Publications by authors named "F E Sharkey"
Background: The incidence and mortality rates of hepatocellular carcinoma among Hispanic individuals in the United States are much higher than in non-Hispanic White people. We conducted multi-omics analyses to elucidate molecular alterations in hepatocellular carcinoma among Hispanic patients.
Methods: Paired tumor and adjacent nontumor samples were collected from 31 Hispanic hepatocellular carcinomas in South Texas for genomic, transcriptomic, proteomic, and metabolomic profiling.
Article Synopsis
- - The study investigates the heightened rates of hepatocellular carcinoma (HCC) among Hispanics in the U.S. by analyzing tumor and adjacent non-tumor samples from Hispanic patients in South Texas through comprehensive multi-omics approaches.
- - Key findings include high mutation frequencies related to the Wnt/β-catenin pathway and the identification of HCC subtypes, where one subtype showed better survival rates associated with immune activity and lower liver function-related gene activity.
- - The research aims to provide insights into specific molecular features and potential biomarkers for HCC among Hispanic patients, laying groundwork for improved therapeutic strategies.
Animal studies have demonstrated the ability of pancreatic acinar cells to transform into pancreatic ductal adenocarcinoma (PDAC). However, the tumorigenic potential of human pancreatic acinar cells remains under debate. To address this gap in knowledge, we expand sorted human acinar cells as 3D organoids and genetically modify them through introduction of common PDAC mutations.
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- The Hippo pathway is increasingly linked to fibroinflammatory diseases, leading researchers to investigate its components by creating knockout mice targeting YAP1 and TAZ to study pancreatic inflammation.
- Mice lacking YAP1 and TAZ showed no major issues, while those lacking LATS1/2 did experience pathological changes, which were reversed by knocking out YAP1 but not TAZ.
- The YAP1/TAZ inhibitor VT-104 was effective in reducing inflammation-related changes, suggesting its potential as a treatment for pancreatitis, although further research is needed to fully understand the mechanisms involved.
Article Synopsis
- ITGA6 is upregulated in hepatocellular carcinoma (HCC) tissues, with its expression linked to worse patient survival.
- Knocking down ITGA6 inhibits HCC cell growth and migration in vitro and slows tumor growth in vivo, suggesting it promotes cancer progression.
- ITGA6 interacts specifically with ITGB4 and regulates its expression, making the α6β4 integrin complex a potential target for HCC therapy.