bims-enbcad Biomed News
on Engineering biology for causal discovery
Issue of 2026–01–11
nineteen papers selected by
Xiao Qin, University of Oxford
  1. Computational generation of high-content digital organs at single-cell resolution.
  2. Colon Organoids as Experimental Models to Study the Effect of Micro-Nanoparticles as a Driver of Early-Onset Colon Cancer.
  3. Noninvasive early detection of colorectal cancer through gut microbiome-derived biomarkers.
  4. A Tissue Renewal-Based Mechanism Drives Colon Tumorigenesis.
  5. The Need for a Systems Biology Approach in Cancer Explained.
  6. Value of Stool-Based Colorectal Cancer Screening: Integrating Real-World Adherence, Detection, and Prevention in a Cohort-Based Modeling Analysis.
  7. The gut microbiome in colorectal cancer: mechanisms of carcinogenesis and emerging microbiota-targeted therapies.
  8. Intratumoral Microbiome: Impact on Cancer Progression and Cellular Immunotherapy.
  9. The metabolism-immune axis in colorectal cancer: remodeling the tumor microenvironment through metabolite signaling.
  10. Circulating Tumor Cells as Diagnostic and Therapeutic Biomarkers in Hepatocellular Carcinoma: Advancing Precision Oncology Through Liquid Biopsy.
  11. Artificial Intelligence in Colonoscopy: A Systematic Review of Adenoma Versus Polyp Detection Rates.
  12. Stool- and Blood-Associated Colorectal Cancer Biomarkers: A Systematic Review.
  13. Microbiome modulation of tumorigenesis and immune responses.
  14. Constructing the spatiotemporal atlas of single-cell lineage trajectories in stereotypic biological structures.
  15. Framework for cancer evolution profiling and interception in colorectal cancer: ASCEND-CRC program.
  16. A guide to cancer screening.
  17. A targeted DNA methylation method for detecting gastrointestinal cancer in circulating cell-free DNA.
  18. Whole genome sequencing data of early- and late-onset colorectal cancer in 99 Korean patients.
  19. Review of Familial Adenomatous Polyposis: Current Understanding and Clinical Management.
  1. Nat Methods. 2026 Jan 06.
    Computational generation of high-content digital organs at single-cell resolution.
      
    DOI:  https://doi.org/10.1038/s41592-025-02996-6
  2. Cells. 2025 Dec 25. pii: 40. [Epub ahead of print]15(1):
    Colon Organoids as Experimental Models to Study the Effect of Micro-Nanoparticles as a Driver of Early-Onset Colon Cancer.
    Zahra Heydari, Gobinda Sarkar, Lauren Helgeson, Estela Mariel Cruz Garcia, Alexandra Ros, Khashayarsha Khazaie, Lisa Boardman.
      Early-onset colorectal cancer (EOCRC) in people < 50 years of age has been rising globally, yet its causes remain unknown. Emerging evidence suggests that environmental factors, including exposure to micro-and nanoplastics (MNPs), may contribute to colorectal carcinogenesis. MNPs can enter the gastrointestinal tract through ingestion, translocate across the epithelial barrier via endocytosis or paracellular pathways, and interact directly with epithelial and immune cells. Once internalized, they may generate events associated with tumor initiation including oxidative stress, disruption of membrane integrity, pro-inflammatory signaling, and disruption of genomic and epigenomic stability. Patient-derived colorectal organoids offer a physiologically relevant and scalable 3D model that closely mimics the cellular architecture and genetic landscape of primary tumors. We highlight how organoid models can be leveraged to study the impact of MNPs on the key processes of inflammation, DNA damage, senescence, and epigenetic modifications. Furthermore, we discuss the application of organoid-based systems to model EOCRC driven by environmental exposures, including the integration of organoid platforms with high-throughput assays, omics profiling, and microfluidics to better capture MNP-induced pathogenic mechanisms. Altogether, colorectal organoids provide a powerful bridge between environmental plastic exposure and EOCRC etiology, offering a tractable platform to identify mechanistic pathways and potential biomarkers of early disease.
