David J. Odde

The paper develops CAMPs, genetically inducible receptors to control cytokine signaling in T cells, to study motility and signaling pathways without paracrine interference.

This study identifies two migratory phenotypes in glioblastoma cells ex vivo, linking them to clinical recurrence and tumor heterogeneity.

This study models CISH-KO TIL therapy in gastrointestinal cancer, finding that T-cell persistence and endogenous competition are key determinants of treatment response.

This study shows that cell migration direction (durotaxis) can be reversed by culturing cells in soft 3D environments, revealing it is influenced by culture conditions rather than being intrinsic.

The paper develops a mechanistic model to predict the efficacy of CISH knockout in TILs and identifies synergistic gene targets to enhance T cell activation.

This study physically optimizes T cells to enhance their ability to sample and engage with pancreatic ductal adenocarcinoma tumor cells, improving therapeutic outcomes.

This study identifies that T cells achieve maximal migration speeds by combining bleb formation with adhesion-based forces, challenging the feasibility of adhesion-free migration.

This study develops an algorithm to analyze T cell migration dynamics using clustering and Hidden Markov Models, finding CD8+ T cells exhibit two distinct migration states in melanoma tumors.

This study identifies UNC-45A as an ATP-independent microtubule severing protein that inhibits repair of defects, leading to microtubule loss and neurite dystrophy in Alzheimer's disease.

The paper investigates how a multi-budding yeast partitions growth equally among its buds, revealing that actin cable networks enable even partitioning without compensatory mechanisms.

This study identifies a motor-clutch mechanism for glioblastoma cell migration in brain tissue, highlighting the roles of integrins, CD44, and myosin motors.

This paper shows UNC-45A increases microtubule curvature and counteracts Taxol's straightening effects, suggesting a role in drug resistance.

The paper identifies a molecular clock mechanism that regulates cell migration in confined spaces through cyclic RhoA activity driven by Ca2+ and GEF-H1 oscillations.

The paper uses a biophysical model of the SARS-CoV-2 viral cycle to identify antiviral targets by analyzing parameter sensitivity and pairwise interactions.