptional plasticity in cancer.
    Simon D Schwarz.
      
    DOI:  https://doi.org/10.1038/s41589-025-02101-0
  8. Cancer Discov. 2026 Jan 21. OF1-OF17
    Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer.
    William C H Cross, Salpie Nowinski, George D Cresswell, Maximilian Mossner, Abhirup Banerjee, Bingxin Lu, Marc J Williams, Georgios Vlachogiannis, Laura J Gay, Ann-Marie Baker, Christopher Kimberley, Frederick J H Whiting, Hayley L Belnoue-Davis, Pierre Martinez, Maria Traki, Viola Walther, Kane Smith, Javier Fernandez-Mateos, Erika Yara-Romero, Erica A Oliveira, Salvatore Milite, Giulio Caravagna, Chela T James, George Elia, Alison Berner, Chang-Ho Ryan Choi, Pradeep Ramagiri, Ritika Chauhan, Nik Matthews, Jamie Murphy, Anthony Antoniou, Susan K Clark, Miriam Mitchison, Jo-Anne Chin Aleong, Enric Domingo, Inmaculada Spiteri, Stuart A C McDonald, Darryl Shibata, Miangela M Laclé, Lai Mun Wang, Morgan Moorghen, Ian P M Tomlinson, Marco Novelli, Marnix Jansen, Alan Watson, Nicola Valeri, Nicholas A Wright, John A Bridgewater, Manuel Rodriguez-Justo, Chris P Barnes, Hemant M Kocher, Simon J Leedham, Andrea Sottoriva, Trevor A Graham.
      Aneuploidy is near-ubiquitous in cancer and contributes to tumor biology. However, the temporal evolutionary dynamics that select for aneuploidy remain uncharacterized. We performed longitudinal genomic analysis of 755 samples from 167 patients with colorectal-derived neoplasias from different stages through metastasis and treatment. Adenomas had few copy number alterations (CNA) and most were subclonal, whereas cancers had many clonal CNAs, suggesting that progression goes through a CNA bottleneck. Individual colorectal cancer glands from the same tumor had similar karyotypes, despite evidence of ongoing instability at the cell level. CNAs in metastatic lesions, after therapy, and in late recurrences were similar to the primary. Mathematical modeling indicated that these data are consistent with the action of negative selection on CNAs that "trap" cancer genomes on a fitness peak characterized by specific CNAs. Hence, progression to colorectal cancer requires traversing a rugged fitness landscape, whereas subsequent CNA evolution is constrained by negative selection.
    SIGNIFICANCE: We profiled 167 long-term responders longitudinally (755 samples), documenting long-term cancer evolution. We found that a genetic bottleneck is required for progression and is associated with dramatic increase in CNAs but decrease in clonal diversity. After initiation, copy number evolution is constrained by negative selection through metastasis and treatment.
    DOI:  https://doi.org/10.1158/2159-8290.CD-24-0813
  9. Nature. 2026 Jan 21.
    Temporal tissue dynamics from a spatial snapshot.
    Jonathan Somer, Shie Mannor, Uri Alon.
      Physiological and pathological processes such as inflammation and cancer emerge from interactions between cells over time1. However, methods to follow cell populations over time within the native context of a human tissue are lacking because a biopsy offers only a single snapshot. Here we present one-shot tissue dynamics reconstruction (OSDR), an approach to estimate a dynamical model of cell populations based on a single tissue sample. OSDR uses spatial proteomics to learn how the composition of cellular neighbourhoods influences division rate, providing a dynamical model of cell population change over time. We apply OSDR to human breast cancer data2-4, and reconstruct two fixed points of fibroblasts and macrophage interactions5,6. These fixed points correspond to hot and cold fibrosis7, in agreement with co-culture experiments that measured these dynamics directly8. We then use OSDR to discover a pulse-generating excitable circuit of T and B cells in the tumour microenvironment, suggesting temporal flares of anticancer immune responses. Finally, we study longitudinal biopsies from a triple-negative breast cancer clinical trial3, in which OSDR predicts the collapse of the tumour cell population in responders but not in non-responders, based on early-treatment biopsies. OSDR can be applied to a wide range of spatial proteomics assays to enable analysis of tissue dynamics based on patient biopsies.
