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Liquid biopsy using circulating tumor DNA (ctDNA) has become one of the most promising approaches in precision oncology, offering a minimally invasive means to track tumor burden, detect minimal residual disease, and monitor treatment response in real time. In colorectal cancer (CRC), ctDNA has been investigated extensively across both localized and advanced disease. In localized CRC, ctDNA testing after surgery provides strong prognostic value, with positivity indicating a high risk of recurrence and negativity correlating with favorable long-term outcomes. ctDNA dynamics during adjuvant therapy can further refine risk stratification, as clearance is associated with improved survival, while persistence signals poor prognosis. Moreover, ctDNA-guided strategies in the adjuvant setting have demonstrated potential to enable safe treatment de-escalation or intensification, tailoring therapy to individual patient risk. In the neoadjuvant setting, particularly in rectal cancer, ctDNA has shown promise as a predictor of pathological response and long-term outcomes, raising the possibility of guiding organ-preserving or intensified treatment strategies. In metastatic CRC, ctDNA serves as a dynamic biomarker for baseline profiling, real-time monitoring of treatment response, and detection of emerging resistance mechanisms, supporting adaptive therapeutic decision-making throughout the disease course. Despite its promise, challenges remain, including variability across assay platforms, risk of false negatives in low-volume disease, lack of standardized thresholds for intervention, and questions of cost-effectiveness. Collectively, ctDNA represents a transformative biomarker in CRC, with ongoing research and harmonization efforts expected to establish its role as a clinical standard for guiding precision treatment.
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Introduction
Liquid biopsy has emerged as one of the most promising innovations in precision oncology, offering a minimally invasive means to access and analyze tumor-derived material in blood and other body fluids. By far the most widely studied analyte is circulating tumor DNA (ctDNA), which provides a direct window into tumor genetics and dynamics [1]. By enabling real-time insights into tumor biology without the need for repeated tissue sampling, ctDNA-based liquid biopsy has the potential to transform how we diagnose, monitor, and treat cancer. Among various tumor types, colorectal cancer (CRC) has stood out as a particularly well-suited setting for the clinical application of ctDNA [2], demonstrating utility in both localized and advanced disease. This review explores the current state of ctDNA analyses in CRC, examining its role as a tool for prognostic insight and its potential trajectory toward becoming an emerging clinical standard.
Localized CRC applications of ctDNA
Increasingly, ctDNA is being investigated not only in the adjuvant setting but also in neoadjuvant applications, where it may help identify patients who could benefit from intensified therapy or safely avoid overtreatment. This growing body of research highlights the potential of ctDNA-guided strategies to refine personalized treatment decisions and improve long-term outcomes (Fig. 1; [3]).
Fig. 1
Clinical integration of ctDNA testing in resectable colorectal cancer (CRC). a In localized stage II–III or resectable stage IV CRC, surgery is the standard of care. Postoperative ctDNA testing within 2–10 weeks can detect minimal residual disease (MRD) and stratify patients by recurrence risk (e.g., CIRCULATE-Japan GALAXY). ctDNA-negative patients may undergo treatment de-escalation (e.g., VEGA, DYNAMIC/DYNAMIC-III trials), whereas ctDNA-positive patients may receive adjuvant chemotherapy (ACT) with possible escalation (e.g., ALTAIR, DYNAMIC-III). Serial ctDNA testing during and after ACT can monitor treatment response and inform prognosis. After treatment completion, regular ctDNA surveillance (e.g., every 4 months for 2 years) may enable earlier detection of recurrence. b In stage II–III rectal cancer, neoadjuvant chemoradiotherapy (nCRT) is recommended before surgery to reduce tumor burden and recurrence risk. ctDNA testing during or at the end of treatment (EOT) can assess response and identify patients at elevated relapse risk, supporting decisions on intensified adjuvant therapy or closer surveillance. After completion of therapy, recurrence surveillance with serial ctDNA testing at regular intervals (e.g., every 4 months during the first 2 years) enables early detection of molecular relapse. Rising ctDNA levels during surveillance may prompt earlier imaging and clinical intervention
Surgery remains the cornerstone of curative-intent treatment for localized CRC [4]. Yet, despite complete macroscopic resection, up to one third of patients will relapse due to microscopic residual disease [5]. Detecting this minimal residual disease (MRD) is a long-standing challenge because traditional surveillance using carcinoembryonic antigen (CEA) levels and imaging lacks sensitivity until disease is clinically overt. ctDNA has provided a solution by acting as a molecular surrogate for MRD [3, 6‐9] with the CIRCULATE-Japan GALAXY study offering the most robust dataset [8]. Enrolling more than 2200 patients with stage II–III colon cancer or resectable stage IV disease, the trial demonstrated that ctDNA positivity within 2–10 weeks after surgery was a powerful predictor of recurrence. Hazard ratios for disease-free survival (DFS) and overall survival (OS) approached 12 and 10, respectively. Nearly 80% of ctDNA-positive patients relapsed, compared to only 13% of ctDNA-negative patients. Equally striking were data on ctDNA clearance. Among ctDNA-positive patients treated with adjuvant chemotherapy (ACT), those achieving clearance had excellent outcomes, with 2‑year DFS over 85–90%. By contrast, persistent ctDNA portended DFS below 5%. Thus, ctDNA serves as both a prognostic biomarker and a dynamic indicator of adjuvant therapy effectiveness.
