By S.-I. Nishikawa, M. Osawa (auth.), O.D. Wiestler, B. Haendler, D. Mumberg (eds.)
This booklet describes the new advancements within the rising box of melanoma stem cells. Their attainable effect for the identity of novel remedy paradigms for melanoma are mentioned. The booklet will customarily be of curiosity to scientists and clinicians curious about melanoma study, or to scholars wishing to go into into this area.
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Extra info for Cancer Stem Cells: Novel Concepts and Prospects for Tumor Therapy
2004). Most strikingly, TPA treatment immediately following the Myc and Ras During Skin Tumorigenesis 21 initial DMBA exposure, or delayed for as long as 1 year after, generates the same number of papillomas with similar latency (Van Duuren et al. 1975). These data suggest that the target cells that carry oncogenic H-Ras have the ability to remain dormant over long periods of time, a feature only attributable to long-lived normal ESCs. In addition, studies using the two-stage carcinogenesis protocol in which the epidermis, but not the hair follicles, has been removed by a specific abrasion technique suggest that the tumor target cells are located in the follicular region (Morris et al.
B. M. 5 β-Catenin β-catenin plays key roles in the Wnt pathway, first by transmitting Wnt signals to the nucleus and second in tumorigenesis, through regulation of oncogenes (including cyclin D1 and c-myc) or by its own sporadic mutations. Overexpression of β-catenin has been reported in lung cancer. It has been reported that increased expression of β-catenin is associated with a high proliferative index, but paradoxically a favorable prognosis (Hommura et al. 2002). Supporting this, two studies reported independently that reduced expression of β-catenin might be associated with a poor prognosis in adenocarcinoma (Retera et al.
Similar to the K14-Myc mice, elimination of Rac1 in the epidermis caused a transient hyperplasia followed by epidermal thinning and finally loss of normal skin function, suggesting ESC depletion. Most strikingly, this phenotype was associated with increased c-Myc expression, and the authors demonstrated that Rac1 negatively regulates c-Myc expression through p21-activated kinase 2 (PAK2) phosphorylation (Benitah et al. 2005). Although the exact mechanism for the loss of ESCs in these models still remains to be elucidated, one plausible explanation is the premature differentiation of ESCs, similar to what has been observed in HSCs overexpressing c-Myc (Wilson et al.