Jennifer M. Kalish

This study identifies fibroadipogenic progenitor cells as non-cell-autonomous regulators of muscle overgrowth in Beckwith-Wiedemann syndrome.

This study shows that DNMT1 is crucial for human trophoblast stem cell proliferation, differentiation, and DNA methylation, linking its dysfunction to recurrent pregnancy loss.

A machine learning model identifies six key phenotypic features to classify Beckwith-Wiedemann spectrum patients and controls with performance comparable to existing clinical criteria.

This study identifies skeletal muscle hypertrophy as the mechanism behind tongue overgrowth in Beckwith-Wiedemann syndrome, revealing subtype-specific myogenic regulatory programs.

This study uses multiomic analysis to identify WNT pathway enrichment and transition cells in BWS hepatoblastoma, revealing unique tumor heterogeneity and potential targets for intervention.

This study uses single-nucleus multiomic analysis to reveal PPARA signaling enrichment and metabolic dysfunction in BWS liver.

This study identifies molecular subgroups and epigenetic alterations in Beckwith-Wiedemann Syndrome and large offspring syndrome across methylome, transcriptome, and chromatin architecture.

The paper uses allele-specific RNA imaging to show that allelic imbalances in tissues can result from transcriptional bursting and low mRNA abundance.