    Keywords:  colorectal cancer; early-onset CRC; micro- and nanoplastics; organoid
    DOI:  https://doi.org/10.3390/cells15010040
  3. Ann Med Surg (Lond). 2026 Jan;88(1): 997-998
    Noninvasive early detection of colorectal cancer through gut microbiome-derived biomarkers.
    Muhammad Shahid Mehmood, Fatima Hajj.
      Colorectal cancer (CRC) remains a major global burden, with 1.9 million new cases and 935000 deaths reported in 2024. Despite available screening tools, nearly 45% of cases are still diagnosed at advanced stages, where the 5-year survival rate falls below 14%, compared to >90% in early detection. The limitations of colonoscopy its invasiveness, cost, and poor compliance (<40% globally) demand innovative, noninvasive diagnostic solutions. Gut microbiome profiling has recently emerged as a transformative approach, with specific bacterial signatures such as Fusobacterium nucleatum, Parvimonas micra, and Peptostreptococcus anaerobius showing AUC values between 0.85 and 0.93 for early CRC identification. Integrating metagenomic and metabolomic data enhances diagnostic accuracy to 89% sensitivity and 91% specificity. Moreover, altered microbial metabolites including decreased short-chain fatty acids and elevated secondary bile acids correlate with a 2.3- to 3.1-fold higher risk of carcinogenesis. Novel CRISPR-Cas13a-based assays further allow sub-attomolar detection of microbial RNA transcripts, underscoring a new frontier in microbiome-driven cancer diagnostics. Collectively, gut microbiome-derived biomarkers represent a noninvasive, mechanistically grounded, and highly sensitive platform for early CRC detection with significant translational potential.
    Keywords:  colorectal cancer; gut microbiome; liquid biopsy; metabolomics; metagenomics; microbial biomarkers; noninvasive diagnostics; precision oncology
    DOI:  https://doi.org/10.1097/MS9.0000000000004353
  4. Cancers (Basel). 2025 Dec 23. pii: 44. [Epub ahead of print]18(1):
    A Tissue Renewal-Based Mechanism Drives Colon Tumorigenesis.
    Ryan M Boman, Gilberto Schleiniger, Christopher Raymond, Juan Palazzo, Anne Shehab, Bruce M Boman.
      Our Goal is to identify how colorectal cancer (CRC) arises in the single-layered cell epithelium (simple columnar epithelium) that lines the luminal surface of the large intestine. Background: We recently reported that the dynamic organization of cells in colonic epithelium is encoded by five biological rules and conjectured that colon tumorigenesis involves an autocatalytic tissue renewal reaction. Introduction Our objective was to define how altered crypt turnover explains tissue disorganization that leads to adenoma morphogenesis and CRC. Hypothesis: Changes in rate of tissue renewal-based cell polymerization leads to epithelial expansion and tissue disorganization during adenoma histogenesis. Methods: Accordingly, we created a computational model that considers the structure of colonic epithelium to be a polymer of cells and that tissue renewal is autocatalytic. Indeed, self-renewal of stem cells in colonic crypts continuously produces cells that act like monomers to form a polymer of cells (an interconnected, continuous cell sheet) in a polymerization-based process. Our model is a system of nonlinear differential equations that simulates changes in human crypt cell population dynamics. Results: We investigated how changes occur in the proportion of different cell types during adenoma development in FAP patients. The results show premalignant colonic crypts have a decreased rate of tissue renewal due to APC-mutation. Discussion: This slower rate of cell polymerization causes a rate-limiting step in the crypt renewal process that expands the proliferative cell population size. Conclusions: Our findings provide a mechanism that explains how a prolonged rate of crypt renewal leads to tissue disorganization with local epithelial expansion, infolding, and contortion during adenoma morphogenesis.
    Keywords:  APC gene; colorectal cancer; familial adenomatous polyposis; systems biology; tissue renewal
    DOI:  https://doi.org/10.3390/cancers18010044
  5. Int J Mol Sci. 2025 Dec 22. pii: 141. [Epub ahead of print]27(1):
    The Need for a Systems Biology Approach in Cancer Explained.
