Breast cancer stem cells: Treatment resistance and therapeutic opportunities

AL-Ejeh, Fares, Smart, Chanel E., Morrison, Brian J., Chenevix-Trench, Georgia, Lopez, J. Alejandro, Lakhani, Sunil R., Brown, Michael P. and Khanna, Kum Kum (2011) Breast cancer stem cells: Treatment resistance and therapeutic opportunities. Carcinogenesis, 32 5: 650-658. doi:10.1093/carcin/bgr028

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Author AL-Ejeh, Fares
Smart, Chanel E.
Morrison, Brian J.
Chenevix-Trench, Georgia
Lopez, J. Alejandro
Lakhani, Sunil R.
Brown, Michael P.
Khanna, Kum Kum
Title Breast cancer stem cells: Treatment resistance and therapeutic opportunities
Journal name Carcinogenesis   Check publisher's open access policy
ISSN 0143-3334
1460-2180
Publication date 2011-05-01
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1093/carcin/bgr028
Open Access Status DOI
Volume 32
Issue 5
Start page 650
End page 658
Total pages 9
Place of publication Oxford, England, U.K.
Publisher Oxford University Press
Language eng
Subject 1306 Cancer Research
Abstract The clinical and pathologic heterogeneity of human breast cancer has long been recognized. Now, molecular profiling has enriched our understanding of breast cancer heterogeneity and yielded new prognostic and predictive information. Despite recent therapeutic advances, including the HER2-specific agent, trastuzumab, locoregional and systemic disease recurrence remain an ever-present threat to the health and well being of breast cancer survivors. By definition, disease recurrence originates from residual treatment-resistant cells, which regenerate at least the initial breast cancer phenotype. The discovery of the normal breast stem cell has reignited interest in the identity and properties of breast cancer stem-like cells and the relationship of these cells to the repopulating ability of treatment-resistant cells. The cancer stem cell model of breast cancer development contrasts with the clonal evolution model, whereas the mixed model draws on features of both. Although the origin and identity of breast cancer stem-like cells is contentious, treatment-resistant cells survive and propagate only because aberrant and potentially druggable signaling pathways are recruited. As a means to increase the rates of breast cancer cure, several approaches to specific targeting of the treatment-resistant cell population exist and include methods for addressing the problem of radioresistance in particular.
Keyword Tumor-initiating cells
Dependent protein-kinase
Epithelial-mesenchymal transition
Dna-damage repair
Carcinoma in-situ
Aldehyde dehydrogenase
Prospective identification
Prognostic-significance
Clinical-implications
Luminal progenitors
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: UQ Centre for Clinical Research Publications
Official 2012 Collection
School of Medicine Publications
 
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