Adjuvant therapy guidance
The DYNAMIC trial in stage II colon cancer provided the first randomized evidence for ctDNA-guided decision-making [10, 11]. In the ctDNA-guided arm, patients received ACT only if postoperative ctDNA was detectable. This approach reduced chemotherapy use from ~28% to 15% without compromising recurrence-free survival. The recently published 5‑year follow-up confirmed non-inferiority for OS between the ctDNA-guided and standard-management groups, reinforcing that ctDNA can enable safe treatment de-escalation without compromising long-term outcomes. Importantly, in ctDNA-positive patients, clearance during or after ACT again predicted excellent long-term outcomes, whereas persistence identified patients with poor prognosis who may require alternative strategies. Building on these results, the ongoing DYNAMIC-III trial is assessing ctDNA guidance in stage III CRC, where baseline relapse risk is higher and the balance between escalation and de-escalation may differ.
Neoadjuvant setting
In locally advanced rectal cancer, ctDNA is detectable in ~75% of patients before neoadjuvant chemoradiotherapy [12]. Detection rates typically drop to ~15–20% prior to surgery. Studies consistently show that ctDNA clearance correlates with pathological complete response and reduced recurrence risk [13‐15]. Conversely, persistent ctDNA identifies patients with elevated relapse risk. These data suggest that ctDNA may guide personalized strategies in the future, such as intensifying therapy for persistent ctDNA or supporting nonoperative management (“watch and wait”) in patients achieving ctDNA clearance alongside clinical and radiologic response.
Surveillance
Beyond the perioperative setting, ctDNA is emerging as a valuable tool for long-term surveillance after curative-intent treatment. While conventional follow-up with CEA and imaging often detects relapse only at advanced stages, ctDNA offers a lead time of several months, with positive predictive values exceeding 90%, thereby enabling earlier identification of molecular relapse [16, 17]. However, the critical question of whether ctDNA-based early detection of recurrence also translates into improved survival remains unanswered. This key issue will likely be clarified by several ongoing interventional clinical trials specifically designed to test whether treatment initiation at the stage of molecular recurrence can alter patient outcomes.
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Metastatic CRC applications of ctDNA
While ctDNA in localized CRC often serves as a binary marker of MRD, in metastatic CRC (mCRC) it is best understood as a dynamic monitoring tool that informs therapeutic choices throughout the disease course [18]. Its value lies in enabling identification of actionable targets, monitoring of emerging resistance, and assessment of treatment response in real time. Together, these applications create an iterative framework where ctDNA continuously guides therapy adaptation. A conceptual framework can be envisioned as a circular loop including baseline profiling, early monitoring, serial surveillance, detection of resistance, and therapy adaptation until the next cycle (Fig. 2).
