No conflicts of interest were declared.
Metaplastic breast carcinoma: tumour histogenesis or dedifferentiation?†
Article first published online: 1 APR 2011
Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
The Journal of Pathology
Volume 224, Issue 4, pages 434–437, August 2011
How to Cite
van Deurzen, C. H., Lee, A. H., Gill, M. S., Menke-Pluijmers, M. B., Jager, A., Ellis, I. O. and Rakha, E. A. (2011), Metaplastic breast carcinoma: tumour histogenesis or dedifferentiation?. J. Pathol., 224: 434–437. doi: 10.1002/path.2872
- Issue published online: 4 JUL 2011
- Article first published online: 1 APR 2011
- Accepted manuscript online: 18 FEB 2011 12:00AM EST
- Manuscript Accepted: 1 FEB 2011
- Manuscript Received: 28 JAN 2011
- Manuscript Revised: 28 JAN 2011
- metaplastic breast carcinoma;
- progenitor cells
Global gene expression profiling studies have classified breast cancer into molecular classes, some of which show similarity to normal mammary cells (ie luminal and basal subtypes) with a subsequent histogenetic implication that reinforced the perception that the phenotype of breast cancer reflects the cell of origin. However, it remains to be determined whether phenotypic changes are the result of malignant transformation of particular cancer stem cells (histogenesis) or specific genetic hits occurring at various stages of carcinogenesis (dedifferentiation). We sought to test the hypothesis that dedifferentiation may be the more likely explanation using in vivo clinical data. Our findings support the hypothesis that at least some metaplastic carcinomas are derived from phenotypic transition from conventional mammary adenocarcinoma either at the in-situ, primary invasive stage or at a distant metastatic site. This observation argues against the cell of origin theory (histogenesis) for breast carcinogenesis and favours the concept of tumour dedifferentiation at later stages. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.