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Modality-Decoupled Federated Learning for Privacy-Preserving Embodied Intelligence in 6G

arXiv:2609.09591v1 Announce Type: cross Abstract: Sixth-generation (6G) wireless networks are expected to provide a key infrastructure for large-scale embodied intelligence, where heterogeneous robots collaborate through low-latency connectivity, edge intelligence, and distributed sensing. Vision-language-action (VLA) models offer a foundation by integrating visual perception, language understanding, and action generation into a unified closed-loop policy. However, training and adapting VLA models to distributed robotic agents introduce challenges in privacy protection, communication efficiency, and model heterogeneity. Existing federated learning (FL) methods overlook the intrinsic differences among vision, language, and action pathways in parameter scale, privacy exposure, update dynamics, and tolerance to compression or perturbation. To address this issue, this article proposes FedMVLA, a modality-decoupled FL framework for privacy-preserving embodied intelligence in 6G networks. FedMVLA incorporates three mechanisms: modality-aware federated aggregation (MAFA), modality-aware privacy allocation (MAPA), and modality-aware communication compression (MACO), together with a modality-sliced transport design that routes the precision-critical action stream through a protected ultra-reliable low-latency slice. A case study on federated robotic manipulation over the Third Generation Partnership Project (3GPP)-based wireless substrate, covering fading, co-channel interference, and malicious jamming, shows that FedMVLA achieves an 84.8% task success rate, exceeds FedAvg by 22.2 percentage points, sustains a widening margin when scaling to 128 clients across eight cells, and reduces the schedule-averaged per-client uplink model-update payload by 95.6% (approximately 96%), while keeping the 95th percentile (p95) of the round-critical uplink completion time near 1.5s.

Circulating Tumor DNA in Cholangiocarcinoma: A Precision Oncology Roadmap

26 March 2026 at 18:00

Cancer Manag Res. 2026 Feb 6;18:574678. doi: 10.2147/CMAR.S574678. eCollection 2026.

ABSTRACT

Cholangiocarcinoma (CCA) is a rare but aggressive malignancy with a rising global incidence and few therapeutic options for advanced disease. In recent decades, precision oncology for CCA has advanced rapidly, particularly through the development of targeted therapies for patients with actionable genetic alterations. These therapies have markedly prolonged survival and improved other clinical outcomes among patients with unresectable, advanced CCA. The implementation of precision oncology largely depends on detecting genetic mutations to guide patient selection and treatment, using tumor tissue biopsies or liquid biopsies, including circulating tumor DNA (ctDNA) from blood or bile. As a minimally invasive biomarker, ctDNA shows great promise for transforming the clinical management of CCA. This review provides a comprehensive overview of the roles of ctDNA in CCA, including early detection, prognostic stratification, minimal residual disease assessment, recurrence monitoring, therapeutic target identification, and treatment response evaluation. A synthesis of existing studies indicates that bile-derived ctDNA shows superior sensitivity compared with blood-based ctDNA in capturing the genetic profiles and heterogeneity of CCA. We also propose an integrative framework that illustrates how ctDNA profiling can inform diagnosis, treatment, and surveillance across the disease continuum. Because research on ctDNA in CCA remains in its infancy, we discuss current challenges and outline future directions for translating these findings into clinical practice. Collectively, the evidence positions ctDNA-particularly bile-derived ctDNA-as a dynamic tool for real-time genomic profiling, sensitive residual disease detection, and therapy monitoring. This integrative framework provides a roadmap for translating these capabilities into clinical practice, with the potential to enable earlier, more personalized interventions and improve outcomes for patients with CCA.

PMID:41883993 | PMC:PMC13012645 | DOI:10.2147/CMAR.S574678

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