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Benvenga S, Koch CA. Molecular pathways associated with aggressiveness of papillary thyroid cancer. Curr Genomics. 2014;15(3):162-70doi: 10.2174/1389202915999140404100958.
Benvenga, S., & Koch, C. A. (2014). Molecular pathways associated with aggressiveness of papillary thyroid cancer. Current genomics, 15(3), 162-70. https://doi.org/10.2174/1389202915999140404100958
Benvenga, Salvatore, and Koch, Christian A. "Molecular pathways associated with aggressiveness of papillary thyroid cancer." Current genomics vol. 15,3 (2014): 162-70. doi: https://doi.org/10.2174/1389202915999140404100958
Benvenga S, Koch CA. Molecular pathways associated with aggressiveness of papillary thyroid cancer. Curr Genomics. 2014 Jun;15(3):162-70. doi: 10.2174/1389202915999140404100958. PMID: 24955023; PMCID: PMC4064555.
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Curr Genomics. 2014 Jun;15(3):162-70. doi: 10.2174/1389202915999140404100958.

Molecular pathways associated with aggressiveness of papillary thyroid cancer.

Current genomics

Salvatore Benvenga, Christian A Koch

Affiliations

  1. Department of Clinical & Experimental Medicine, Section of Endocrinology, University of Messina, Messina, Italy.
  2. Division of Endocrinology, University of Mississippi Medical Center, Jackson, MS, USA ; GV (Sonny) Montgomery VA Medical Center, Jackson, MS, USA.

PMID: 24955023 PMCID: PMC4064555 DOI: 10.2174/1389202915999140404100958

Abstract

The most common thyroid malignancy is papillary thyroid cancer (PTC). Mortality rates from PTC mainly depend on its aggressiveness. Geno- and phenotyping of aggressive PTC has advanced our understanding of treatment failures and of potential future therapies. Unraveling molecular signaling pathways of PTC including its aggressive forms will hopefully pave the road to reduce mortality but also morbidity from this cancer. The mitogen-activated protein kinase and the phosphatidylinositol 3-kinase signaling pathway as well as the family of RAS oncogenes and BRAF as a member of the RAF protein family and the aberrant expression of microRNAs miR-221, miR-222, and miR-146b all play major roles in tumor initiation and progression of aggressive PTC. Small molecule tyrosine kinase inhibitors targeting BRAF-mediated events, vascular endothelial growth factor receptors, RET/PTC rearrangements, and other molecular targets, show promising results to improve treatment of radioiodine resistant, recurrent, and aggressive PTC.

Keywords: BRAF; P13/Akt; Papillary thyroid cancer; Signaling; Tyrosine kinase; VEGF.

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