Introduction: Medullary thyroid carcinoma (MTC) is a neuroendocrine cancer originating from calcitonin-producing C-cells. Surgical resection is the most effective treatment currently available. Understanding the molecular pathways mediating MTC is crucial for the development of novel therapies. Cyclin-dependent kinase 5 (Cdk5) and its activators, p35 and p25, have recently been implicated in MTC etiology. P25 is a cleavage product of p35 and the binding of p25 to Cdk5 leads to aberrant Cdk5 activity.
Aim(s): We present a new mouse model in which inducible expression of p25 (p25OE) in thyroid C-cells led to tumorigenesis and lethal MTC.
Materials and methods: Conditional p25OE was driven by a NSE promoter via a tetracycline transactivator system.
Conference: 10th Annual ENETS Conference 2013 (2013)
Category: Epidemiology/Natural history/Prognosis - Registries, nationwide and regional surveys
Presenting Author: Dr Karine Pozo
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