    Hehuan Zhu, Xi Zhang, Ehsan Nazemalhosseini-Mojarad, Jessica Roelands, Lysanne D A N de Muynck, Cor J Ravensbergen, Rachel Hoorntje, Imke Stouten, Marianne Hokland, Alexander L Vahrmeijer, Rob A E M Tollenaar, Edwin Koster, Peter J K Kuppen.
      Traditionally, scientists tend to approach cancer research in a reductionistic way: aiming at uncovering underlying, separate components in malignant processes. And indeed, great progress has been made by reducing the development of a tumor to single, specific genes and mutations. For instance, familial adenomatous polyposis (FAP) could be reduced to a germline mutation in the Adenomatous Polyposis Coli (APC) gene. The escape of tumor cells from immune surveillance could be reduced to the tumor expression of immune checkpoints, resulting in new approaches in tumor therapy by applying immune checkpoint inhibitors. However, a germline mutation in APC is not 1:1 related to colorectal cancer (CRC), and only some patients respond to immune checkpoint inhibitors. The point here is that biological systems, also comprising cancer, have properties that cannot be reduced to single components. The cooperation of the single components results in new, emergent properties. The outcome of an interaction in a complex network, like the immune system, depends on the many cell types involved and the numerous molecules that interact and activate or inhibit pathways. The way the composing elements are organized is a causal factor in itself for any emergent property. The rise of genomic analysis at the end of the previous century, enabling us to sequence a full genome at the DNA and RNA levels, has initiated an awareness of the need for 'systems biology': to consider a full system and how it is organized, in all of its aspects, to understand biological pathways and their outcomes. In this review, we outline the prospects and limitations of systems biology in cancer research and propose a causal framework that integrates upward and downward causation and multiple realizability to understand the emergent properties of tumors that determine the dynamics of tumor development.
    Keywords:  cancer; downward causation; emergent property; molecular biology; systems biology; upward causation
    DOI:  https://doi.org/10.3390/ijms27010141
  6. J Clin Med. 2025 Dec 20. pii: 41. [Epub ahead of print]15(1):
    Value of Stool-Based Colorectal Cancer Screening: Integrating Real-World Adherence, Detection, and Prevention in a Cohort-Based Modeling Analysis.
    A Mark Fendrick, Derek W Ebner, Michael Dore, Chris Estes, Gustavus Aranda, Mohammad Dehghani.
      Background/Objectives: Modeling analyses for colorectal cancer (CRC) screening focusing solely on the costs of screening do not fully capture the value of screening programs. We evaluated the clinical and economic effects of CRC stool-based screening tests, including impacts on cancer-related outcomes. Methods: A cohort-based decision-analytic cost-estimator model estimated outcomes for a single round of screening with next-generation multi-target stool DNA (ng mt-sDNA) test or fecal immunochemical test (FIT) from a US payer perspective. Undiagnosed cancers were assumed to become symptomatic (and detected) within 10 years. Clinical assumptions, advanced precancerous lesion and CRC prevalence, and test performance inputs were from clinical trial data. Adherence rates for initial screening and follow-up colonoscopy after a positive result were from real-world data. Input costs included the screening tests, follow-up colonoscopy (with and without polypectomy), and CRC treatment. Results: Compared with FIT, more individuals completed ng mt-sDNA (321,000 vs. 713,000, respectively), leading to the detection of more CRC cases (436 with FIT vs. 2235 with ng mt-sDNA), more advanced precancerous lesions, and more CRC at earlier stages. The cost of screening per patient screened was USD 801 for ng mt-sDNA and USD 124 for FIT. Follow-up colonoscopy cost was USD 149 million with ng mt-sDNA versus USD 22 million with FIT, whereas CRC treatment costs were lower for ng mt-sDNA (USD 1423 million versus USD 1474 million, respectively). When accounting for both direct and CRC averted costs, the total cost of screening and treatment was USD 1383 million with ng mt-sDNA versus USD 1427 million with FIT. Conclusions: Higher screening costs with ng mt-sDNA versus FIT are counterbalanced by savings realized from enhanced CRC prevention and earlier detection due to the superior test performance and better adherence with ng mt-sDNA.
