Genomic Instability as Mechanism in Thyroid Cancer Development

Abstract

Introduction: Thyroid cancer arises in the context of numerous risk factors that reflect the intrinsically high proliferative potential of thyroid follicular cells. Among these factors, genomic instability has emerged as a fundamental mechanism driving thyroid tumorigenesis. Objective: This review aims to elucidate the role of genomic instability in the pathogenesis of thyroid cancer, examining the molecular alterations and key oncogenes implicated in tumor initiation and progression. Methods: An analysis of current cytogenetic and molecular studies was conducted to synthesize the knowledge surrounding genetic mutations and chromosomal aberrations associated with both benign and malignant thyroid lesions. Results: Genomic instability contributes significantly to thyroid tumor development through the accumulation of genetic alterations affecting crucial signaling pathways. These alterations influence tumor phenotype and behavior across different stages of progression. Moreover, advances in diagnostic technologies have improved the identification of novel gene variants and the characterization of molecular profiles linked to specific thyroid tumor phenotypes. Conclusion: Understanding the molecular underpinnings of genomic instability offers critical insights into thyroid carcinogenesis and highlights potential targets for diagnostic and therapeutic refinement. The principal oncogenes driving this process represent promising focal points for future research.