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First published online May 28, 2004
doi: 10.1242/10.1242/dev.01233


Development 131, 2763-2768 (2004)
Published by The Company of Biologists 2004


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Stem cells, plasticity and cancer - uncomfortable bed fellows

Alan Trounson

Monash Immunology and Stem Cell Laboratories, Faculty of Medicine, Monash University, Wellington Road, Clayton, Victoria, 3800, Australia



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Fig. 1. Stem cells and cancer phenotype. Slowly renewing stem cells that exist within a niche may be subject to mutation, and to gene silencing or upregulated expression. This might be one reason for the delay between an effector stimulus and the cancer phenotype appearing, and might also explain the heterogeneity of cells in tumours. If stem cells or their progenitors escape from the regulation of specific genes, signalling pathways might activate genes, resulting in their escaping from apoptosis and their activating ß-catenin, and/or oncogenes and tumour suppression pathways.

 


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Fig. 2. Detection of a male fumarylacetoacetate hydrolase (Fah)-expressing hepatocyte after transplantation of female GMP (granulocyte/macrophage progenitors) into a male Fah-/- mouse. The presence of donor-specific Fah protein (red, left panel) and host-derived Y chromosome signals (pink, right panel) in the same cell indicate that this trinucleated hepatocyte originates from fusion with a transplanted female (X chromosomes are stained green) myelomonocytic cell. Sequential Fah immunocytochemistry and X/Y FISH were provided by Holger Willenbring and Yassmine Akkari (Department of Molecular and Medical Genetics, Oregon Health and Science University).

 





© The Company of Biologists Ltd 2004