    Keywords:  adherence; colorectal cancer; cost; screening; sensitivity; specificity; stool test
    DOI:  https://doi.org/10.3390/jcm15010041
  7. Discov Oncol. 2026 Jan 07.
    The gut microbiome in colorectal cancer: mechanisms of carcinogenesis and emerging microbiota-targeted therapies.
    Yue Li, Xingyu Shen, Deqiang Wang, Kang Sun.
      
    Keywords:  Carcinogenesis; Chemoresistance; Colorectal cancer; Fecal microbial transplantation; Microbiome
    DOI:  https://doi.org/10.1007/s12672-025-04367-1
  8. Cancers (Basel). 2025 Dec 29. pii: 100. [Epub ahead of print]18(1):
    Intratumoral Microbiome: Impact on Cancer Progression and Cellular Immunotherapy.
    Georgy Leonov, Antonina Starodubova, Oleg Makhnach, Dmitry Goldshtein, Diana Salikhova.
      The intratumoral microbiota, comprising bacteria, fungi, and viruses within the tumor microenvironment, actively influences carcinogenesis. Key mechanisms include the induction of host DNA damage, modulation of critical oncogenic signaling pathways such as WNT-β-catenin, NF-κB, and PI3K, and the orchestration of inflammatory processes. The microbiome's interaction with the host immune system is complex and bidirectional. On one hand, specific microbes can foster a pro-tumorigenic niche by suppressing the activity of cytotoxic T cells and natural killer (NK) cells or by promoting the accumulation of immunosuppressive cell types like tumor-associated macrophages (TAMs). On the other hand, microbial components can serve as neoantigens for T cell recognition or produce metabolites that reprogram the immune landscape to enhance anti-tumor responses. The composition of this microbiome is emerging as a crucial factor influencing the outcomes of immunotherapies. Prospective investigations in cancer immunotherapy ought to prioritize mechanistic inquiry employing integrative multi-omics methodologies. The execution of meticulously designed clinical trials for the validation of microbial biomarkers, and the systematic, evidence-based development of microbiome-targeted therapeutic interventions aimed at enhancing antitumor immune responses.
    Keywords:  CAR-T cells; antitumor immunity; cell therapy; gut-tumor axis; immune response; intratumoral microbiome; tumor microenvironment
    DOI:  https://doi.org/10.3390/cancers18010100
  9. Front Immunol. 2025 ;16 1735873
    The metabolism-immune axis in colorectal cancer: remodeling the tumor microenvironment through metabolite signaling.
    Shaofan Hu, Hui Heng, Fang Yang, Meng Wang, Guoxiang Liu, Yuancai Xiang, Hongming Miao.
      Metabolic reprogramming is a defining hallmark of tumors, and plays a pivotal role in sustaining malignant growth by rewiring core bioenergetic and biosynthetic pathways. Beyond supporting tumor cell proliferation, survival, and metastasis, it profoundly shapes the tumor microenvironment through nutrient competition, accumulation of immunosuppressive metabolites, and modulation of immune cell function, thereby facilitating immune evasion and therapy resistance. This review comprehensively elaborates on metabolic reprogramming in colorectal cancer, covering key alterations in glucose metabolism (Warburg effect), tricarboxylic acid cycle remodeling, lipid biosynthesis/oxidation, cholesterol metabolism, and amino acid (glutamine, methionine, tryptophan, arginine) metabolism. It further dissects how these metabolic shifts impact the tumor microenvironment in colorectal cancer, including their effects on effector immune cells (CD8+ T cells, NK cells), immunosuppressive populations (Tregs, MDSCs, M2-TAMs), and antigen-presenting cells. Additionally, this review highlights the role of the gut microbiota and their metabolites (e.g., SCFAs, secondary bile acids and indoles) in remodeling the immune microenvironment via metabolic crosstalk. Overall, this work provides a comprehensive understanding of CRC metabolic reprogramming and its microenvironmental impacts, offering critical insights to guide the development of novel metabolism-targeted therapeutic strategies for CRC.
    Keywords:  colorectal cancer (CRC); gut microbiota; immune evasion; metabolic reprogramming; metabolism-targeted therapy; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2025.1735873
  10. J Gastroenterol Hepatol. 2026 Jan 05.
    Circulating Tumor Cells as Diagnostic and Therapeutic Biomarkers in Hepatocellular Carcinoma: Advancing Precision Oncology Through Liquid Biopsy.
    Mutaz Jamal Al-Khreisat, Munthar Kadhim-Abosaoda, Namim Abas Ibrahim, Ms Malathi H, Priya Priyadarshini-Nayak, V Sathiya-Priya, Gurjant Singh, Ashish Singh Chauhan.
      Circulating tumor cells (CTCs) are emerging as promising biomarkers in hepatocellular carcinoma (HCC), offering noninvasive insight into tumor biology, progression, and treatment response. Advances in enrichment and single-cell technologies have enabled the characterization of CTCs at genomic, transcriptomic, epigenetic, and proteomic levels. CTC detection correlates with tumor stage, vascular invasion, and alpha-fetoprotein levels, supporting their role in early diagnosis and staging. Specific surface markers such as epithelial cell adhesion molecule, GPC3, ASGPR, and stem cell-associated antigens like CD90 and CD133 help classify CTC subtypes with prognostic and therapeutic relevance. Mesenchymal and hybrid phenotypes, identified via epithelial-to-mesenchymal transition markers, are linked to recurrence and metastasis. Furthermore, CTCs provide a platform for companion diagnostics by reflecting mutational and resistance profiles, particularly in the context of targeted therapies and immune checkpoint inhibitors. Despite current limitations in standardization, sensitivity, and scalability, the integration of CTC analysis into clinical practice holds potential to enhance precision medicine strategies in HCC.
    Keywords:  biomarkers; circulating tumor cells; hepatocellular carcinoma; liquid biopsy; precision oncology
    DOI:  https://doi.org/10.1111/jgh.70197
  11. Cureus. 2025 Dec;17(12): e98528
    Artificial Intelligence in Colonoscopy: A Systematic Review of Adenoma Versus Polyp Detection Rates.
    Waseem Rabba, Fatima Asif, Muhammad Y Younis, Haris Nasrullah, Laraib Fatima, Muhammad A Arif.
      Colonoscopy is the gold standard in the prevention of colorectal cancer, but the miss rates of adenoma are high, which restricts its efficacy. To improve lesion recognition, artificial intelligence (AI), especially computer-aided detection (CADe) systems, has been introduced. The aim of this systematic review was to compare AI-assisted colonoscopy in terms of its ability to improve adenoma detection rate (ADR) and polyp detection rate (PDR). An extensive search was performed on PubMed, Embase, and Cochrane Library from 2015 to 2025. There were 17 randomized controlled trials (RCTs) comparing the use of AI-assisted colonoscopy with normal colonoscopy. The methodological quality measure of the included RCTs was Cochrane Risk of Bias 2.0 (RoB 2.0), which subdivided the studies based on low risk, some concerns, or high risk of bias based on whether they were biased in this or that domain. The robVis tool was used to produce the visual summaries. AI-aided colonoscopy effectively enhanced both adenoma detection rate (ADR) and polyp detection rate (PDR) in all of the included studies over conventional colonoscopy. In adenoma detection, accuracy was more than 85%, and in polyp detection, more than 90%. The advantage was also found especially in the detection of small and flat adenomas, which are very often missed in routine practice. The use of AI in colonoscopy is strongly associated with an increase in the detection rate of adenoma and polyps, minimizing the risk of underdiagnosis. The results highlight the clinical promise of AI in the form of a decision-support tool across gastroenterologists and suggest that AI can be applied to enhance the outcomes of preventive and screening colorectal cancer. Future research should be cost-efficient and practical, and combined with some clinical activities.
    Keywords:  adenoma detection rate; artificial intelligence; colonoscopy; computer-aided detection; polyp detection rate
    DOI:  https://doi.org/10.7759/cureus.98528
  12. Cancers (Basel). 2025 Dec 27. pii: 96. [Epub ahead of print]18(1):
    Stool- and Blood-Associated Colorectal Cancer Biomarkers: A Systematic Review.
    Pumelela Hallom, Pragalathan Naidoo, Sibusiso Senzani, Sayed S Kader, Zilungile L Mkhize-Kwitshana.