    DOI:  https://doi.org/10.1038/s41586-025-09876-1
  10. Nat Genet. 2026 Jan 22.
    Genomic evolution of pancreatic cancer at single-cell resolution.
    Haochen Zhang, Palash Sashittal, Elias-Ramzey Karnoub, Akhil Jakatdar, Shigeaki Umeda, Jungeui Hong, Anne Marie Noronha, Agustin Cardenas, Amanda Erakky, Caitlin A McIntyre, Akimasa Hayashi, Nicolas Lecomte, Marc Hilmi, Wungki Park, Nan Pang, Eileen M O'Reilly, Alice C Wei, Benjamin J Raphael, Christine A Iacobuzio-Donahue.
      Most evolutionary studies on pancreatic cancer rely on bulk sequencing, yet clonal evolution happens at the single-cell level. We used single-nucleus DNA sequencing to study 137,491 single nuclei from 24 pancreatic neoplasms reflecting various clinical scenarios. We found higher frequencies of somatic alterations to driver genes that bulk studies indicate; many manifest as copy number alterations and account for the majority of spatial heterogeneity. In pancreatic cancers with canonical KRAS oncogenic mutations, we found likely varied dependence on the genotype that may signify differential response to KRAS inhibition. In pancreatic cancers with germline heterozygous BRCA2 mutations, we discovered varied mechanisms and timing of inactivation of the wild-type allele that sculpted differential evolutionary trajectories. Inactivation of tumor-intrinsic response to transforming growth factor-β happens through various mechanisms, takes place after oncogenesis and coincides with invasion and metastasis, reflecting increasing selective pressure for the phenotype later in pancreatic ductal adenocarcinoma development.
    DOI:  https://doi.org/10.1038/s41588-025-02468-9
  11. bioRxiv. 2025 Dec 11. pii: 2025.12.08.693051. [Epub ahead of print]
    Haruka Resolves Perturbation Response Heterogeneity in Spatial Cell Niches.
    Yan Cui, Jasmine Blandin, Kipp Weiskopf, Na Sun.
      Understanding how tissues remodel in response to perturbations requires computational tools that can untangle condition-specific changes from the conserved tissue architecture. We present Haruka, a spatially aware contrastive learning framework that identifies salient (condition-specific) and background (shared) spatial domains across tissue slices and experimental conditions. Haruka integrates contrastive variational inference with an auxiliary microenvironment reconstruction task, enabling the model to learn spatial-context-informed embeddings that capture both perturbation effects and local neighborhood context. Through benchmarking on simulated and real datasets, Haruka outperforms state-of-the-art methods in detecting spatially heterogeneous responses. Applied to diverse spatial omics platforms, Haruka distinguished immunotherapy responders in melanoma, traced fibrosis progression in human lung tissue, and mapped treatment-resistant microenvironments in KRAS G12D -mutated lung cancer. Thus, Haruka provides a generalizable framework for spatial contrastive analysis, enabling systematic dissection of tissue organization, cellular plasticity, and microenvironmental remodeling across disease, development, and therapeutic response.
    DOI:  https://doi.org/10.64898/2025.12.08.693051
  12. Front Cell Infect Microbiol. 2025 ;15 1685862
    Emerging technologies and current challenges in intratumoral microbiota research.
    Zhiyue Wang, Tianqi Zhang, Yang Liu.
      Intratumoral microbiota are now recognized as an integral component of the tumor microenvironment, affecting tumor initiation, metastatic potential, immune modulation, and treatment response. However, their extremely low biomass poses significant challenges for accurate detection, functional interpretation, and reproducibility, largely because the detection process is highly susceptible to environmental contamination. Standardization of analytical procedures has not yet been established; consequently, variability in sampling protocols, sequencing workflows, and bioinformatic pipelines further complicates cross-study comparisons and hampers the consolidation of robust evidence in this field. Recent advances in technology have begun to provide opportunities to overcome these barriers. Improved contamination-control strategies and more sophisticated decontamination algorithms have enhanced the reliability of microbial detection in low-biomass tissues. High-resolution approaches, such as single-cell RNA sequencing, spatial transcriptomics and optimized anaerobic cultivation, enable the sensitive identification, spatial localization, and mechanistic study of tumor associated microbes. Parallel developments in genome-resolved and enzyme-level analysis reveal microbial metabolic pathways that shape immune responses, drug resistance, and tumor progression. Organoid-based co-culture models further provide physiologically relevant platforms to dissect host-microbe-immune interactions and interpret microbiota-driven modulation of therapeutic responses. Integrating microbiome data with clinical and multi-omics profiles, assisted by artificial intelligence, is accelerating biomarker discovery and informing microbe-guided therapeutic strategies. Taken together, the standardization of research strategies, combined with the application of advanced detection technologies, is propelling the field beyond descriptive profiling toward mechanistic understanding and clinical translation, thereby unlocking the potential of intratumoral microbiota for precision oncology.
