Christopher J. Tape

GeoSinkhorn Flow converts static phenoscapes into dynamic ones by learning perturbation-conditioned transport trajectories that respect the phenoscape's geometry and generalize to unseen conditions.

This study identifies that epithelial stem cell fate, not DNA damage, determines chemoradiotherapy response in rectal cancer by analyzing patient-derived organoids and using SPARTA to validate findings.

This study identifies stromal prostaglandin E2 as a key regulator of cell-fate plasticity in colorectal cancer, showing it converts chemosensitive stem cells into chemorefractory, prometastatic cells.

This study maps the NFκB pathway in T-cells using CRISPR screens and identifies novel regulators that enhance cytotoxicity and cytokine production.

The paper develops multi-regional gastric assembloids from patient-derived organoids to model parietal cell maturation and antral foveolar hyperplasia in genetic disorders.

ProMPt is a syngeneic mouse platform modeling prostate cancer heterogeneity, revealing MYC's role in progression and showing that MAPK inhibition plus translation blockade synergistically suppresses castration-resistant tumors.

The paper identifies a post-transcriptional regulatory checkpoint, ZFP36/ZFP36L1, that controls CD4+ T cell cytotoxicity and response to immunotherapy.

The paper shows that T-cell activation is initiated by partial CD45 exclusion at sub-micron contacts, leading to strong activation and cytotoxicity through small signaling changes.

SIGNAL-seq measures RNA and PTMs in single cells to analyze inter- and intra-cellular signaling in the tumor microenvironment.

The paper uses single-cell analyses to show that oncogenic PIK3CAH1047R reduces IGF1 signaling specificity and enhances EGF responses, leading to increased phenotypic heterogeneity.