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In addition, two recent reports have suggested that the ALK fusion, TPM4\u2010ALK, may be involved in the genesis of a subset of esophageal squamous cell carcinomas. While the cause\u2010effect relationship between ALK fusions and malignancies such as ALCL and IMT is very well established, more circumstantial links implicate the involvement of the full\u2010length, normal ALK receptor in the genesis of additional malignancies including glioblastoma, neuroblastoma, breast cancer, and others; in these instances, ALK is believed to foster tumorigenesis following activation by autocrine and\/or paracrine growth loops involving the reported ALK ligands, pleiotrophin (PTN) and midkine (MK). There are no currently available ALK small\u2010molecule inhibitors approved for clinical cancer therapy; however, recognition of the variety of malignancies in which ALK may play a causative role has recently begun to prompt developmental efforts in this area. This review provides a succinct summary of normal ALK biology, the confirmed and putative roles of ALK fusions and the full\u2010length ALK receptor in the development of human cancers, and efforts to target ALK using small\u2010molecule kinase inhibitors. \u00a9 2007 Wiley Periodicals, Inc. Med Res Rev, 28, No. 3, 372\u2013412, 2008<\/jats:p>","DOI":"10.1002\/med.20109","type":"journal-article","created":{"date-parts":[[2007,8,10]],"date-time":"2007-08-10T20:17:02Z","timestamp":1186777022000},"page":"372-412","source":"Crossref","is-referenced-by-count":110,"title":["Development of anaplastic lymphoma kinase (ALK) small\u2010molecule inhibitors for cancer therapy"],"prefix":"10.1002","volume":"28","author":[{"given":"Rongshi","family":"Li","sequence":"first","affiliation":[]},{"given":"Stephan 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