    Keywords:  anaerobic bacteria; artificial intelligence; intratumoral microbiota; organoid models; tumor microenvironment
    DOI:  https://doi.org/10.3389/fcimb.2025.1685862
  13. Nat Methods. 2026 Jan 22.
    It's poster time.
    Vivien Marx.
      
    DOI:  https://doi.org/10.1038/s41592-025-03001-w
  14. NPJ Biofilms Microbiomes. 2026 Jan 23.
    Gut microbiome-driven colorectal cancer via immune, metabolic, neural, and endocrine axes reprogramming.
    Jhommara Bautista, Mónica Lamas-Maceiras, Camila Hidalgo-Tinoco, Antonio Guerra-Guerrero, Anapaula Betancourt-Velarde, Andrés López-Cortés.
      Colorectal cancer (CRC) is a leading cause of cancer mortality worldwide and is increasingly recognized as the outcome of complex host-microbe interactions. Beyond established genetic and environmental drivers, the gut microbiome has emerged as a causal and mechanistic contributor to CRC initiation, progression, and therapy response. This review synthesizes current molecular, ecological, and translational evidence to explain how gut microbial communities reprogram immune, metabolic, neural, and endocrine networks within the tumor microenvironment. CRC-associated dysbiosis is characterized by enrichment of pathobionts such as Fusobacterium nucleatum, pks⁺ Escherichia coli, and enterotoxigenic Bacteroides fragilis, and by loss of protective, short-chain-fatty-acid-producing commensals. These microbes promote carcinogenesis through genotoxin-induced DNA damage, epithelial barrier disruption, metabolic rewiring, and chronic inflammation that collectively sustain immune suppression and tumor growth. Defined mutational signatures from bacterial metabolites, including colibactin, cytolethal distending toxin, and indolimines, now directly link microbial exposures to human cancer genomes. By integrating these findings, this review conceptualizes CRC as a biofilm-structured, microbiome-driven ecosystem disease, where polymicrobial consortia coordinate barrier breakdown, immune evasion, and metabolic cooperation. Finally, we highlight emerging microbiota-targeted strategies, including dietary modulation, pre- and probiotics, postbiotics, bacteriophage therapy, engineered live biotherapeutics, and fecal microbiota transplantation, that translate these insights into precision prevention and therapy. Through this integrative framework, the review aims to reposition the microbiome from a correlative feature to a tractable determinant of CRC pathogenesis and treatment response.
    DOI:  https://doi.org/10.1038/s41522-025-00883-8
  15. Acta Biomater. 2026 Jan 20. pii: S1742-7061(26)00054-1. [Epub ahead of print]
    Bioengineering multicellular tumor spheroids with tunable extracellular matrix deposition.
    Alessandro Motta, Rasika Daware, Alessia Nucci, Saskia Breuel, Saskia von Stillfried, Jochen Maurer, Peter Boor, Danny Jonigk, Fabian Kiessling, Twan Lammers, Alexandros Marios Sofias, Federica De Lorenzi.
