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Nevertheless, most patients treated using this approach experience local recurrence, so it is essential to identify ways to enhance tumor response. We previously reported that <jats:styled-content style=\"fixed-case\">PDT<\/jats:styled-content> transiently activates <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3 in lung and ovarian cancer cells and inhibiting <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content> via erlotinib can increase <jats:styled-content style=\"fixed-case\">PDT<\/jats:styled-content> sensitivity. Additionally, we have seen higher <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content> expression associating with worse outcomes after Photofrin\u2010mediated <jats:styled-content style=\"fixed-case\">PDT<\/jats:styled-content> for <jats:styled-content style=\"fixed-case\">MPM<\/jats:styled-content>, and the extensive desmoplastic reaction associated with <jats:styled-content style=\"fixed-case\">MPM<\/jats:styled-content> influences tumor phenotype and therapeutic response. Since extracellular matrix (<jats:styled-content style=\"fixed-case\">ECM<\/jats:styled-content>) proteins accrued during stroma development can alter <jats:styled-content style=\"fixed-case\">EGF<\/jats:styled-content> signaling within tumors, we have characterized novel 3D models of <jats:styled-content style=\"fixed-case\">MPM<\/jats:styled-content> to determine their response to erlotinib combined with Photofrin\u2010<jats:styled-content style=\"fixed-case\">PDT<\/jats:styled-content>. Our <jats:styled-content style=\"fixed-case\">MPM<\/jats:styled-content> cell lines formed a range of acinar phenotypes when grown on <jats:styled-content style=\"fixed-case\">ECM<\/jats:styled-content> gels, recapitulating the locally invasive phenotype of <jats:styled-content style=\"fixed-case\">MPM<\/jats:styled-content> in pleura and endothoracic fascia. Using these models, we confirmed that <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content> inhibition increases <jats:styled-content style=\"fixed-case\">PDT<\/jats:styled-content> cytotoxicity. Together with emerging evidence that <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content> inhibition may improve survival of lung cancer patients through immunologic and direct cell killing mechanisms, these results suggest erlotinib\u2010enhanced <jats:styled-content style=\"fixed-case\">PDT<\/jats:styled-content> may significantly improve outcomes for <jats:styled-content style=\"fixed-case\">MPM<\/jats:styled-content> patients.<\/jats:p>","DOI":"10.1111\/php.13067","type":"journal-article","created":{"date-parts":[[2018,11,30]],"date-time":"2018-11-30T07:55:03Z","timestamp":1543564503000},"page":"397-405","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Modeling Epidermal Growth Factor Inhibitor\u2010mediated Enhancement of Photodynamic Therapy Efficacy Using 3D Mesothelioma Cell 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