H. Levine

This paper develops a computational-experimental framework to explain the spatial heterogeneity of cancer stem cells in the tumor microenvironment, showing that Notch-JAG1 signaling and inflammatory cytokines drive CSC distribution and stemness.

The paper investigates CD8+ T cell infiltration into tumor-cell clusters in TNBC, proposing a chemo-repellent mechanism and ruling out collagen fiber restrictions.

This study presents a mechanical model of cell migration that reproduces durotaxis and contact guidance by simulating cell-substrate interactions through focal adhesions.

The paper develops a computational model to explore the interactions between EMT, CSCs, and Notch-Jagged signaling, revealing how hybrid E/M cells with stemness traits and enhanced Notch-Jagged signaling contribute to therapeutic resistance.

This study uses molecular dynamics simulations to investigate how phosphorylation of PAGE4 affects its structure and interactions with AP-1 and AR, revealing conformational switching linked to prostate cancer progression.

The paper develops a model to study how mechanical properties of transcription affect gene expression and DNA structure in multi-gene systems.

The paper identifies interconnected feedback loops among ESRP1, HAS2, and CD44 that regulate ZEB1 levels and drive epithelial-hybrid-mesenchymal transition in cancer, with ESRP1 as a key regulatory node.

This study identifies modularity in metabolic gene expression as a prognostic biomarker for hepatocellular carcinoma, correlating higher modularity with worse patient outcomes.

This study uses hierarchical organization metrics to show that gene expression networks in IBC are more organized and linked to worse outcomes and epithelial traits in metastatic breast cancer.

This study shows Numb stabilizes a hybrid E/M phenotype by inhibiting Notch-driven full EMT, correlates with poor cancer survival, and predicts its role in tumor-initiation.

This study investigates the mechanism behind long-range alignment of fibroblasts, showing that local interactions are insufficient and proposing a non-local interaction involving the extracellular matrix.

This paper examines the role of EMT and MET in metastasis, arguing that these processes are not binary and proposes alternative mechanisms beyond the traditional EMT-MET model.

This paper reviews how quantitative mathematical models have advanced understanding of epithelial-mesenchymal plasticity in tumors by explaining data, guiding experiments, and improving conceptual frameworks.

This review discusses molecular mechanisms enabling CTC clusters formation and their higher metastatic potential, using Inflammatory Breast Cancer as an example.

The paper uses experimental and theoretical approaches to evaluate two models of EMT dynamics, finding experimental evidence supporting the ternary chimera switch model over the cascading bistable switches model.