Fig. 2
ctDNA-guided therapy adaptation in metastatic colorectal cancer (mCRC). Schematic of the ctDNA analysis loop for continuous monitoring and treatment adaptation. At baseline, ctDNA profiling identifies actionable tumor mutations (e.g., RAS, BRAF). After systemic therapy initiation (chemotherapy ± targeted agents), early ctDNA testing at 2–4 weeks can distinguish rapid declines (treatment response) from minimal or no decline (potential treatment failure). Ongoing monitoring every 1–3 months enables early detection of rising ctDNA, prompting imaging or therapy adjustments before radiologic progression. ctDNA can also reveal emergent resistance mutations (e.g., RAS/BRAF), guiding therapy adaptation through alternative agents, clinical trials, or anti-EGFR rechallenge if wild-type status re-emerges. The cycle then repeats with new baseline profiling for subsequent therapy lines. Green indicates treatment response (low ctDNA), and red indicates progression risk
Identification of actionable targets and baseline profiling
Management of mCRC typically begins with baseline ctDNA profiling to establish the molecular landscape of the tumor. Key alterations of interest include RAS, BRAF, HER2, and other actionable variants that determine eligibility for targeted therapies such as anti-EGFR antibodies in RAS/BRAF wild-type disease. Unlike tissue biopsy, ctDNA reflects contributions from all metastatic sites, thereby capturing intra-patient heterogeneity that may influence treatment sensitivity [19‐21]. This comprehensive molecular view not only guides initial treatment selection but also provides a reference baseline for subsequent monitoring.
Response monitoring
One of the unique strengths of ctDNA is its ability to provide early efficacy readouts [18]. Quantitative declines within 2–4 weeks of treatment initiation often correlate with radiographic response and prolonged survival [22, 23]. Conversely, a lack of decline may indicate primary resistance, allowing for earlier reassessment of the treatment strategy and minimizing exposure to ineffective therapy. Ongoing monitoring every 1–3 months enables the detection of molecular progression before radiologic confirmation, prompting proactive imaging and timely therapy adjustments. Thus, rising ctDNA levels can act as an early warning signal, offering an opportunity to intervene sooner than traditional modalities.
Identification of actionable targets and resistance
A major strength of ctDNA is its ability to detect emerging resistance mechanisms during therapy. Under selective pressure from targeted agents, resistant clones may expand, often before radiologic progression is apparent. ctDNA can identify alterations such as acquired RAS or EGFR mutations [24‐26], HER2 amplification, or rare but actionable gene fusions. These insights allow clinicians to anticipate therapeutic failure and adjust strategies accordingly. For example, in patients who develop RAS mutations under anti-EGFR therapy, subsequent ctDNA testing can reveal reversion to wild-type status after treatment withdrawal. This enables the use of anti-EGFR rechallenge, a strategy supported by multiple studies showing median PFS of 3–4 months OS of around 10 months [27].
Prognostic assessment
Independent of molecular profiling, resistance monitoring, or dynamic response assessment, absolute ctDNA levels carry prognostic value in mCRC [28]. High baseline ctDNA concentrations are consistently associated with greater tumor burden, more aggressive biology, and worse survival [29, 30]. Importantly, however, there are currently no universally established cut-offs to define “high” or “low” ctDNA, as values vary depending on assay platform, patient characteristics, and disease context. Despite this lack of standardization, across multiple studies, the relationship is consistent: Higher ctDNA levels invariably predict poorer outcomes.
Discussion
The integration of ctDNA into CRC management brings both significant opportunities and notable challenges. One of the major strengths of ctDNA in this disease setting is the relatively high shedding rate of tumor-derived DNA, which makes assays more sensitive in CRC than in many other solid tumors. This facilitates reliable detection even at earlier disease stages. Moreover, ctDNA reflects contributions from all metastatic sites, thereby capturing tumor heterogeneity more comprehensively than a single-site tissue biopsy. The minimally invasive nature of blood sampling further enables serial testing, providing real-time insights into tumor dynamics without the need for repeated invasive procedures. Importantly, ctDNA is versatile: In localized disease, it serves as a marker of MRD, while in metastatic settings it functions as a tool for detecting evolving resistance and guiding therapy adaptation.
Despite these advantages, important challenges remain. Even in CRC, false negatives are possible, particularly in patients with very low-volume disease or in sanctuary sites where DNA shedding is minimal. Standardization is another critical hurdle: Variability in pre-analytical handling, sequencing platforms [31], and data interpretation and reporting [32] limits comparability across studies and complicates the establishment of universal clinical guidelines. Furthermore, while the potential of serial monitoring is clear, the optimal frequency of testing and the precise thresholds that should trigger therapeutic changes have not yet been universally defined. Finally, questions of cost-effectiveness and reimbursement persist, and until robust health-economic data are available, routine clinical adoption may be constrained in many healthcare systems. Taken together, ctDNA in CRC exemplifies both the promise and the complexity of translating liquid biopsy into clinical practice.
