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One of the most critical checkpoint pathways responsible for mediating tumor\u2010induced immune suppression is the programmed death\u20101 (\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    \u20101) pathway, normally involved in promoting tolerance and preventing tissue damage in settings of chronic inflammation. Many human solid tumors express\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    ligand 1 (\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    \u2010L1), and this is often associated with a worse prognosis. Tumor\u2010infiltrating lymphocytes from patients with cancer typically express\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    \u20101 and have impaired antitumor functionality. Proof\u2010of\u2010concept has come from several preclinical studies in which blockade of\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    \u20101 or\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    \u2010L1 enhanced T\u2010cell function and tumor cell lysis. Three monoclonal antibodies against\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    \u20101, and one against\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    \u2010L1, have reported phase 1 data. All four agents have shown encouraging preliminary activity, and those that have been evaluated in larger patient populations appear to have encouraging safety profiles. Additional data are eagerly awaited. This review summarizes emerging clinical data and potential of\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    \u20101 pathway\u2013targeted antibodies in development. If subsequent investigations confirm the initial results, it is conceivable that agents blocking the\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    \u20101\/\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    \u2010L1 pathway will prove valuable additions to the growing armamentarium of targeted immunotherapeutic agents.\n                  <\/jats:p>","DOI":"10.1002\/cam4.106","type":"journal-article","created":{"date-parts":[[2013,7,22]],"date-time":"2013-07-22T00:38:57Z","timestamp":1374453537000},"page":"662-673","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":339,"title":["<scp>PD<\/scp>\n                    \u20101 as a potential target in cancer therapy"],"prefix":"10.1002","volume":"2","author":[{"given":"David F.","family":"McDermott","sequence":"first","affiliation":[{"name":"Biologic Therapy Program Beth Israel Deaconess Medical Center Boston Massachusetts"},{"name":"Harvard Medical School Boston Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael B.","family":"Atkins","sequence":"additional","affiliation":[{"name":"Georgetown\u2010Lombardi Cancer Center Georgetown University School of Medicine Washington District of Columbia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,7,21]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ctrv.2007.04.003"},{"key":"e_1_2_12_3_1","doi-asserted-by":"crossref","first-page":"201","DOI":"10.5489\/cuaj.853","article-title":"Interferon\u2010alfa in the treatment of patients with inoperable locally advanced or metastatic renal cell carcinoma: a systematic review","volume":"4","author":"Canil C.","year":"2010","journal-title":"Can. 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