A5028553990- Retinal Development and Disorders
- Ocular Oncology and Treatments
- Ubiquitin and proteasome pathways
- Melanoma and MAPK Pathways
- Cancer Genomics and Diagnostics
- Protein Degradation and Inhibitors
- Monoclonal and Polyclonal Antibodies Research
- Cell Adhesion Molecules Research
- Microtubule and mitosis dynamics
- Prostate Cancer Treatment and Research
- Receptor Mechanisms and Signaling
- Protein Kinase Regulation and GTPase Signaling
- Cutaneous Melanoma Detection and Management
- Genomics and Chromatin Dynamics
- Mechanisms of cancer metastasis
- Cancer Mechanisms and Therapy
- Chronic Myeloid Leukemia Treatments
- Click Chemistry and Applications
- Prostate Cancer Diagnosis and Treatment
- Brucella: diagnosis, epidemiology, treatment
- Cancer Cells and Metastasis
- RNA Research and Splicing
- Colorectal Cancer Treatments and Studies
- Salmonella and Campylobacter epidemiology
- Prion Diseases and Protein Misfolding
Memorial Sloan Kettering Cancer Center
2016-2023
Cornell University
2016-2023
Kettering University
2020
University of Newcastle Australia
1985
Uveal melanoma (UM) is characterized by mutually exclusive activating mutations in GNAQ, GNA11, CYSLTR2, and PLCB4, four genes a linear pathway to activation of PLCβ almost all tumors loss BAP1 the aggressive subset. We generated mice with melanocyte-specific expression GNA11Q209L without homozygous Bap1 loss. The recapitulated human Gq-associated melanomas, they developed pigmented neoplastic lesions from melanocytes skin non-cutaneous organs, including eye leptomeninges, as well at...
Uveal melanoma is the most common eye cancer in adults and clinically genetically distinct from skin cutaneous melanoma. In a subset of cases, oncogenic driver an activating mutation CYSLTR2, gene encoding G protein-coupled receptor cysteinyl-leukotriene 2 (CysLTR2). The mutant CYSLTR2 encodes for CysLTR2-L129Q receptor, with substitution Leu to Gln at position 129 (3.43). ability cause malignant transformation has been hypothesized result constitutive activity, but how could escape...
The mechanisms underlying
Fusion between TMPRSS2 and ERG, placing ERG under the control of promoter, is most frequent genetic alteration in prostate cancer, present 40–50% cases. The fusion event an early, if not initiating, implicating TMPRSS2-positive epithelial cell as cancer origin fusion-positive cancer. To introduce alterations into Tmprss2-positive cells mice a temporal-specific manner, we generated Tmprss2-CreERT2 knock-in mouse. We found robust tamoxifen-dependent Cre activation luminal but basal cells, well...
Abstract The G protein-coupled receptor (GPCR) cysteinyl-leukotriene 2 (CysLTR2) with a single amino acid mutation at position 3.43 (Leu replaced Gln 129 in transmembrane helix 3) causes uveal melanoma humans. ability of CysLTR2-L129Q to cause malignant transformation has been hypothesized result from constitutive activity. We show that is constitutively active mutant (CAM) strongly drives Gq/11 signaling pathways melan-a melanocytes and HEK293T cells culture. However, the only very weakly...
<p>raw uncropped labeled western blots</p>
<p>Supplementary figures S1-S6 with figure legends.</p>
<div>AbstractPurpose:<p>All uveal melanoma and a fraction of other subtypes are driven by activation the G-protein alpha-q (Gα<sub>q</sub>) pathway. Targeting these melanomas has proven difficult despite advances in molecular understanding key driver signaling pathways disease pathogenesis. Inhibitors Gα<sub>q</sub> have shown promising preclinical results, but their therapeutic activity distinct mutational contexts <i>in vivo</i> remained...
<div>AbstractPurpose:<p>All uveal melanoma and a fraction of other subtypes are driven by activation the G-protein alpha-q (Gα<sub>q</sub>) pathway. Targeting these melanomas has proven difficult despite advances in molecular understanding key driver signaling pathways disease pathogenesis. Inhibitors Gα<sub>q</sub> have shown promising preclinical results, but their therapeutic activity distinct mutational contexts <i>in vivo</i> remained...
<p>Supplementary figures S1-S6 with figure legends.</p>
<p>raw uncropped labeled western blots</p>