Conclusion
Circulating tumor (ctDNA) is a powerful biomarker in colorectal cancer, enabling sensitive detection of minimal residual disease and real-time monitoring of treatment response. Ongoing prospective trials, technological advances, and harmonization efforts will be essential to fully establish ctDNA as a clinical standard, ensuring that its considerable strengths can be realized while its current limitations are systematically addressed.
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Conflict of interest
K. Jonas, S. Andaloro and E. Heitzer declare that they have no competing interests.
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Patelli G, Lazzari L, Crisafulli G, Sartore-Bianchi A, Bardelli A, Siena S, Marsoni S. Clinical utility and future perspectives of liquid biopsy in colorectal cancer. Commun Med (lond). 2025;5:137. https://doi.org/10.1038/s43856-025-00852-4.CrossRefPubMed
3.
Hoang T, Choi MK, Oh JH, Kim J. Utility of circulating tumor DNA to detect minimal residual disease in colorectal cancer: A systematic review and network meta-analysis. Int J Cancer. 2025;157:722–40. https://doi.org/10.1002/ijc.35442.CrossRefPubMed
Mo S, Ye L, Wang D, Han L, Zhou S, Wang H, Dai W, Wang Y, Luo W, Wang R, et al. Early Detection of Molecular Residual Disease and Risk Stratification for Stage I to III Colorectal Cancer via Circulating Tumor DNA Methylation. JAMA Oncol. 2023;9:770–8. https://doi.org/10.1001/jamaoncol.2023.0425.CrossRefPubMedPubMedCentral
8.
Nakamura Y, Watanabe J, Akazawa N, Hirata K, Kataoka K, Yokota M, Kato K, Kotaka M, Kagawa Y, Yeh KH, et al. ctDNA-based molecular residual disease and survival in resectable colorectal cancer. Nat Med. 2024;30:3272–83. https://doi.org/10.1038/s41591-024-03254-6.CrossRefPubMedPubMedCentral
9.
Pellatt AJ, Bent A, Hornstein N, Parseghian C, Huey R, Raghav K, Morris V, Overman M, Morelli P, Willis J, et al. Phase II Trial of TAS-102 in Colorectal Cancer Patients With Circulating Tumor DNA-Defined Minimal Residual Disease After Adjuvant Therapy: INTERCEPT–TT. Jco Precis Oncol. 2025;9:e2500142. https://doi.org/10.1200/PO-25-00142.CrossRefPubMed
10.
Tie J, Cohen JD, Lahouel K, Lo SN, Wang Y, Kosmider S, Wong R, Shapiro J, Lee M, Harris S, et al. Circulating Tumor DNA Analysis Guiding Adjuvant Therapy in Stage II Colon Cancer. N Engl J Med. 2022;386:2261–72. https://doi.org/10.1056/NEJMoa2200075.CrossRefPubMedPubMedCentral
11.
Tie J, Wang Y, Lo SN, Lahouel K, Cohen JD, Wong R, Shapiro JD, Harris SJ, Khattak A, Burge ME, et al. Circulating tumor DNA analysis guiding adjuvant therapy in stage II colon cancer: 5‑year outcomes of the randomized DYNAMIC trial. Nat Med. 2025;31:1509–18. https://doi.org/10.1038/s41591-025-03579-w.CrossRefPubMed
Zhou J, Wang C, Lin G, Xiao Y, Jia W, Xiao G, Liu Q, Wu B, Wu A, Qiu H, et al. Serial Circulating Tumor DNA in Predicting and Monitoring the Effect of Neoadjuvant Chemoradiotherapy in Patients with Rectal Cancer: A Prospective Multicenter Study. Clin Cancer Res. 2021;27:301–10. https://doi.org/10.1158/1078-0432.CCR-20-2299.CrossRefPubMed
14.
