A5038964119- Bladder and Urothelial Cancer Treatments
- Cancer Immunotherapy and Biomarkers
- Immunotherapy and Immune Responses
- Ferroptosis and cancer prognosis
- Epigenetics and DNA Methylation
- Cancer, Hypoxia, and Metabolism
- Histone Deacetylase Inhibitors Research
- Tryptophan and brain disorders
- Electroconvulsive Therapy Studies
- Esophageal Cancer Research and Treatment
- Urinary Bladder and Prostate Research
- Viral-associated cancers and disorders
- Urinary and Genital Oncology Studies
UNC Lineberger Comprehensive Cancer Center
2016-2019
University of North Carolina at Chapel Hill
2018
Communities In Schools of Orange County
2017
Segeberger Kliniken
2016
We report the discovery of a claudin-low molecular subtype high-grade bladder cancer that shares characteristics with homonymous breast cancer. Claudin-low tumors were enriched for multiple genetic features including increased rates RB1, EP300, and NCOR1 mutations; frequency EGFR amplification; decreased FGFR3, ELF3, KDM6A PPARG amplification. While showed highest expression immune gene signatures, they also demonstrated patterns consistent those observed in active immunosuppression. This...
Abstract Introduction: High-grade, muscle-invasive bladder cancer has recently been shown to harbor intrinsic molecular subtypes with distinct biologic features. Current murine models of cancer, including the prominent carcinogen induced model MB49, do not account for subtype specific characteristics, leaving a gap in available tools understanding differences cancer. We have developed and validated immunocompetent, we used these assess differential responses immune checkpoint inhibition....
<div>Abstract<p>High-grade urothelial cancer contains intrinsic molecular subtypes that exhibit differences in underlying tumor biology and can be divided into luminal-like basal-like subtypes. We describe here the first subtype-specific murine models of bladder show Upk3a-Cre<sup>ERT2</sup>; Trp53<sup>L/L</sup>; Pten<sup>L/L</sup>; Rosa26<sup>LSL-Luc</sup> (UPPL, luminal-like) BBN (basal-like) tumors are more faithful to human than...
<p>Supplemental Figure Legends</p>
<p>Supplemental Figure 1: Inactivation of Pten and Trp53 in Keratin 5 expressing cells does not result bladder cancer. Supplemental 2: Histologic features BBN induced tumors. 3: Generation KT normal urothelial comparison to MB49 3T3 cells. 4: Hierarchical clustering MB49, BBN963, UPPL1541 cell lines line derived 5: IPA Pathways enriched BBN963 versus 6: tumors are more mesenchymal than 7: Immune Gene Signatures correlation between tumor-infiltrating lymphocyte phenotype tumor size. 8:...
<p>Supplemental Figure Legends</p>
<p>Supplemental Figure 1: Inactivation of Pten and Trp53 in Keratin 5 expressing cells does not result bladder cancer. Supplemental 2: Histologic features BBN induced tumors. 3: Generation KT normal urothelial comparison to MB49 3T3 cells. 4: Hierarchical clustering MB49, BBN963, UPPL1541 cell lines line derived 5: IPA Pathways enriched BBN963 versus 6: tumors are more mesenchymal than 7: Immune Gene Signatures correlation between tumor-infiltrating lymphocyte phenotype tumor size. 8:...
<div>Abstract<p>High-grade urothelial cancer contains intrinsic molecular subtypes that exhibit differences in underlying tumor biology and can be divided into luminal-like basal-like subtypes. We describe here the first subtype-specific murine models of bladder show Upk3a-Cre<sup>ERT2</sup>; Trp53<sup>L/L</sup>; Pten<sup>L/L</sup>; Rosa26<sup>LSL-Luc</sup> (UPPL, luminal-like) BBN (basal-like) tumors are more faithful to human than...
You have accessJournal of UrologyBladder Cancer: Basic Research & Pathophysiology IV1 Apr 2017MP88-20 ESTABLISHMENT OF NOVEL MOUSE BLADDER CANCER CELL LINES MIMICKING INTRINSIC SUBTYPE HUMAN INVASIVE RYOICHI SAITO, Christof Smith, Jordan Kardos, Lisa Bixby, Shengjie Chai, Jeffrey Damrauer, Takanobu Utsumi, Sara Wobker, Bhavani Krishnan, Osamu Ogawa, Benjamin Vincent, and William Kim SAITORYOICHI SAITO More articles by this author , SmithChristof Smith KardosJordan Kardos BixbyLisa Bixby...
Abstract Aberrant chromatin remodeling by epigenetic modifier proteins such as histone deacetylases (HDACs) is common within many types of cancer, including muscle-invasive bladder cancer (MIBC). The removal acetyl groups from the lysine residues histones leads to transcriptional silencing that promotes tumor growth and potentially enhances cells' ability evade host immune response. Therefore, HDACs present themselves attractive targets for therapy. Histone deacetylase inhibitors (HDACi)...