By Otmar D. Wiestler (Editor), Bernhard Haendler (Editor), Dominik Mumberg (Editor)
Melanoma stem cells have initially been pointed out in leukemia and later in different stable tumor varieties. they've got very varied homes from the majority of the tumor as they divide even more slowly and feature very effective drug resistance mechanisms. present remedies may principally spare melanoma stem cells. This ebook appears at contemporary advancements within the box of melanoma stem cells and the potential influence for the id of novel therapy paradigms for melanoma.
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Extra resources for Cancer Stem Cells: Novel Concepts and Prospects for Tumor Therapy (Ernst Schering Foundation Symposium Proceedings 06.5)
Surprisingly, this response appears to be mediated by a single gene, p21CIP1 , which needs to be controlled/repressed by c-Myc in this scenario. Thus, while oncogenic Ras drives the senescence-promoting activity of p21CIP1 , it simultaneously eliminates this antioncogenic effect by stabilizing the p21CIP1 22 A. Trumpp repressor c-Myc (Fig. 1). This again points toward c-Myc as a putative drug target. In the past, anti-Myc therapy has usually been discarded as a therapeutic regime, given the belief that c-Myc function is essential for the proliferation of many, if not all, cells in our body.
2004). Blockade of Wnt-1 signaling induces apoptosis in vitro 38 B. M. Jablons and suppresses tumor growth in vivo (He et al. 2004). Similar results were observed in head and neck squamous cell carcinoma (Rhee et al. 2002), suggesting that Wnt-1 signaling is a key mediator of apoptosis in epithelial cancers. 3, is highly expressed in fetal lung and weakly expressed in placenta (Katoh 2001a). The link between Wnt-2 and tumorigenesis was first proposed after data indicated that Wnt-2 was amplified in human cancers (Yoshida et al.
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 28 29 30 31 35 37 37 39 40 41 42 42 44 46 47 Abstract. The Wnt signal transduction pathway plays important roles during embryo development, regulating cell proliferation and survival of immature cells. However, its improper function can lead to harmful consequences for humans, such as aberrant cell proliferation and, therefore, cancer. Increasing evidence suggests that stem cells may be the source of mutant cells that cause cancers to develop and proliferate.
Cancer Stem Cells: Novel Concepts and Prospects for Tumor Therapy (Ernst Schering Foundation Symposium Proceedings 06.5) by Otmar D. Wiestler (Editor), Bernhard Haendler (Editor), Dominik Mumberg (Editor)