Clinical Outcome, Role of BRAF\(^{V600E}\), and Molecular Pathways in Papillary Thyroid Microcarcinoma: Is It an Indolent Cancer or an Early Stage of Papillary Thyroid Cancer?
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Clinical Outcome, Role of BRAF\(^{V600E}\), and Molecular Pathways in Papillary Thyroid Microcarcinoma: Is It an Indolent Cancer or an Early Stage of Papillary Thyroid Cancer?
| Title: | Clinical Outcome, Role of BRAF\(^{V600E}\), and Molecular Pathways in Papillary Thyroid Microcarcinoma: Is It an Indolent Cancer or an Early Stage of Papillary Thyroid Cancer? |
| Author: |
Pontecorvi, Alfredo; Nucera, Carmelo
Note: Order does not necessarily reflect citation order of authors. |
| Citation: | Nucera, Carmelo, and Alfredo Pontecorvi. 2012. Clinical outcome, role of BRAF\(^{V600E}\), and molecular pathways in papillary thyroid microcarcinoma: Is it an indolent cancer or an early stage of papillary thyroid cancer? Frontiers in Endocrinology 3:33. |
| Full Text & Related Files: |
3355963.pdf (1.137Mb; PDF) 
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| Abstract: | Most human thyroid cancers are differentiated papillary carcinomas (PTC). Papillary thyroid microcarcinomas (PTMC) are tumors that measure 1 cm or less. This class of small tumors has proven to be a very common clinical entity in endocrine diseases. PTMC may be present in 30–40% of human autopsies and is often identified incidentally in a thyroid removed for benign clinical nodules. Although PTMC usually has an excellent long-term prognosis, it can metastasize to neck lymph nodes; however deaths related to this type of thyroid tumor are very rare. Few data exist on molecular pathways that play a role in PTMC development; however, two molecules have been shown to be associated with aggressive PTMC. S100A4 (calcium-binding protein), which plays a role in angiogenesis, extracellular matrix remodeling, and tumor microenvironment, is over-expressed in metastatic PTMC. In addition, the BRAF\(^{V600E}\) mutation, the most common genetic alteration in PTC, is present in many PTMC with extra thyroidal extension and lymph node metastasis. Importantly, recently developed selective [e.g., PLX4720, PLX4032 (Vemurafenib, also called RG7204)] or non-selective (e.g., Sorafenib) inhibitors of BRAF\(^{V600E}\) may be an effective treatment for patients with BRAFV600E-expressing PTMCs with aggressive clinical–pathologic features. Here, we summarize the clinical outcome, cancer genetics, and molecular mechanisms of PTMC. |
| Published Version: | doi:10.3389/fendo.2012.00033 |
| Other Sources: | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3355963/pdf/ |
| Terms of Use: | This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA |
| Citable link to this page: | http://nrs.harvard.edu/urn-3:HUL.InstRepos:10385012 |
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