Akiyoshi T, Shinozaki E, Maeda Y, Taguchi S, Chino A, Hanaoka Y, Toda S, Matoba S, Tin A, Spickard E, et al. Circulating Tumor DNA Longitudinal Analysis During Total Neoadjuvant Therapy and Non-operative Management for Locally Advanced Rectal Cancer: A Biomarker Study from the NOMINATE Trial. Clin Cancer Res. 2025; https://doi.org/10.1158/1078-0432.CCR-25-1242.CrossRefPubMed
15.
Kim JK, Alden AJ, Knaus S, Thakkar R, Moudgill L, Chudzinski A, Cavallaro P, Martinez C, Bennett RD, Marcet J. Circulating Tumor DNA Detects Minimal Residual Disease in Patients with Locally Advanced Rectal Cancer After Total Neoadjuvant Therapy. Cancers (basel). 2025; https://doi.org/10.3390/cancers17152560.CrossRefPubMedPubMedCentral
16.
Parikh AR, Van Seventer EE, Siravegna G, Hartwig AV, Jaimovich A, He Y, Kanter K, Fish MG, Fosbenner KD, Miao B, et al. Minimal Residual Disease Detection using a Plasma-only Circulating Tumor DNA Assay in Patients with Colorectal Cancer. Clin Cancer Res. 2021;27:5586–94. https://doi.org/10.1158/1078-0432.CCR-21-0410.CrossRefPubMedPubMedCentral
17.
Reinert T, Henriksen TV, Christensen E, Sharma S, Salari R, Sethi H, Knudsen M, Nordentoft I, Wu HT, Tin AS, et al. Analysis of Plasma Cell-Free DNA by Ultradeep Sequencing in Patients With Stages I to III Colorectal Cancer. JAMA Oncol. 2019;5:1124–31. https://doi.org/10.1001/jamaoncol.2019.0528.CrossRefPubMedPubMedCentral
18.
Holz A, Paul B, Zapf A, Pantel K, Joosse SA. Circulating tumor DNA as prognostic marker in patients with metastatic colorectal cancer undergoing systemic therapy: A systematic review and meta-analysis. Cancer Treat Rev. 2025;139:102999. https://doi.org/10.1016/j.ctrv.2025.102999.CrossRefPubMed
19.
Ciardiello D, Boscolo Bielo L, Napolitano S, Martinelli E, Troiani T, Nicastro A, Latiano TP, Parente P, Maiello E, Avallone A, et al. Comprehensive genomic profiling by liquid biopsy captures tumor heterogeneity and identifies cancer vulnerabilities in patients with RAS/BRAF(V600E) wild-type metastatic colorectal cancer in the CAPRI 2‑GOIM trial. Ann Oncol. 2024;35:1105–15. https://doi.org/10.1016/j.annonc.2024.08.2334.CrossRefPubMed
20.
Wang W, Huang Y, Kong J, Lu L, Liao Q, Zhu J, Wang T, Yan L, Dai M, Chen Z, et al. Plasma ctDNA enhances the tissue-based detection of oncodriver mutations in colorectal cancer. Clin Transl Oncol. 2024;26:1976–87. https://doi.org/10.1007/s12094-024-03422-7.CrossRefPubMedPubMedCentral
21.
Nakamura Y, Olsen S, Zhang N, Liao J, Yoshino T. Comprehensive Genomic Profiling of Circulating Tumor DNA in Patients with Previously Treated Metastatic Colorectal Cancer: Analysis of a Real-World Healthcare Claims Database. Curr Oncol. 2022;29:3433–48. https://doi.org/10.3390/curroncol29050277.CrossRefPubMedPubMedCentral
22.
Ahn DH, Barzi A, Ridinger M, Samuelsz E, Subramanian RA, Croucher PJP, Smeal T, Kabbinavar FF, Lenz HJ. Onvansertib in Combination with FOLFIRI and Bevacizumab in Second-Line Treatment of KRAS-Mutant Metastatic Colorectal Cancer: A Phase Ib Clinical Study. Clin Cancer Res. 2024;30:2039–47. https://doi.org/10.1158/1078-0432.CCR-23-3053.CrossRefPubMedPubMedCentral
23.