      The tumor microenvironment is complex and cannot be adequately recapitulated using conventional two-dimensional in vitro assays. Three-dimensional multicellular tumor spheroids (MCTS) offer a versatile platform to study heterotypic cell interactions, extracellular matrix (ECM) deposition, and drug screening in a controlled setting. Although technical advances have been made, there is still a lack of standardization among the different MCTS-forming methodologies. In fibroblast-containing MCTS, it is unclear how the initial cancer cell-fibroblast ratio affects MCTS architecture, functionality, and resemblance to in vivo tumors. Here, we systematically investigated how varying stromal content shapes MCTS architectural, molecular, and functional characteristics. Four cancer cell lines with distinct in vivo stromal signatures were co-cultured with fibroblasts at defined ratios to generate spheroids with increasing stromal content. At defined time points, spheroids were analyzed via histology, live fluorescence microscopy, immunofluorescence, flow cytometry, and gene expression assays to quantify growth kinetics, cell organization, proliferation, ECM deposition, and phenotypic states. We demonstrated that cancer cell identity and fibroblast proportion determine spheroid compactness, internal architecture, desmoplastic activity, and proliferation. Notably, fibroblast-rich spheroids displayed an increased ECM deposition and upregulation of genes related to fibroblast activation and ECM remodeling. These trends observed in MCTS were in line with patterns identified in in vivo mouse xenograft and patient-derived samples. Finally, a drug testing proof-of-concept validation revealed that increasing stromal content reduces sensitivity to chemotherapeutics, with cancer cell-fibroblast MCTS recapitulating treatment responses more accurately than cancer cell homospheroids. Taken together, our study enables the standardization of parameters and identification of variables that influence the desmoplastic reaction within MCTS. This knowledge may contribute to the manufacturing of MCTS with desired morphological and functional features, aiming to support their integration in bioreactor-based advanced in vitro models for tackling complex biological questions. STATEMENT OF SIGNIFICANCE: We established a reproducible strategy to engineer fibroblast-containing multicellular tumor spheroids (MCTS) with tunable stromal content and desmoplastic activity. By systematically varying the cancer cell-fibroblast ratio, we demonstrated a proportional and controllable increase in extracellular matrix deposition. Furthermore, fibroblast inclusion induced coordinated transcriptional, secretory, and functional changes that scale with stromal abundance and recapitulate key tumor-type-specific phenotypic states observed in murine xenografts and human tumor specimens. Together, these findings provide a standardized and scalable framework for generating MCTS with defined stromal properties, enhancing the relevance and reproducibility of 3D in vitro tumor models. This platform enables controlled interrogation of tumor-stroma interactions and offers a practical foundation for studying stromal modulation of therapy response.
    Keywords:  Bioengineering; extracellular matrix; fibrosis; multicellular tumor spheroids; tumor microenvironment
    DOI:  https://doi.org/10.1016/j.actbio.2026.01.038
  16. Open Biol. 2026 Jan 21. pii: 250282. [Epub ahead of print]16(1):
    Decoding 'Wntch': the intertwined Wnt and Notch pathways in development and disease.
    Fabio Turetti, Marek Dokoupil, Giovanna M Collu, Jakub Harnos, Jan Mašek.
      Multicellularity emerges from the ability of cells to undergo functional differentiation. One of the key mechanisms that enables this coordination is cellular signalling-a series of molecular interactions within or between cells that induce changes in cell behaviour or gene expression. As the body plan of multicellular organisms becomes more complex, so does the sophistication of their signalling systems. The Wnt and Notch pathways are central to regulating cell fate, tissue development and maintenance in all studied metazoa. Affecting overlapping biological processes, often within short developmental time windows, these molecular systems appear to be functionally interconnected, leading to the proposal of a 'Wntch' signalling concept. This concept implies that Wnt and Notch modules do not operate as isolated linear pathways but form a coherent network that integrates signals to ensure precise control of developmental and physiological outcomes. In this review, we synthesize both past and recent insights into the direct crosstalk of Wnt and Notch signalling molecules, examine crosstalk within the context of recently developed assays such as single-cell RNA sequencing and proximity labelling, and discuss the broader implications of this interplay in development and disease.
    Keywords:  Notch signalling; Wnt signalling; embryonic development; protein–protein interactions ; signalling crosstalk
    DOI:  https://doi.org/10.1098/rsob.250282
  17. Asian Pac J Cancer Prev. 2026 Jan 01. pii: 92003. [Epub ahead of print]27(1): 1
    From Evidence to Action: Reinforcing FIT as the Cornerstone of Colorectal Cancer Prevention Worldwide.
    Anwar Ali Khan, Raja Muhammad Umer Panhwar.
      
    Keywords:  Colorectal cancer (CRC); Global Health; cancer screening; early detection; fecal immunochemical test (FIT)
    DOI:  https://doi.org/10.31557/APJCP.2026.27.1.1
  18. Nat Biomed Eng. 2026 Jan;10(1): 4
    Morphological evaluation of brain organoids.
    Sadra Bakhshandeh.
      
    DOI:  https://doi.org/10.1038/s41551-025-01566-7
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