❌

Reading view

Contextual Control without Memory Growth in a Context-Switching Task

arXiv:2604.03479v1 Announce Type: new Abstract: Context-dependent sequential decision making is commonly addressed either by providing context explicitly as an input or by increasing recurrent memory so that contextual information can be represented internally. We study a third alternative: realizing contextual dependence by intervening on a shared recurrent latent state, without enlarging recurrent dimensionality. To this end, we introduce an intervention-based recurrent architecture in which a recurrent core first constructs a shared pre-intervention latent state, and context then acts through an additive, context-indexed operator. We evaluate this idea on a context-switching sequential decision task under partial observability. We compare three model families: a label-assisted baseline with direct context access, a memory baseline with enlarged recurrent state, and the proposed intervention model, which uses no direct context input to the recurrent core and no memory growth. On the main benchmark, the intervention model performs strongly without additional recurrent dimensions. We also evaluate the models using the conditional mutual information (I(C;O | S)) as a theorem-motivated operational probe of contextual dependence at fixed latent state. For task-relevant phase-1 outcomes, the intervention model exhibits positive conditional contextual information. Together, these results suggest that intervention on a shared recurrent state provides a viable alternative to recurrent memory growth for contextual control in this setting.
  •  

Molecular and Phenotypic Characterization of Fluid-Derived Patient-Derived Cell and Organoid Models in Advanced Gastric Cancer

J Gastric Cancer. 2026 Apr;26(2):260-278. doi: 10.5230/jgc.2026.26.e19.

ABSTRACT

PURPOSE: Patient-derived cells (PDCs) and patient-derived organoids (PDOs) are complementary preclinical models widely used in translational cancer research. However, their molecular and functional differences have not been systematically characterized. This study established and analyzed paired PDC and PDO models derived from the same gastric cancer ascites to delineate platform-dependent molecular and functional profiles.

MATERIALS AND METHODS: Malignant ascites or pleural fluid obtained from 6 patients with advanced gastric cancer were used to establish paired PDC and PDO models. All pairs underwent comprehensive multi-omics profiling, integrating genomic, transcriptomic, and proteomic data. Phenotypic characterization included morphological, histological, proliferative, and cell cycle analyses. Drug sensitivity assays were performed using 4 chemotherapeutic agents commonly used to treat gastric cancer.

RESULTS: The 6 paired PDC and PDO models exhibited distinct morphological characteristics. Whole-genome analyses demonstrated high concordance among primary tumors, PDCs, and PDOs, confirming tumor representation across platforms. Multi-omics profiling identified platform-dependent molecular signatures; PDOs were enriched for extracellular matrix remodeling and stemness, whereas PDCs displayed proliferation- and immune-related signatures. Clinically relevant biomarkers, including HER2 and MET alterations, were concordant with primary tumors. Notably, drug responses differed between platforms and patients, indicating platform-dependent and patient-specific chemosensitivity.

CONCLUSIONS: Paired PDC and PDO models derived from the same patients preserved core patient-specific tumor characteristics while exhibiting distinct molecular and functional profiles. These findings underscore the culture platform as a critical determinant of experimental outcomes and therapeutic responses. Therefore, careful selection of an appropriate preclinical model is essential to accurately address biological questions and optimize precision oncology strategies.

PMID:41942359 | DOI:10.5230/jgc.2026.26.e19

  •  

Molecular and Phenotypic Characterization of Fluid-Derived Patient-Derived Cell and Organoid Models in Advanced Gastric Cancer

J Gastric Cancer. 2026 Apr;26(2):260-278. doi: 10.5230/jgc.2026.26.e19.

ABSTRACT

PURPOSE: Patient-derived cells (PDCs) and patient-derived organoids (PDOs) are complementary preclinical models widely used in translational cancer research. However, their molecular and functional differences have not been systematically characterized. This study established and analyzed paired PDC and PDO models derived from the same gastric cancer ascites to delineate platform-dependent molecular and functional profiles.

MATERIALS AND METHODS: Malignant ascites or pleural fluid obtained from 6 patients with advanced gastric cancer were used to establish paired PDC and PDO models. All pairs underwent comprehensive multi-omics profiling, integrating genomic, transcriptomic, and proteomic data. Phenotypic characterization included morphological, histological, proliferative, and cell cycle analyses. Drug sensitivity assays were performed using 4 chemotherapeutic agents commonly used to treat gastric cancer.

RESULTS: The 6 paired PDC and PDO models exhibited distinct morphological characteristics. Whole-genome analyses demonstrated high concordance among primary tumors, PDCs, and PDOs, confirming tumor representation across platforms. Multi-omics profiling identified platform-dependent molecular signatures; PDOs were enriched for extracellular matrix remodeling and stemness, whereas PDCs displayed proliferation- and immune-related signatures. Clinically relevant biomarkers, including HER2 and MET alterations, were concordant with primary tumors. Notably, drug responses differed between platforms and patients, indicating platform-dependent and patient-specific chemosensitivity.

CONCLUSIONS: Paired PDC and PDO models derived from the same patients preserved core patient-specific tumor characteristics while exhibiting distinct molecular and functional profiles. These findings underscore the culture platform as a critical determinant of experimental outcomes and therapeutic responses. Therefore, careful selection of an appropriate preclinical model is essential to accurately address biological questions and optimize precision oncology strategies.

PMID:41942359 | PMC:PMC13053824 | DOI:10.5230/jgc.2026.26.e19

  •  
❌