Recent

advances in the stem cell technology have made it possible to understand diverse biological and molecular mechanisms that control the disease process; however, the validity of the origin of CSCs and their distinct role in thyroid cancer still uphold a great interest. Stem cells are the Linsitinib ic50 population of cells that have a tremendous potential for self-renewal and can differentiate into various specialized cells in the body. These are distinguished from other cell types by two important properties. Firstly, they have the ability for self-renewal through continuous cell division and secondly, under specialized circumstances, they can be induced to become tissue/organ specific cells carrying their designated functions. Among these cells, of particular importance are (1) Embryonic stem cells (ESCs) – which are pluripotent cells that divide infinitely and give rise to ectodermal, endodermal and mesodermal cells; and (2) Somatic stem cells (SSC) – also known as adult stem cells, are tissue specific cells with limited life-span that give rise to all cells in a particular lineage, for instance thyroid follicular cells or hematopoietic cells. However, the putative role of ESC and SSC in adult thyroid pathophysiology still remains

to be proven. A sub-type of cancer cells that has recently gained much recognition are CSCs, also referred to as Tumor-initiating cells (TICs)[6-8]. These cells possess characteristics associated with normal stem cells with a remarkable potential to reconstitute and sustain tumor growth. However, it does not infer their origin from a normal stem cell. It has been reported that basal-like epithelial cells can de-differentiate into stem-like cell[9]. Moreover, existing literature illustrates that CSCs may depend on a specific microenvironment or the niche for sustained stem-cell like properties[6,10]. One such example of CSCs niche is hypoxia of cancer where these cells

undergo continued proliferation on exposure to increased free radical generation within the tumor. Therefore, several studies have attempted to identify the niche that necessitates Entinostat these cells to sustain and promote tumor growth. In 1997, Bonnet et al[11] were the first to provide conclusive evidence of CSCs in leukemia. The isolated leukemic cells expressed cell surface markers CD34 but lacked CD38. On injection into an immunodeficient mice, these cells initiated tumor with similar histological features of the parental tumor[11]. In 2002, Ignatova et al[12] were the first to isolate CSCs from human brain gliomas which were described to be clonogenic with special sphere-forming property. Since then there have been many published clinical researches that have successfully identified CSCs in solid cancers of breast, colon, pancreas, prostate and ovary[13-15].