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Unmasking FCGR2B as a high-grade serous ovarian cancer specific marker of immune suppression and tumor progression through multi-omics mining

Transl Oncol. 2026 Apr 3;67:102748. doi: 10.1016/j.tranon.2026.102748. Online ahead of print.

ABSTRACT

BACKGROUND: Epithelial ovarian cancer (EOC) encompasses five major histological subtypes with marked genetic, immunological, and clinical heterogeneity. While genome-wide association studies (GWAS) have identified subtype-specific risk loci, a critical gap remains in understanding how plasma proteins influence immune-cell traits and contribute to EOC pathogenesis.

METHODS: We integrated subtype-stratified GWAS data from two EOC cohorts with plasma proteomics and immune-cell traits to construct protein-immune-EOC regulatory landscapes using a three-stage Mendelian randomization framework. Single-cell RNA-seq and multiplex immunofluorescence were employed to delineate the cellular distribution and spatial context of causal proteins. Subsequent analyses characterized immune infiltration, macrophage polarization, and clinicopathological associations. Drug-gene correlations were used to identify potential therapeutic targets, and transcriptomic analyses were applied to delineate the underlying transcriptional landscape.

RESULTS: We identified 20 subtype-specific protein-immune-EOC regulatory axes, with FCGR2B emerging as a causal plasma protein in immune regulation and high-grade serous ovarian cancer (HGSOC) progression. FCGR2B was highly expressed in tumor-associated macrophages and was associated with an M2-like polarization phenotype. Functional characterization revealed that FCGR2B was associated with shorter progression-free survival and an immunosuppressive tumor microenvironment. Transcriptomic analyses revealed altered NF-ΞΊB signaling upon FCGR2B knockdown, and drug-response data suggested a potential association between high FCGR2B expression and sensitivity to NF-ΞΊB inhibitors.

CONCLUSIONS: These findings delineate subtype-specific genetically informed protein-immune regulatory landscapes in EOC and identify FCGR2B as a key immunoregulatory and prognostic biomarker in HGSOC, suggesting FCGR2B as a potential therapeutic vulnerability that warrants further investigation.

PMID:41934917 | DOI:10.1016/j.tranon.2026.102748

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Memory Bear AI Memory Science Engine for Multimodal Affective Intelligence: A Technical Report

arXiv:2603.22306v1 Announce Type: new Abstract: Affective judgment in real interaction is rarely a purely local prediction problem. Emotional meaning often depends on prior trajectory, accumulated context, and multimodal evidence that may be weak, noisy, or incomplete at the current moment. Although multimodal emotion recognition (MER) has improved the integration of text, speech, and visual signals, many existing systems remain optimized for short-range inference and provide limited support for persistent affective memory, long-horizon dependency modeling, and robust interpretation under imperfect input. This technical report presents the Memory Bear AI Memory Science Engine, a memory-centered framework for multimodal affective intelligence. Instead of treating emotion as a transient output label, the framework models affective information as a structured and evolving variable within a memory system. It organizes processing through structured memory formation, working-memory aggregation, long-term consolidation, memory-driven retrieval, dynamic fusion calibration, and continuous memory updating. At its core, multimodal signals are transformed into structured Emotion Memory Units (EMUs), enabling affective information to be preserved, reactivated, and revised across interaction horizons. Experimental results show consistent gains over comparison systems across benchmark and business-grounded settings, with stronger accuracy and robustness, especially under noisy or missing-modality conditions. The framework offers a practical step from local emotion recognition toward more continuous, robust, and deployment-relevant affective intelligence.
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