A5007554036- Pancreatic and Hepatic Oncology Research
- Pancreatic function and diabetes
- Cancer Cells and Metastasis
- Glycosylation and Glycoproteins Research
- Cancer, Hypoxia, and Metabolism
- Epigenetics and DNA Methylation
- Renal and related cancers
- RNA modifications and cancer
- Cancer Research and Treatments
- Cancer Genomics and Diagnostics
- Ubiquitin and proteasome pathways
- Cancer, Lipids, and Metabolism
- Prostate Cancer Treatment and Research
- Peptidase Inhibition and Analysis
- FOXO transcription factor regulation
- Monoclonal and Polyclonal Antibodies Research
- Pluripotent Stem Cells Research
- Cytokine Signaling Pathways and Interactions
- Neuroendocrine Tumor Research Advances
- Glioma Diagnosis and Treatment
- Galectins and Cancer Biology
- Metabolism, Diabetes, and Cancer
- Cancer Mechanisms and Therapy
- Molecular Biology Techniques and Applications
- Hippo pathway signaling and YAP/TAZ
University of Nebraska Medical Center
2016-2024
Nebraska Medical Center
2019-2024
Columbia University
2024
Abstract Background Differential expression of mucins has been associated with several cancers including colorectal cancer (CRC). In normal physiological conditions, secretory mucin MUC5AC is not expressed in the colonic mucosa, whereas its aberrant observed during development colon and precursor lesions. To date, molecular mechanism CRC progression drug resistance remains obscure. Methods was determined tissue microarray by immunohistochemistry. A RNA interference CRISPR/Cas9-mediated...
Glioblastoma (GBM) is an aggressive brain tumor with universal recurrence and poor prognosis. The largely driven by chemoradiation resistant cancer stem cells (CSCs). Epidermal growth factor receptor (EGFR) its mutant EGFRvIII are amplified in ~ 60% 30% of GBM patients, respectively; however, therapies targeting EGFR have failed to improve disease outcome. EGFRvIII-mediated cross-activation tyrosine kinase receptor, cMET, regulates CSC maintenance promote recurrence. Here, we evaluated the...
Purpose: MUC16, a tumor biomarker and cell surface-associated mucin, is overexpressed in various cancers; however, its role lung cancer pathogenesis unknown. Here, we have explored the mechanistic of MUC16 cancer.Experimental Design: To identify functional stable knockdown was carried cells with two different shRNAs. Clinical significance evaluated patient tissues using IHC. We generated genetically engineered mouse model (KrasG12D; AdCre) to evaluate preclinical MUC16.Results: (P = 0.03) as...
Abstract Background Several reports have shown the role of glycosylation in pancreatic cancer (PC), but a global systematic screening specific glycosyltransferases (glycoTs) its progression remains unknown. Methods We demonstrate rigorous top-down approach using TCGA-based RNA-Seq analysis, multi-step validation RT-qPCR, immunoblots and immunohistochemistry. identified six unique glycoTs (B3GNT3, B4GALNT3, FUT3, FUT6, GCNT3 MGAT3) PC pathogenesis studied their function CRISPR/Cas9-based KD...
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal types cancer, as it commonly metastasizes to liver resulting in an overall poor prognosis. However, molecular mechanism involved metastasis remains poorly understood. Here, we aimed identify MUC16-mediated PDAC-liver metastasis. Previous studies demonstrated that MUC16 and its C-terminal (Cter) domain are aggressiveness PDAC. In this study, observed Cter expression significantly high human PDAC tissues, organoids, metastatic...
MUC16/CA125 is one of the few oldest cancer biomarkers still used in current clinical practice. As mesothelium an abundant source MUC16 and a major contributor to stromal heterogeneity PDAC, we investigated regulation tumor compartments individually. The trajectories constructed using single-cell transcriptomes cells from KPC tumors demonstrated continuity trajectory path between MUC16-expressing mesothelial other CAF subsets. Further, tissues whole-body knockout (KPCM) showed dysregulation...
Cisplatin- and gemcitabine-based chemotherapeutics represent a mainstay of cancer therapy for most solid tumors; however, resistance limits their curative potential. Here, we identify RNA polymerase II-associated factor 1 (PAF1) as common driver cisplatin gemcitabine in human cancers (ovarian, lung, pancreas). Mechanistically, cisplatin- gemcitabine-resistant cells show enhanced DNA repair, which is inhibited by PAF1 silencing. We demonstrate an increased interaction with RAD52 resistant...