To date, however, no studies have definitely indicated that stem cells are responsible for thyroid carcinogenesis. markers c-KIT and THY-1 DASA-58 were negative. Sensitivity to chemotherapy agents was investigated, showing remarkable resistance to chemotherapy-induced apoptosis in ARO/CD133poswhen compared with ARO/CD133negcells. == Conclusions/Significance == We describe CD133poscells in ATC cell lines. ARO/CD133poscells exhibit stem cell-like features – such as high proliferation, self-renewal ability, expression of OCT-4 – and are characterized by higher resistance to chemotherapy. The simultaneous positivity for thyroid specific factor TTF-1 and onfFN suggest DASA-58 they might represent putative thyroid cancer stem-like cells. Ourin vitrofindings might provide new insights for novel therapeutic approaches. == Introduction == Anaplastic thyroid carcinoma (ATC) is one of the most aggressive endocrine tumors with morphological features of undifferentiated neoplasm. Patients with ATC have a poor prognosis with a mean survival time of 26 months. Surgery, radiotherapy and chemotherapy do not improve survival rate[1]. Recently, adult stem cells were identified in human thyroid glands[2]. These cells express several specific markers, such as the nuclear transcription factor OCT-4 (also known as OCT-3, OCT-3/4) and the endodermal markers GATA-4 and HNF4[2][4]. A link between DASA-58 stem and cancer cells has been suggested in various tissues where cancer cells are supposed to derive from immature progenitors or stem cells[5]. Cancer stem cells (CSCs) have been found in leukemia[6], glioblastoma[7], breast[8], prostate[9], gastric[10], lung[11], and colon[12]cancer. These cells, which represent only a small population within the bulk of the tumor, possess the simultaneous ability to self-renew and differentiate into other cytotypes[13]. The stem-like phenotype has proved to be capable of resisting conventional therapies, thus leading to disease relapse even when the primary lesion has been eradicated[14],[15]. To date, however, no studies have definitely indicated that stem cells are responsible DASA-58 for thyroid carcinogenesis. However, the rarity and rapid growth pattern of ATC resembles the nature of stem cells. Only one study has described a very small population, termed MAPK10 side population, enriched for stem cells among thyroid cancer cell lines[16]. In addition, the hypothesis of fetal cell carcinogenesis, in which cancer cells are derived from the remnants of fetal thyroid cells instead of adult thyrocytes, has been proposed[17]. Several markers have been identified for the characterization of CSCs. Human CD133, a highly conserved antigen homologue of mouse Prominin-1, was originally identified in a subpopulation of CD34+hematopoietic cells derived from human fetal liver and bone marrow[18][19]. CD133 has been used for the identification and isolation of a putative CSC population from several human cancers[20],[21]. In addition, the expression of CD133posCSCs in hepatocellular carcinoma (HCC) was shown to confer chemoresistancein vitro[14]. However, its biological function remains unknown. The transcription factor OCT-4 is considered a main regulator of human embryonic stem cell pluripotency and self-renewal capacities[22]. Interestingly, these stem-cell properties are attributed to OCT-4A, DASA-58 a splice variant of the OCT-4 gene located in the nucleus[23],[24]. The aim of the present study was to investigate the expression of putative stem cell markers in established human ATC cell lines, such as ARO, KAT-4, KAT-18 and FRO. We identified CD133poscells in ARO and KAT-4 cell lines. This subset was characterized by higherin-vitroproliferation, self-renewal and colony forming ability. ARO/CD133poswere more resistant than ARO/CD133negcells to chemotherapy-induced apoptosis. In addition, ARO/CD133poscells expressed the thyroblast specific transcription factor TTF-1 and the stem cell marker OCT-4, whereas they were.