      Background/Objectives: Colorectal cancer (CRC) is a major contributor to cancer-related deaths worldwide. While existing screening tools are effective, their high cost and limited availability restrict widespread adoption, particularly in low- and middle-income settings. The identification of affordable, non-invasive biomarkers is therefore critical to improve early CRC detection and survival outcomes. Methods: A systematic literature search was performed through PubMed, ScienceDirect, Medline, ISI Web of Knowledge, and Google Scholar to identify studies reporting stool- and blood-based biomarkers for CRC detection. Data were extracted using a standardized template, including study details, specimen type, detection method, and diagnostic performance parameters such as sensitivity and specificity. Results: DNA methylation biomarkers demonstrated high diagnostic potential. Syndecan 2 (SDC2) and Short Stature Homeobox 2 (SHOX2) achieved a combined stool sensitivity of 91.35%. Other methylation markers, including NDRG4, SEPT9, and BCAT1, showed a composite sensitivity of 82.7%. Plasma-based methylation markers such as GATA5, FOXE1, and SYNE1 reported sensitivities ranging from 18-47% and specificities of 93-99%. Hypermethylation of SFRP2 and WIF-1 achieved 81.3% sensitivity in CRC and precursor lesions. Matrix metalloproteinases (MMP-2 and MMP-9) were elevated in CRC patients, with stool MMP-9 yielding 72.2% sensitivity and 95% specificity. A stool gene panel (UBE2N, IMPDH1, DYNC1LI1, HRASLS2) reached 96.6% sensitivity and 89.7% specificity, while a methylation-based panel (ALX4, BMP3, NPTX2, RARB, SDC2, SEPT9, VIM) achieved 90.7% sensitivity. MicroRNAs (miR-21, miR-92a, miR-223, miR-182) showed excellent diagnostic performance, with sensitivities exceeding 96% and specificities above 75%. Conclusions: DNA methylation and microRNA biomarkers hold strong promises for non-invasive CRC screening. Multi-marker panels demonstrate superior diagnostic accuracy and may provide a cost-effective, scalable approach for early CRC detection in resource-limited settings.
    Keywords:  biomarkers; blood; colorectal cancer; non-invasive screening methods; stool
    DOI:  https://doi.org/10.3390/cancers18010096
  13. J Biomed Sci. 2026 Jan 05. 33(1): 4
    Microbiome modulation of tumorigenesis and immune responses.
    Yuning Chen, Ying Fang, Zibai Lyu, Yanxin Tian, Siyue Niu, Yan-Ruide Li, Lili Yang.
      The microbiome has emerged as a critical, context-dependent regulator of tumorigenesis and anticancer immunity, capable of either promoting cancer progression or protecting against malignancy. This dual role is mediated by multiple interconnected mechanisms-including chronic inflammation, modulation of immune responses, and alterations in host metabolic signaling. These microbiome-cancer interactions vary across organs, influencing malignancies in the colon, breast, lung, and beyond. Clinically, the microbiome significantly affects patient responses to cancer therapies, particularly immunotherapies such as immune checkpoint blockade (ICB) and chimeric antigen receptor (CAR)-T cell therapy. Although emerging therapeutic strategies aimed at modulating the microbiome have shown promising early results, challenges remain, including individual microbiome variability and the dynamic interplay between the immune system and microbial communities. Nevertheless, harnessing the microbiome holds significant potential to transform precision oncology, offering personalized cancer prevention and treatment strategies tailored to each patient's unique microbial ecosystem.
    Keywords:  Cancer immunotherapy; Dysbiosis; Immune modulation; Microbial metabolites; Microbiome; Microbiome-targeted therapies; Tumorigenesis
    DOI:  https://doi.org/10.1186/s12929-025-01208-9
  14. iScience. 2026 Jan 16. 29(1): 114307
    Constructing the spatiotemporal atlas of single-cell lineage trajectories in stereotypic biological structures.
    Ran Wang, Xianfa Yang, Chengfei Lian, Jianjie Wang, Jiehui Chen, Yun Qian, Yaochen Xu, Liantang Wang, John C Marioni, Patrick P L Tam, Naihe Jing.
