Jennifer P. Morton

TiSAM improves whole-slide image segmentation by fusing spatial and histopathology features, achieving high accuracy across diverse datasets and scanners.

This paper develops a 2D hydrogel platform to study how mechanical and biochemical cues influence acinar-to-ductal metaplasia in pancreatic cells.

The paper compares primary and liver PDAC lesions using single-cell transcriptomics to identify MET as a target in pancreatic cancer metastasis.

This study shows that arginine depletion induces senescence and stress response in pancreatic cancer cells, making them susceptible to senolysis and stress response inhibition.

This paper shows that pulsed narmafotinib priming improves chemotherapy response in pancreatic cancer by reducing fibrosis and enhancing treatment efficacy.

This study shows that viscosity, not just elasticity, drives EMT in pancreatic intraepithelial neoplasia using hydrogel models.

This study shows that proteostatic failure in ER-phagy, driven by Kras, leads to protein aggregates that prime acinar-ductal metaplasia and pancreatic cancer.

This study shows that genetic mutations in PDAC affect blood biomarker profiles, suggesting genotype-specific biomarkers are needed for early detection.

This paper shows that ROCK2 inhibition reduces ECM remodelling and cell growth while impairing migration and invasion in breast cancer models.

This study shows that activating PP2A-B56 in PDAC increases EGFR signaling and promotes tumor growth, suggesting a new therapeutic target.

This study identifies PIKfyve as a targetable vulnerability in pancreatic cancer by showing its role in lipid metabolism and synthetic lethality with KRAS-MAPK inhibitors.

This study shows that oncogenic KRAS cells in the adult pancreas evade elimination by using Wnt signaling and cell dormancy.

This study shows that loss of wild-type Kras enhances oncogenic Kras signaling and promotes pancreatic ductal adenocarcinoma, while also increasing sensitivity to MEK1/2 inhibitors.

The paper shows that ionizing radiation enhances immunotherapy in pancreatic cancer by increasing tissue-resident NK cells that support CD8 T cell activity through cDC1-dependent mechanisms.

This study shows that wild-type KRAS suppresses tumour growth and metastasis in KRAS mutant colorectal cancer while enhancing resistance to MEK inhibition.