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Identification of new ALK and RET gene fusions from colorectal and lung cancer biopsies. KIF5B-RET fusions in lung adenocarcinoma. Germ-line mutations of the RET proto-oncogene in multiple endocrine neoplasia type 2A. PTC is a novel rearranged form of the ret proto-oncogene and is frequently detected in vivo in human thyroid papillary carcinomas. Isolation of ret proto-oncogene cDNA with an amino-terminal signal sequence. Assignment of multiple endocrine neoplasia type 2A to chromosome 10 by linkage. Human ret proto-oncogene mapped to chromosome 10q11.2.
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This article describes the first isolation of RET as well as the first demonstration of its oncogenic activity. Activation of a novel human transforming gene, ret, by DNA rearrangement. FDA approves selpercatinib pralsetinib may soon follow. New therapeutic approaches to treat medullary thyroid carcinoma. Schlumberger, M., Carlomagno, F., Baudin, E., Bidart, J. Although expanded clinical validation in future trials is needed, the sustained antitumoural activity and the improved safety profile of these novel compounds is opening a new exciting era in precision oncology for RET-driven cancers. However, remarkable progress has been achieved with the identification of novel potent and selective RET kinase inhibitors for the treatment of advanced thyroid cancer.
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In clinical practice, use of multikinase inhibitors in patients with advanced thyroid cancer resulted in therapeutic efficacy, which was associated with frequent and sometimes severe adverse effects. This approach was initially achieved using multikinase inhibitors, which affect multiple deregulated pathways that include RET kinase. Thus, RET kinase inhibition is an attractive therapeutic target in patients with RET alterations. RET rearrangements and mutations of extracellular cysteines facilitate dimerization and kinase activation, whereas mutations in the RET kinase coding domain drive dimerization-independent kinase activation. By contrast, single amino acid substitutions and small insertions and/or deletions are typical of hereditary and sporadic medullary thyroid carcinoma. RET gene rearrangements are observed in papillary thyroid carcinoma, which result in RET fusion products. Since the discovery of the RET receptor tyrosine kinase in 1985, alterations of this protein have been found in diverse thyroid cancer subtypes.