Posters should be on display from Thursday morning through Friday evening, but it is recommended that all posters remain on display through Sunday so they are available for viewing both at the designated time with the authors (see below) and informally (without authors) at coffee breaks and lunch.
Invited Speaker (10:20am – 11:05am) Treatment Manifestations of an Endoglin Antibody Dr. Theuer will discuss non-clinical and clinical data with the TRC105 endolgin antibody. TRC105 causes many of the small vessel manifestations of HHT (i.e., mucocutaneous telangiectasia), when dosed to cancer patients as a single agent or when combined with chemotherapy or inhibitors of the VEGF pathway. Similarly, an antibody to activin-like kinase 1 (ALK1) and a fusion protein targeting bone morphogenic protein 9 (BMP9), also produce small vessel manifestations of HHT. The consistency of small vessel manifestations of HHT following treatment with each of these three therapeutics reinforce recent... Read More
Invited Speaker (1:30pm – 2:15pm) Therapeutic potential of ALK1 activating drugs in HHT models Hereditary hemorrhagic telangiectasia (HHT) is a vascular disorder arising from aberrant endothelial cell-driven hypervascularization, and caused by loss-of-function mutations in the BMP9-ALK1-Smad1/5/8 signaling pathway. Interventions that would activate ALK1 signaling might therefore have therapeutic potential in HHT. By screening the NIH clinical collections of FDA-approved drugs, we have recently identified several molecules capable of activating ALK1 signaling in BMP9-challenged C2C12 reporter cells. In human primary endothelial cells (HUVECs), the most potent drug identified, tacrolimus (FK506), activated Smad1/5/8 and opposed the pro-angiogenic transcriptional response of ALK1 loss-of-function... Read More
Invited Speaker (8:00am – 8:45am) Endoglin Controls Blood Vessel Diameter Through Endothelial Cell Shape Changes Dr. Siekmann will present data on the role of endoglin in establishing the hierarchical patterning of the vascular tree. His results show that loss of endoglin leads to an increase in endothelial cell areas, thereby precipitating arterial-venous malformations. Dr. Siekmann suggests that changes in endothelial cell shapes contribute to the manifestation of HHT phenotypes. Oral Presentations (8:45am – 9:45am)