Jesse Kreger

The paper shows HDAC1 inhibition in MDSCs increases Malat1, decreases pSTAT3, induces apoptosis and cell cycle arrest, and reduces T cell suppression.

The paper develops mathematical models and Bayesian inference methods to analyze tumor-immune dynamics in metastatic breast cancer, revealing immune suppressive parameters as key predictors of response to immunotherapy.

The paper investigates how myeloid-T cell interactions and B cell activation influence response to checkpoint inhibition in metastatic breast cancer using multi-omics and computational methods.

The paper shows that clonal hematopoiesis later in life is driven by stem cell variation established before birth, using CpG methylation patterns in twins.

This study shows CXCL12 gradients around TMEM doorways promote tumor cell invasion and create immunosuppressive niches by affecting CD8+ T cell function and distribution.

The paper characterizes a novel syngeneic murine breast cancer model (NT2.5-LM) that exhibits rapid and widespread metastases, enabling study of metastatic progression and therapeutic responses.

The paper identifies gene expression changes in Nipbl+/- mouse embryos during gastrulation that link Nipbl-deficiency to birth defects via mesoderm lineage misallocation and Nanog overexpression.

This study develops a mathematical model to analyze MDSC dynamics in metastatic niches, showing that MDSC delays and suppression capabilities significantly impact metastasis outcomes.