Jonathan Robert Brody

This study identifies impaired adipose anabolism in pancreatic cancer cachexia and shows that HuR inhibition restores adipose anabolism in mice.

The paper identifies global 3'UTR lengthening in SCNC through APA and develops a neural network model to classify SCNC using APA signatures.

The paper identifies resistance mechanisms to KRAS-MEK pathway targeting in PDAC by analyzing clinical trial data and multi-omics profiles, showing that KRAS/MYC co-gain correlates with resistance and that co-targeting these genes is synergistic.

This paper introduces a dual-contrast microCT protocol to track tumor growth, metastasis, and cachexia in murine PDAC models over time.

This study shows that HuR promotes immune evasion in PDAC by inhibiting T cell infiltration and function, suggesting HuR as a therapeutic target with immunotherapy.

This study develops a novel pancreatic cancer mouse model by expressing Myc and mutant Kras in adult acinar cells, showing metastasis and therapeutic resistance similar to human PDAc.

This study shows PIN1 promotes cellular plasticity and immune changes in chronic pancreatitis, with genetic or pharmacological inhibition reducing disease severity.

This study shows that HuR in pancreatic cancer cells enhances angiogenesis by modulating extracellular vesicle signaling to endothelial cells, increasing their migratory and tube-forming abilities while reducing ICAM-1 expression.