Cancer Immunity, Vol. 9, p. 4 (23 April 2009) Submitted: 26 August 2008. Resubmitted: 29 January 2009. Accepted: 27 March 2009.
Zahra Madjd1,2,3, Ali Zare Mehrjerdi1,3, Ali Mohammad Sharifi2, Saadat Molanaei4, Shahriar Zohourian Shahzadi1 and Mohsen Asadi-Lari3,5
1Department of Pathology, Iran University of Medical Sciences, Tehran, Iran
2Cellular Molecular Research Centre, Iran University of Medical Sciences, Tehran, Iran
3Oncopathology Research Centre, Iran University of Medical Sciences, Tehran, Iran
4Department of Pathology, Milad Hospital, Tehran, Iran
5Department of Epidemiology, Iran University of Medical Sciences, Tehran, Iran
Communicated by: LJ Old
Breast tumours consist of phenotypically diverse populations of breast cancer cells of which only a minority has the ability to form new tumours. The capacity for breast tumour development has been shown to be restricted to breast cancer stem cells with the CD44+/CD24(-/low) phenotype. These cells can resist apoptosis through mechanisms such as the regulation of Bcl-2. Identification of this population of cells is important because of its implication in the development of new therapeutic strategies. One hundred and forty-six primary operable breast cancer patients were investigated in order to identify the population of CD44+ and Bcl-2+ cells in paraffin-embedded tissues by immunohistochemistry. The prevalence of these phenotypes was then correlated with clinicopathological features. CD44 and Bcl-2 expression was detected in 86% and 82% of breast tumours, respectively. There was no significant correlation between CD44+ tumour cell prevalence and tumour characteristics, whereas the prevalence of CD44+ cells was associated with higher levels of Bcl-2 expression (P = 0.004). In univariate analysis, Bcl-2 expression was correlated with breast tumours of lower grade (P < 0.001) and fewer lymphatic metastases (P < 0.05). Our findings suggest that the prevalence of CD44+ tumour cells as a subpopulation of breast cancer stem cells was of no clinicopathological significance, but was correlated with higher Bcl-2 expression. This population of tumour cells may thus be more resistant to apoptosis. Targeting these cells in combination with current treatments may be more effective in treating breast cancer patients.
Copyright © 2009 by Zahra Madjd