A5038274192- Pancreatic and Hepatic Oncology Research
- Peptidase Inhibition and Analysis
- Protease and Inhibitor Mechanisms
- Cancer Research and Treatments
- interferon and immune responses
- RNA modifications and cancer
- Biochemical and Molecular Research
- Cancer Genomics and Diagnostics
- RNA Research and Splicing
- Chronic Lymphocytic Leukemia Research
- Cancer Cells and Metastasis
- Acute Lymphoblastic Leukemia research
- Cytokine Signaling Pathways and Interactions
- Genomics and Chromatin Dynamics
- Angiogenesis and VEGF in Cancer
- Advanced Breast Cancer Therapies
- Cancer, Hypoxia, and Metabolism
- Protein Degradation and Inhibitors
- Immune cells in cancer
- RNA regulation and disease
- Epigenetics and DNA Methylation
- Bladder and Urothelial Cancer Treatments
- Phagocytosis and Immune Regulation
- Nanoplatforms for cancer theranostics
- Microtubule and mitosis dynamics
Roswell Park Comprehensive Cancer Center
2013-2025
Cancer Genetics (United States)
2013-2015
Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease that lacks effective treatment options, highlighting the need for developing new therapeutic interventions. Here, we assessed response to pharmacologic inhibition of KRAS, central oncogenic driver PDAC. In a panel PDAC cell lines, KRASG12D with MRTX1133 yielded variable efficacy in suppressing growth and downstream gene expression programs 2D cultures. On basis CRISPR-Cas9 loss-of-function screens, ITGB1 was identified...
Cellular responses to the loss of genomic stability are well-established, while how mammalian cells respond chromatin destabilization is largely unknown. We previously found that DNA demethylation on p53-deficient background leads transcription repetitive heterochromatin elements, followed by an interferon response, a phenomenon we named TRAIN (Transcription Repeats Activates INterferon). Here, report curaxin, anticancer small molecule, destabilizing nucleosomes via disruption histone/DNA...
Abstract Cyclin dependent kinase 2 (CDK2) regulates cell cycle and is an emerging target for cancer therapy. There are relatively small numbers of tumor models that exhibit strong dependence on CDK2 undergo G1 arrest following inhibition. The expression P16INK4A cyclin E1 determines this sensitivity to co-expression these genes occurs in breast patients highlighting their clinical significance as predictive biomarkers CDK2-targeted therapies. In genetically independent CDK2, pharmacological...
Genetic and epigenetic alterations have been identified as to contribute directly or indirectly the generation of transitional cell carcinoma urinary bladder (TCC-UB).We previously found that amplification chromosome 6p22 is significantly associated with muscle-invasive rather than superficial TCC-UB.Here, we demonstrated Sox4, one candidate oncogenes located within amplicon, confers cancer stem (CSC) properties.Down-regulation Sox4 led inhibition migration, colony formation well...
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease for which new therapeutic interventions are needed. Here we assessed the cellular response to pharmacological KRAS inhibition, target central oncogenic factor in PDAC. In a panel of PDAC cell lines, pharmaceutical inhibition G12D allele, with MRTX1133 yields variable efficacy suppression growth and downstream gene expression programs 2D culture. CRISPR screens identify drivers enhanced that regulate focal adhesion signaling...
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<p>Transcriptome data</p>
<p>Supplementary information</p>
<p>Transcriptome data</p>
<div>Abstract<p>Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease that lacks effective treatment options, highlighting the need for developing new therapeutic interventions. Here, we assessed response to pharmacologic inhibition of KRAS, central oncogenic driver PDAC. In a panel PDAC cell lines, KRAS<sup>G12D</sup> with MRTX1133 yielded variable efficacy in suppressing growth and downstream gene expression programs 2D cultures. On basis CRISPR-Cas9...
<div>Abstract<p>Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease that lacks effective treatment options, highlighting the need for developing new therapeutic interventions. Here, we assessed response to pharmacologic inhibition of KRAS, central oncogenic driver PDAC. In a panel PDAC cell lines, KRAS<sup>G12D</sup> with MRTX1133 yielded variable efficacy in suppressing growth and downstream gene expression programs 2D cultures. On basis CRISPR-Cas9...
Abstract The anticancer activity of genotoxic agents has been intensively studied, while the mechanisms action drugs destabilizing epigenome are far less understood. We previously found that DNA hypomethylation in absence p53 leads to transcriptional desilencing repetitive elements, such as pericentromeric repeats and endogenous retroelements, which is associated with an interferon type I response, a phenomenon we named TRAIN ( T ranscription R epeats A ctivates IN terferon). Here, report...