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Bio AI Agent: A Multi-Agent Artificial Intelligence System for Autonomous CAR-T Cell Therapy Development with Integrated Target Discovery, Toxicity Prediction, and Rational Molecular Design

By: Yi Ni Β· Liwei Zhu Β· Shuai Li
13 November 2025 at 13:00
arXiv:2511.08649v1 Announce Type: cross Abstract: Chimeric antigen receptor T-cell (CAR-T) therapy represents a paradigm shift in cancer treatment, yet development timelines of 8-12 years and clinical attrition rates exceeding 40-60% highlight critical inefficiencies in target selection, safety assessment, and molecular optimization. We present Bio AI Agent, a multi-agent artificial intelligence system powered by large language models that enables autonomous CAR-T development through collaborative specialized agents. The system comprises six autonomous agents: Target Selection Agent for multi-parametric antigen prioritization across >10,000 cancer-associated targets, Toxicity Prediction Agent for comprehensive safety profiling integrating tissue expression atlases and pharmacovigilance databases, Molecular Design Agent for rational CAR engineering, Patent Intelligence Agent for freedom-to-operate analysis, Clinical Translation Agent for regulatory compliance, and Decision Orchestration Agent for multi-agent coordination. Retrospective validation demonstrated autonomous identification of high-risk targets including FcRH5 (hepatotoxicity) and CD229 (off-tumor toxicity), patent infringement risks for CD38+SLAMF7 combinations, and generation of comprehensive development roadmaps. By enabling parallel processing, specialized reasoning, and autonomous decision-making superior to monolithic AI systems, Bio AI Agent addresses critical gaps in precision oncology development and has potential to accelerate translation of next-generation immunotherapies from discovery to clinic.

Multiple time points for detecting circulating tumor DNA to monitor the response to neoadjuvant therapy in breast cancer: a meta-analysis

23 January 2025 at 19:00

BMC Cancer. 2025 Jan 22;25(1):115. doi: 10.1186/s12885-025-13526-0.

ABSTRACT

BACKGROUND: Not all breast cancer (BC) patients can benefit from neoadjuvant therapy (NAT). A poor response may result in patients missing the best opportunity for treatment, ultimately leading to a poor prognosis. Thus, to identify an effective predictor that can assess and predict patient response at early time points, we focused on circulating tumor DNA (ctDNA), which is a vital noninvasive liquid biopsy biomarker. We performed a meta-analysis to explore the predictive value of response by monitoring ctDNA at four time points of NAT using pathologic complete response (pCR) and residual cancer burden (RCB).

METHODS: By searching Embase, PubMed, the Cochrane Library, and the Web of Science until December 24, 2023, we selected studies concerning the relationship between ctDNA and response or prognosis. We analysed the results at the following various time points: baseline (T0), first cycle of NAT (T1), mid-treatment (MT), and end of NAT (EOT). pCR and RCB were used to evaluate the response as the primary endpoint. The secondary endpoint was to investigate the relationship between ctDNA and prognosis. Odds ratios (ORs) and hazard ratios (HRs) were used as effect indicators.

RESULTS: Thirteen reports from twelve studies were eligible for inclusion in this meta-analysis. The results demonstrated that ctDNA negativity was associated with pCR at T1 (OR = 0.34; 95% CI: 0.21-0.57), MT (OR = 0.35; 95% CI: 0.20-0.60), and EOT (OR = 0.38; 95% CI: 0.22-0.66). When RCB was used to evaluate responses, ctDNA negativity was associated with RCB-0/I at the MT (OR = 0.34; 95% CI: 0.21-0.55) and EOT (OR = 0.26; 95% CI: 0.15-0.46). Furthermore, ctDNA positivity at T1 predicted a worse prognosis for patients (HR = 2.73; 95% CI: 1.29-5.75). We also performed a subgroup analysis to more accurately assess the predictive value of ctDNA for triple-negative breast cancer.

CONCLUSIONS: Our meta-analysis suggested that the ctDNA status at the early stage of NAT can predict patient response, which provides evidence for adjusting personalized treatment strategies and improving patient survival.

PROSPERO REGISTRATION NUMBER: CRD42024496465.

PMID:39844103 | PMC:PMC11752932 | DOI:10.1186/s12885-025-13526-0

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