Abstract
Apoptosis is an active biologic process that represents a form of programmed cellular suicide, activated either by genetic factors or by cellular lesions caused by various extracellular traumatic agents. The alterations of its functional mechanisms control cellular homeostasis are involved in the genesis of many illnesses. There are different control systems that can both stimulate and inhibit apoptosis, such as the p53 and Bcl-2 proteins. Different injuries may cause a rapid increase in the levels of p53 and the activation of the complex mechanism which leads either to damage repair or cellular apoptosis. The concept of tumor growth as a dynamic balance between cellular development and death is well applicable to differentiated thyroid carcinomas, which are generally not highly invasive and present excellent prognosis. On the contrary, in aggressive anaplastic thyroid carcinoma there is an increase in p53, whereas in normal thyroid cells there is a high expression of Bcl-2, so as to interfere with apoptosis when physiologic hormone levels are normal. However, only some of the biomolecular mechanisms behind the genesis of thyroid tumors have been explained, and the role of apoptosis in thyroid diseases has not been well defined. This review provides information about relationship between apoptosis and thyroid diseases.
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