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Molecular Alterations in Thyroid Carcinoma
Mohamed Rizwan Haroon Al Rasheed1, Bin Xu1
1Department of Pathology, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA.
Abstract:
Thyroid carcinoma is the most common cancer in the endocrine system. Recent advances, using next-generation sequencing, have shed light on the molecular pathogenesis of thyroid cancer. Constitutional activation of the mitogen-activated protein kinase pathway through RAS mutation, BRAF mutation, and/or fusions involving receptor tyrosine kinase (eg, (REarranged during Transfection) RET-PTC) plays a central role in tumorigenesis and opens doors to promising tyrosine kinase inhibitor therapy. Several molecular signatures, such as TERT promoter mutation and TP53 mutation, are associated with tumor progression. This article provides a concise and updated summary of the main genetic alterations in thyroid carcinoma.
Insights
Thyroid carcinoma, the most common endocrine cancer, is driven by genetic alterations like RAS and BRAF mutations. These molecular changes in the mitogen-activated protein kinase pathway are key targets for new tyrosine kinase inhibitor therapies.
Area of Science:
- Endocrinology
- Oncology
- Molecular Biology
Background:
- Thyroid carcinoma is the most prevalent endocrine system malignancy.
- Next-generation sequencing has advanced understanding of thyroid cancer's molecular basis.
- Constitutive activation of the mitogen-activated protein kinase (MAPK) pathway is crucial in thyroid tumorigenesis.
Purpose of the Study:
- To provide a concise and updated summary of the primary genetic alterations in thyroid carcinoma.
- To highlight the role of specific mutations and fusions in thyroid cancer development.
- To discuss the implications of these molecular findings for targeted therapies.
Main Methods:
- Review of recent advances in next-generation sequencing.
- Analysis of molecular pathogenesis of thyroid cancer.
- Identification of key genetic alterations and molecular signatures.
Main Results:
- RAS mutations, BRAF mutations, and RET-PTC fusions are central to MAPK pathway activation and tumorigenesis.
- TERT promoter and TP53 mutations are linked to tumor progression.
- These genetic alterations offer potential targets for tyrosine kinase inhibitor therapy.
Conclusions:
- Understanding the genetic landscape of thyroid carcinoma is critical for diagnosis and treatment.
- Targeting activated molecular pathways presents a promising therapeutic strategy.
- Continued research into molecular signatures will refine prognostication and treatment selection.
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