      Spatial transcriptomics technologies have emerged as instrumental tools for elucidating cellular heterogeneity and molecular regulation within the complex tissue microenvironment, but are constrained by insufficient gene recovery or an inability to achieve intact single-cell resolution. By integrating spatial transcriptomics and single-cell RNA sequencing technologies, we develop a mathematical method of single-cell resolved spatiotemporal (SCST) mapping that comprises tiered algorithms for constructing the spatial molecular atlas of the biospecimen at single-cell resolution across a timeline of development. The embedded spatial-smoothing algorithm in SCST significantly enhances the spatial mapping accuracy of single cells, thereby improving the fidelity of the annotation of cell identity to the equivalent in vivo cell type. Through 3D mathematical modeling, SCST facilitates the spatial reconstruction of a single-cell molecular atlas and the delineation of cellular heterogeneity. When integrated with temporal data, SCST can also delineate the spatiotemporal lineage trajectory at single-cell resolution in a developing biological entity.
    Keywords:  Computational bioinformatics; Developmental biology; Transcriptomics
    DOI:  https://doi.org/10.1016/j.isci.2025.114307
  15. Cancer Cell. 2026 Jan 08. pii: S1535-6108(25)00550-1. [Epub ahead of print]
    Framework for cancer evolution profiling and interception in colorectal cancer: ASCEND-CRC program.
    Salvador Alonso, Kanwal Raghav, Van K Morris, Kristin Alfaro-Munoz, Tanios Bekaii-Saab, Timothy L Cannon, Ryan B Corcoran, Nicholas Duesbery, Manju George, David Hsu, Christopher Lieu, Anirban Maitra, Dipen Maru, Jasmine A McQuerry, David Menter, Jonathan Mizrahi, Kimmie Ng, Aparna Parikh, Kunal Rai, Michelle C Sangar, Kenna R Shaw, John Paul Shen, John H Strickler, Ann D Feehan, Alda L Tam, Guglielmo Vetere, Rona Yaeger, Ying Yuan, Xiling Shen, Andrea H Bild, Scott Kopetz.
      Cancer evolution is a complex and dynamic process, yet most treatment strategies remain static. Infrequent tumor sampling has limited our ability to counteract the transient adaptive states that precede resistance. To address this gap, ARPA-H launched the ADAPT program, an initiative aimed at transforming cancer care by aligning therapies with real-time tumor evolution. Within this framework, the ASCEND-CRC trial aims to uncover early adaptive mechanisms and identify biomarkers to guide therapeutic decision-making in metastatic colorectal cancer (CRC). The study moves beyond single pre-treatment biomarkers by integrating multimodal profiling to longitudinally track tumor evolution and define an actionable set of dynamic biomarkers that inform treatment decisions. Together with other ADAPT initiatives, ASCEND-CRC represents a paradigm shift in precision oncology, establishing a scalable platform to intercept resistance.
    DOI:  https://doi.org/10.1016/j.ccell.2025.12.016
  16. Nat Rev Clin Oncol. 2026 Jan 07.
    A guide to cancer screening.
    Stephen W Duffy, Judith Offman.
      The aim of cancer screening is to identify pre-malignant conditions, which can be removed or treated, or earlier-stage disease, for which treatment is more likely to be curative, in non-symptomatic individuals. Currently, screening programmes are being consolidated for five cancer types (breast, prostate, cervical, colorectal and lung) and several other cancer types are the focus of specific initiatives. Cancer screening is at a point of potential major transformation owing to technological advances in detection. In this Review, we first recapitulate the general principles of cancer screening. We then provide a timely overview of the current screening practices for breast, cervical, colorectal, prostate and lung cancer, addressing major challenges and potential future changes in practice. We also discuss other malignancies for which screening initiatives might be worth considering. Finally, we highlight technological developments in cancer detection that might hold promise for screening an increasing number of cancers in the future, notably some that reflect unmet needs.
    DOI:  https://doi.org/10.1038/s41571-025-01112-z
  17. iScience. 2026 Jan 16. 29(1): 114342
    A targeted DNA methylation method for detecting gastrointestinal cancer in circulating cell-free DNA.
    Zhaoyu Jiang, Yuqing Guo, Yongqu Lu, Kun Qian, Xiaomeng Liu, Siyi Lu, Jie Ren, Fuchou Tang, Wei Fu, Lu Wen, Xin Zhou.
