In the last decade, the incidence of malignant thyroid cancer has increased worldwide. This escalation has derived either from a precocious individualization of small carcinomas or a major occurrence of large carcinomas. As a counterweight to early diagnosis, the mortality has not decreased but has rather increased. Epithelial malignant cancers of the thyroid emerge as nodules set up by two different cellular types such as follicular and parafollicular cells, namely C cells. The former, producing thyroid hormones, develop either well differenced thyroid carcinomas (WDTC) or anaplastic carcinomas; while the latter, secreting calcitonin, make up medullary thyroid carcinomas (MTC). WDTC account for 90% of all thyroid cancers and are classified as papillary thyroid cancer (PTC) (80–85%), follicular thyroid cancer (FTC) (10–15%) and Hurtle cell carcinoma (HCC) (3–5%). Overall, WDTC have good prognosis with disease free survival close to 95% for PTC and 80% for FTC. ATC are occurring in 1 to 2% of thyroid cancers and display a poor prognosis. MTC include the remaining 5 to 9% of thyroid cancer and show a relatively poor prognosis. Multiple gene mutations and rearrangements harbour in thyroid cancers. Affected genes include RET, BRAF, PI3KCA, RAS, MET and Galectin. Chromosomal rearrangements involve especially chromosome 7 and 10. Morphology of cells already plays a main role for identification of cancer in nodules and to drive patients toward appropriate treatments. The latest is that molecular medicine may work in diagnostic identification of thyroid cancers as a marker and therefore, could modify the flow chart for management of thyroid nodules.

Cancer Thyroid Nodule: Knowing is Doing

TROVATO, Maria Concetta
2015-01-01

Abstract

In the last decade, the incidence of malignant thyroid cancer has increased worldwide. This escalation has derived either from a precocious individualization of small carcinomas or a major occurrence of large carcinomas. As a counterweight to early diagnosis, the mortality has not decreased but has rather increased. Epithelial malignant cancers of the thyroid emerge as nodules set up by two different cellular types such as follicular and parafollicular cells, namely C cells. The former, producing thyroid hormones, develop either well differenced thyroid carcinomas (WDTC) or anaplastic carcinomas; while the latter, secreting calcitonin, make up medullary thyroid carcinomas (MTC). WDTC account for 90% of all thyroid cancers and are classified as papillary thyroid cancer (PTC) (80–85%), follicular thyroid cancer (FTC) (10–15%) and Hurtle cell carcinoma (HCC) (3–5%). Overall, WDTC have good prognosis with disease free survival close to 95% for PTC and 80% for FTC. ATC are occurring in 1 to 2% of thyroid cancers and display a poor prognosis. MTC include the remaining 5 to 9% of thyroid cancer and show a relatively poor prognosis. Multiple gene mutations and rearrangements harbour in thyroid cancers. Affected genes include RET, BRAF, PI3KCA, RAS, MET and Galectin. Chromosomal rearrangements involve especially chromosome 7 and 10. Morphology of cells already plays a main role for identification of cancer in nodules and to drive patients toward appropriate treatments. The latest is that molecular medicine may work in diagnostic identification of thyroid cancers as a marker and therefore, could modify the flow chart for management of thyroid nodules.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3066909
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