Moser T, Waldispuehl-Geigl J, Belic J, Weber S, Zhou Q, Hasenleithner SO, Graf R, Terzic JA, Posch F, Sill H, et al. On-treatment measurements of circulating tumor DNA during FOLFOX therapy in patients with colorectal cancer. Npj Precis Oncol. 2020;4:30. https://doi.org/10.1038/s41698-020-00134-3.CrossRefPubMedPubMedCentral
24.
Arena S, Bellosillo B, Siravegna G, Martinez A, Canadas I, Lazzari L, Ferruz N, Russo M, Misale S, Gonzalez I, et al. Emergence of Multiple EGFR Extracellular Mutations during Cetuximab Treatment in Colorectal Cancer. Clin Cancer Res. 2015;21:2157–66. https://doi.org/10.1158/1078-0432.CCR-14-2821.CrossRefPubMed
25.
Misale S, Yaeger R, Hobor S, Scala E, Janakiraman M, Liska D, Valtorta E, Schiavo R, Buscarino M, Siravegna G, et al. Emergence of KRAS mutations and acquired resistance to anti-EGFR therapy in colorectal cancer. Nature. 2012;486:532–6. https://doi.org/10.1038/nature11156.CrossRefPubMedPubMedCentral
26.
Siravegna G, Mussolin B, Buscarino M, Corti G, Cassingena A, Crisafulli G, Ponzetti A, Cremolini C, Amatu A, Lauricella C, et al. Clonal evolution and resistance to EGFR blockade in the blood of colorectal cancer patients. Nat Med. 2015;21:795–801. https://doi.org/10.1038/nm.3870.CrossRefPubMedPubMedCentral
27.
Sartore-Bianchi A, Pietrantonio F, Lonardi S, Mussolin B, Rua F, Crisafulli G, Bartolini A, Fenocchio E, Amatu A, Manca P, et al. Circulating tumor DNA to guide rechallenge with panitumumab in metastatic colorectal cancer: the phase 2 CHRONOS trial. Nat Med. 2022;28:1612–8. https://doi.org/10.1038/s41591-022-01886-0.CrossRefPubMedPubMedCentral
28.
Zhou Q, Chen X, Zeng B, Zhang M, Guo N, Wu S, Zeng H, Sun F. Circulating tumor DNA as a biomarker of prognosis prediction in colorectal cancer: a systematic review and meta-analysis. J Natl Cancer Cent. 2025;5:167–78. https://doi.org/10.1016/j.jncc.2024.05.007.CrossRefPubMed
29.
Unseld M, Belic J, Pierer K, Zhou Q, Moser T, Bauer R, Piringer G, Gerger A, Siebenhuner A, Speicher M, et al. A higher ctDNA fraction decreases survival in regorafenib-treated metastatic colorectal cancer patients. Results from the regorafenib’s liquid biopsy translational biomarker phase II pilot study. Int J Cancer. 2021;148:1452–61. https://doi.org/10.1002/ijc.33303.CrossRefPubMed
30.
Unseld M, Kuhberger S, Graf R, Beichler C, Braun M, Dandachi N, Heitzer E, Prager GW. Circulating tumor DNA (ctDNA) trajectories predict survival in trifluridine/tipiracil-treated metastatic colorectal cancer patients. Mol Oncol. 2025;19:2120–32. https://doi.org/10.1002/1878-0261.13755.CrossRefPubMedPubMedCentral
31.
Lockwood CM, Borsu L, Cankovic M, Earle JSL, Gocke CD, Hameed M, Jordan D, Lopategui JR, Pullambhatla M, Reuther J, et al. Recommendations for Cell-Free DNA Assay Validations: A Joint Consensus Recommendation of the Association for Molecular Pathology and College of American Pathologists. J Mol Diagn. 2023;25:876–97. https://doi.org/10.1016/j.jmoldx.2023.09.004.CrossRefPubMed
32.
de Jager VD, Giacomini P, Fairley JA, Toledo RA, Patton SJ, Joosse SA, Koch C, Deans ZC, c. Group Pantel EWK, et al. Reporting of molecular test results from cell-free DNA analyses: expert consensus recommendations from the 2023 European Liquid Biopsy Society ctDNA Workshop. eBioMedicine. 2025;114:105636. https://doi.org/10.1016/j.ebiom.2025.105636.CrossRefPubMedPubMedCentral
