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Direct Targeting of RET Aberrations Moves Closer to the Clinic

William Pass, DVM
Published: Monday, Dec 10, 2018
Dr Alexander Drilon

Alexander Drilon, MD
Research on the proto-oncogene RET has accelerated exponentially since 1985, when Masahide Takahashi, MD, PhD, and colleagues first reported a fusion rearrangement in lymphoma DNA.1 Early progress was slow. Other investigators noted RET abnormalities—both fusions and mutations—in papillary thyroid cancer (PTC), in multiple endocrine neoplasia type 2 (MEN2), and after radiation exposure, but targeted interventions were still on the distant horizon.2-4

fusion partners, and researchers are optimistic about the value of RET inhibition across tumor types. How this inhibition will be accomplished—by selective agents, custom-tailored multikinase inhibitors, or in combination with other therapies—has yet to be determined.

Pathways Involving RET

RET is a transmembrane glycoprotein receptor tyrosine kinase (RTK) encoded by RET, which is located on chromosome 10.9 During embryogenesis, RET aids in development of the enteric nervous system and kidneys; throughout life, in the homeostasis of multiple tissues.10,11

RET Aberrations

With knowledge of associations between RET and downstream cell proliferation pathways, it follows logically that cancer might result from RET dysfunction. Such dysfunction can be retraced to various RET aberrations, which are divided into 2 types: chromosomal rearrangements (fusions) or mutations.1
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