      Colorectal cancer (CRC) and gastric cancer (GC) are leading causes of cancer-related mortality. However, cost-effective methods for simultaneous detection of CRC and GC in circulating cell-free DNA (cfDNA) remain insufficiently explored. To address this, we developed targeted methylated CpG tandem amplification and sequencing (tMCTA-seq), a PCR-based method utilizing a set of locus-specific primers with a universal CGCGCGG primer, and targeted a panel of 110 loci. The method demonstrated high technical sensitivity below one haploid genome equivalent. Using a repeated nested cross-validation framework, the ensemble model, applied to 448 plasma samples (170 CRC, 101 GC, and 177 control participants), achieved areas under the curve (AUCs) of 0.928 (88.2% sensitivity and 90.7% specificity) for CRC and 0.926 (86.7% sensitivity and 94.4% specificity) for GC on the test set. Furthermore, tMCTA-seq differentiated between CRC and GC (AUC = 0.819). Thus, tMCTA-seq is a cost-effective, methylation-based approach for simultaneous detection of and differentiation between two major gastrointestinal cancers in blood.
    Keywords:  Biochemistry; Cancer
    DOI:  https://doi.org/10.1016/j.isci.2025.114342
  18. Sci Data. 2026 Jan 08.
    Whole genome sequencing data of early- and late-onset colorectal cancer in 99 Korean patients.
    Jae-Yoon Kim, Ye Jin Ha, Seung-Jin Park, Sun-Woo Lee, Seon-Yeop Kim, Seung-Eun Oh, Jong-Lyul Park, Ka Hee Tak, Yong Sik Yoon, Jong Lyul Lee, Seon-Young Kim, Chan Wook Kim.
      Colorectal cancer (CRC) is the third most prevalent cancer type worldwide. Despite improvements in screening programs, the incidence of early-onset CRC (EOCRC) in patients under 50 years old is rapidly increasing, including in Korea, in contrast to the decreasing trend of late-onset CRC (LOCRC). However, a comprehensive biological understanding of CRC's coding and non-coding variants, onset-dependent prognostic variables, and the genetic and transcriptomic differences between EOCRC and LOCRC remains limited. To provide insights into this, we present a high-quality multi-omics dataset consisting of whole genome sequencing (WGS) and RNA sequencing (RNA-seq) data from 49 EOCRC and 50 LOCRC patients. WGS was performed using the DNBSEQ-T7 platform, generating 1.409 billion reads at an average depth of 37.70×. RNA-seq data previously generated from the same samples are included to support integrative analysis. This dataset enables comprehensive exploration of genomic and transcriptomic alterations in CRC and serves as a valuable resource for identifying onset-specific biomarkers and molecular features, ultimately supporting improved diagnosis and therapeutic strategies.
    DOI:  https://doi.org/10.1038/s41597-025-06517-0
  19. JCO Oncol Pract. 2026 Jan 06. OP2500553
    Review of Familial Adenomatous Polyposis: Current Understanding and Clinical Management.
    Jared R Hendren, Elissa Dabaghi, Josh Sommovilla, David Liska.
      Familial adenomatous polyposis (FAP) is an autosomal dominant hereditary colorectal cancer (CRC) syndrome caused by germline pathogenic variants in the adenomatous polyposis coli (APC) gene. FAP is typically characterized by the development of hundreds to thousands of adenomatous polyps throughout the colon and rectum, with a nearly 100% chance of developing CRC if left untreated. Duodenal cancer is the second leading cause of cancer for patients with FAP; however, gastric cancer has become more prevalent in recent years with improved surveillance of the colon, rectum, and duodenum. Patients frequently develop other extracolonic manifestations including desmoid disease, which holds the highest extracolonic mortality risk, and thyroid nodules, which are more frequently associated with the cribriform morular variant of papillary thyroid cancer. Management of FAP is complex, and patients require frequent and lifelong surveillance. This review will discuss the current understanding and clinical management of FAP as well as innovations and challenges in clinical practice.
    DOI:  https://doi.org/10.1200/OP-25-00553
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