Anti-ELTD1 mmAb or scFV therapy is effective in a highly aggressive (G55) orthotopic rodent xenograft model of GBM: it reduces tumor volumes and increases animal survival, it reduces tumor microvascularity and angiogenesis, and it reduces tumor cell proliferation and migration and increases tumor cell apoptosis. Unlike bevacizumab (VEGF mAb), using an antibody against ELTD1 does not cause hemorrhage.
Dr. Deshmukh has discovered that anti-vimentin Ab is readily detected in the sera of primary SjD patients. Presence of anti-vimentin Ab is associated with higher severity of oral and ocular features of the disease.
Dr. Farris has identified a set of autoantibodies that classifies 46% Ro Neg patients as SjD resulting in reduced lip biopsies. Additionally, SjD classification of these patients via the novel antigens will improve treatment and patient stratification in clinical trials.
Dr. Jeffries has identified ‘first of kind’ epigenetic DNA methylation biomarkers easily measured in peripheral blood that are used to predict OA progression. His algorithm shows high specificity and sensitivity across different cohorts.
Dr. Griffin has discovered that, YK-4-279, an ETS inhibitor, selectively regresses slow-flow neovascular tufts in the OIR retina but spares healthy vessels with normal blood flow. ETS inhibitors could be used to regress pathological vessels in humans with RoP, DR, age-associated macular degeneration or venous malformations.
Dr. Jeffries has identified that gut microbiome transplantation from OA-protected MRL mice into OA susceptible B6 mice reduces OA histopathology. OA protection correlates with certain gut microbiome clades; particularly, p_Actinobacteria, p_Bacteroidetes (particularly f_Dehalobacteriaceae), and o_Burkholderiales.
Dr.Srinivasan has discovered that PROX1 deficiency leads to cardiac valve disease via dysregulation of PDGF-β signaling pathway. Inhibition of PDGF-β signaling partially rescues aortic valve function in Prox1 mice
Dr. Lee has identified a novel mechanism to treat metabolic cardiomyopathy. He has demonstrated that inhibition of SARM1 elevates NAD+ levels and ameliorates metabolic cardiomyopathy.
Dr. Ahamed has shown that platelet-derived TGF-β1 directly contributes to aortic stenosis (AS) progression. Atherosclerosis prone LDLR mice lacking platelet-derived TGF-β1 were protected from developing AS. Thiol-Reactive compounds, including NAC and galunisertive (LY2157299), significantly attenuated AS progression in LDLR mice by blocking platelet-derived TGF-β1 activation.
Dr. Xia has discovered that the S1P defect causes impaired activation of GlcNAc-1-phosphotransferase and of the ER stress transducer BBF2H77, resulting in abnormal secretion of lysosomal enzymes and ER retention of collagens in chondrocytes. Cartilage related disorders, which account for the majority of skeletal dysplasia, are associated with ER stress. Dr. Xia’s data indicates that treatment of these cartilage related disorders with PBA, BIX or AMO would improve bone function by manipulating ER stress and result in enhanced collagen secretion and reduced chondrocyte apoptosis.