title: RET revisited: expanding the oncogenic portfolio.
abstract: The RET receptor tyrosine kinase is crucial for normal development but also contributes to pathologies that reflect both the loss and the gain of RET function. Activation of RET occurs via oncogenic mutations in familial and sporadic cancers - most notably, those of the thyroid and the lung. RET has also recently been implicated in the progression of breast and pancreatic tumours, among others, which makes it an attractive target for small-molecule kinase inhibitors as therapeutics. However, the complex roles of RET in homeostasis and survival of neural lineages and in tumour-associated inflammation might also suggest potential long-term pitfalls of broadly targeting RET.
authors.affiliation: Division of Cancer Biology and Genetics, Cancer Research Institute and Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario K7L 3N6, Canada.
authors.forename: Lois M
authors.initials: LM
authors.lastname: Mulligan
mesh_terms: D000818:Animals; D006801:Humans; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D051096:Proto-Oncogene Proteins c-ret / Q000235:genetics / Q000378:metabolism*
chemical_list: D051096:Proto-Oncogene Proteins c-ret