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Cutaneous cancer stem cell maintenance is dependent on beta-catenin signalling (2008)

I. Malanchi ; H. Peinado ; D. Kassen ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 452(7187): 650-3. doi: 10.1038/nature06835.

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Publication Date: 2008-04-04

Description: Continuous turnover of epithelia is ensured by the extensive self-renewal capacity of tissue-specific stem cells. Similarly, epithelial tumour maintenance relies on cancer stem cells (CSCs), which co-opt stem cell properties. For most tumours, the cellular origin of these CSCs and regulatory pathways essential for sustaining stemness have not been identified. In murine skin, follicular morphogenesis is driven by bulge stem cells that specifically express CD34. Here we identify a population of cells in early epidermal tumours characterized by phenotypic and functional similarities to normal bulge skin stem cells. This population contains CSCs, which are the only cells with tumour initiation properties. Transplants derived from these CSCs preserve the hierarchical organization of the primary tumour. We describe beta-catenin signalling as being essential in sustaining the CSC phenotype. Ablation of the beta-catenin gene results in the loss of CSCs and complete tumour regression. In addition, we provide evidence for the involvement of increased beta-catenin signalling in malignant human squamous cell carcinomas. Because Wnt/beta-catenin signalling is not essential for normal epidermal homeostasis, such a mechanistic difference may thus be targeted to eliminate CSCs and consequently eradicate squamous cell carcinomas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malanchi, Ilaria -- Peinado, Hector -- Kassen, Deepika -- Hussenet, Thomas -- Metzger, Daniel -- Chambon, Pierre -- Huber, Marcel -- Hohl, Daniel -- Cano, Amparo -- Birchmeier, Walter -- Huelsken, Joerg -- England -- Nature. 2008 Apr 3;452(7187):650-3. doi: 10.1038/nature06835.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ecole Polytechnique Federale de Lausanne/ISREC (Swiss Institute for Experimental Cancer Research) and National Center of Competence in Research Molecular Oncology, Chemin des Boveresses 155, 1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18385740" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Antigens, CD34/metabolism ; Cell Line, Tumor ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Epidermis/pathology ; Humans ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplastic Stem Cells/*metabolism/*pathology ; *Signal Transduction ; Skin Neoplasms/*pathology ; beta Catenin/*metabolism

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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Interactions between cancer stem cells and their niche govern metastatic colonization (2011)

I. Malanchi ; A. Santamaria-Martinez ; E. Susanto ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 481(7379): 85-9. doi: 10.1038/nature10694.

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Publication Date: 2011-12-14

Description: Metastatic growth in distant organs is the major cause of cancer mortality. The development of metastasis is a multistage process with several rate-limiting steps. Although dissemination of tumour cells seems to be an early and frequent event, the successful initiation of metastatic growth, a process termed 'metastatic colonization', is inefficient for many cancer types and is accomplished only by a minority of cancer cells that reach distant sites. Prevalent target sites are characteristic of many tumour entities, suggesting that inadequate support by distant tissues contributes to the inefficiency of the metastatic process. Here we show that a small population of cancer stem cells is critical for metastatic colonization, that is, the initial expansion of cancer cells at the secondary site, and that stromal niche signals are crucial to this expansion process. We find that periostin (POSTN), a component of the extracellular matrix, is expressed by fibroblasts in the normal tissue and in the stroma of the primary tumour. Infiltrating tumour cells need to induce stromal POSTN expression in the secondary target organ (in this case lung) to initiate colonization. POSTN is required to allow cancer stem cell maintenance, and blocking its function prevents metastasis. POSTN recruits Wnt ligands and thereby increases Wnt signalling in cancer stem cells. We suggest that the education of stromal cells by infiltrating tumour cells is an important step in metastatic colonization and that preventing de novo niche formation may be a novel strategy for the treatment of metastatic disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malanchi, Ilaria -- Santamaria-Martinez, Albert -- Susanto, Evelyn -- Peng, Hong -- Lehr, Hans-Anton -- Delaloye, Jean-Francois -- Huelsken, Joerg -- England -- Nature. 2011 Dec 7;481(7379):85-9. doi: 10.1038/nature10694.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ecole Polytechnique Federale de Lausanne, Swiss Institute for Experimental Cancer Research and National Center of Competence in Research Molecular Oncology, 1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22158103" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Breast Neoplasms/pathology ; Cell Adhesion Molecules/genetics/metabolism ; Female ; Lung Neoplasms/secondary ; Mice ; Mice, Inbred C57BL ; Neoplasm Metastasis/*pathology ; Neoplastic Stem Cells/metabolism/*pathology ; Stem Cell Niche/*physiology ; Stromal Cells/metabolism ; Wnt Signaling Pathway

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics