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Members of the <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010<jats:italic>\u03b2<\/jats:italic> superfamily, <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010<jats:italic>\u03b2<\/jats:italic>1, <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010<jats:italic>\u03b2<\/jats:italic>3, and <jats:styled-content style=\"fixed-case\">BMP<\/jats:styled-content>9, are key propagators of both inhibition and initiation of angiogenesis. <jats:styled-content style=\"fixed-case\">HHT<\/jats:styled-content>, characterized by AVM and capillary bed defects, is caused by germline mutations in the <jats:italic><jats:styled-content style=\"fixed-case\">ENG<\/jats:styled-content><\/jats:italic> and <jats:italic><jats:styled-content style=\"fixed-case\">ACVRL<\/jats:styled-content>1\/<jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content>1<\/jats:italic> genes, respectively. Clinical symptoms include epistaxis and GI hemorrhage. The membranous receptors endoglin and <jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content>1 activate proliferation and migration of endothelial cells during the angiogenic process via the downstream intracellular <jats:styled-content style=\"fixed-case\">SMAD<\/jats:styled-content> signaling pathway. Endothelial cell senescence or activation is dependent on the type of cytokine, ligand concentration, cell\u2013cell interaction, and a multitude of other signaling molecules. Endoglin and <jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content>1 receptor levels in tumor vasculature correlate inversely with prognosis in humans, whereas in mice, endoglin deficiency decelerates tumor progression. Therefore, endoglin and <jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content>1 have been identified as potential therapeutic targets for antibody treatment in various cancers. Early phase clinical trials in humans are currently underway to evaluate the efficacy and safety of biological therapy targeting endoglin\/<jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content>1\u2010mediated cells signaling.<\/jats:p>","DOI":"10.1111\/micc.12099","type":"journal-article","created":{"date-parts":[[2014,2,17]],"date-time":"2014-02-17T02:43:37Z","timestamp":1392605017000},"page":"93-103","source":"Crossref","is-referenced-by-count":40,"title":["<scp>TGF<\/scp>\u2010<i>\u03b2<\/i> &amp; <scp>BMP<\/scp> Receptors Endoglin and <scp>ALK<\/scp>1: Overview of their Functional Role and Status as Antiangiogenic Targets"],"prefix":"10.1111","volume":"21","author":[{"given":"Leon","family":"Jonker","sequence":"first","affiliation":[{"name":"North Cumbria University Hospitals NHS Trust Carlisle 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