A5006056754- Histone Deacetylase Inhibitors Research
- Peptidase Inhibition and Analysis
- Cytokine Signaling Pathways and Interactions
- Inflammatory mediators and NSAID effects
- Macrophage Migration Inhibitory Factor
- Click Chemistry and Applications
- Nuclear Receptors and Signaling
- Signaling Pathways in Disease
- FOXO transcription factor regulation
- Phosphodiesterase function and regulation
- Galectins and Cancer Biology
- 14-3-3 protein interactions
- Glioma Diagnosis and Treatment
- Synthesis and Catalytic Reactions
- Protein Degradation and Inhibitors
- Genomic variations and chromosomal abnormalities
- Calcium signaling and nucleotide metabolism
- Advanced NMR Techniques and Applications
- Neuroscience of respiration and sleep
- Cancer Genomics and Diagnostics
- Shoulder and Clavicle Injuries
- Melanoma and MAPK Pathways
- Neurofibromatosis and Schwannoma Cases
- Ubiquitin and proteasome pathways
- Nerve Injury and Rehabilitation
Detroit Medical Center
2024
Virginia Commonwealth University
2016-2022
Virginia Cancer Institute
2020
VCU Massey Comprehensive Cancer Center
2020
Dana-Farber Cancer Institute
2011-2012
Pediatric low-grade gliomas (PLGGs) are among the most common solid tumors in children but, apart from BRAF kinase mutations or duplications specific subclasses, few genetic driver events known. Diffuse PLGGs comprise a set of uncommon subtypes that exhibit invasive growth and therefore especially challenging clinically. We performed high-resolution copy-number analysis on 44 formalin-fixed, paraffin-embedded diffuse to identify recurrent alterations. exhibited fewer such alterations than...
Stat5a is a transcription factor utilized by several cytokine/hormone receptor signaling pathways that promotes of genes associated with proliferation, differentiation, and survival cancer cells. However, there are currently no clinically approved therapies directly target Stat5a, despite ample evidence it contributes to breast pathogenesis. Here, deacetylation the coactivator chromatin-remodeling protein HMGN2 on lysine residue K2 HDAC6 Stat5a-mediated growth. inhibition both in vitro vivo...
Whole-genome copy number analysis platforms, such as array comparative genomic hybridization (aCGH) and single nucleotide polymorphism (SNP) arrays, are transformative research discovery tools. In cancer, the identification of aberrations with these approaches has generated important diagnostic prognostic markers, critical therapeutic targets. While robust for basic studies, reliable whole-genome been unsuccessful in routine clinical practice due to a technical limitations. Most important,...
Case: A 60-year-old man sustained a massive irreparable rotator cuff tear and axillary nerve palsy with deltoid dysfunction after an anterior shoulder dislocation. He underwent staged reverse end-to-side radial-to-axillary transfer return of function allowing for subsequent arthroplasty. At 1 year postoperatively, he returned to full activity. Conclusion: Irreparable tears complicated by can be effectively treated approach followed
Prolactin (PRL) and its receptor (PRLr) play important roles in the pathogenesis of breast cancer. Cyclophilin A (CypA) is a cis-trans peptidyl-prolyl isomerase (PPI) that constitutively associated with PRLr facilitates activation tyrosine kinase Jak2. Treatment non-immunosuppressive prolyl inhibitor NIM811 or CypA short hairpin RNA inhibited PRL-stimulated signaling, cancer cell growth, migration. Transcriptomic analysis revealed two-thirds top 50 PRL-induced genes reduction gene pathways...
Abstract The hormone prolactin has been implicated in breast cancer pathogenesis and regulates chromatin engagement by the transcription factor, STAT5A. STAT5A is known to inducibly bind promoters cis-regulatory elements genome-wide, though mechanisms which it exerts specificity regulation of target gene expression remain enigmatic. We previously identified HDAC6 HMGN2 as cofactors that facilitate prolactin-induced, STAT5A-mediated expression. Here, multicondition STAT5A, HDAC6,...
<div>Abstract<p>Stat5a is a transcription factor utilized by several cytokine/hormone receptor signaling pathways that promotes of genes associated with proliferation, differentiation, and survival cancer cells. However, there are currently no clinically approved therapies directly target Stat5a, despite ample evidence it contributes to breast pathogenesis. Here, deacetylation the Stat5a coactivator chromatin-remodeling protein HMGN2 on lysine residue K2 HDAC6 Stat5a-mediated...
<div>Abstract<p>Stat5a is a transcription factor utilized by several cytokine/hormone receptor signaling pathways that promotes of genes associated with proliferation, differentiation, and survival cancer cells. However, there are currently no clinically approved therapies directly target Stat5a, despite ample evidence it contributes to breast pathogenesis. Here, deacetylation the Stat5a coactivator chromatin-remodeling protein HMGN2 on lysine residue K2 HDAC6 Stat5a-mediated...
<p>S3. Bufexamac and tubacin inhibit the tumorigenic properties of breast cancer cell in vitro.</p>
<p>Supplemental Information text</p>
<p>S1. Specificity of α-ac-K2-HMGN2 antibody. S2. HDAC6 inhibition impairs Stat5a-mediated signaling. S3. Bufexamac and tubacin inhibit the tumorigenic properties breast cancer cell in vitro. S4. inhibits MDA-MB-231 tumor growth vivo. S5. treatment viability triple-negative WHIM2 PDX cells.</p>
<p>Supplemental Table S1. Primers used for mutagenesis.</p>
<p>Supplemental Table S2. Primers used for qPCR.</p>
<p>S5. Bufexamac treatment impairs the viability of triple-negative WHIM2 PDX cells.</p>
<p>S2. HDAC6 inhibition impairs Stat5a-mediated signaling.</p>
<p>S4. Bufexamac inhibits MDA-MB-231 tumor growth in vivo.</p>
<p>S5. Bufexamac treatment impairs the viability of triple-negative WHIM2 PDX cells.</p>
<p>Supplemental Table S2. Primers used for qPCR.</p>
<p>S4. Bufexamac inhibits MDA-MB-231 tumor growth in vivo.</p>
<p>Supplemental Table S1. Primers used for mutagenesis.</p>
<p>S1. Specificity of α-ac-K2-HMGN2 antibody. S2. HDAC6 inhibition impairs Stat5a-mediated signaling. S3. Bufexamac and tubacin inhibit the tumorigenic properties breast cancer cell in vitro. S4. inhibits MDA-MB-231 tumor growth vivo. S5. treatment viability triple-negative WHIM2 PDX cells.</p>
<p>Supplemental Information text</p>
<p>S3. Bufexamac and tubacin inhibit the tumorigenic properties of breast cancer cell in vitro.</p>