Journal
PIGMENT CELL & MELANOMA RESEARCH
Volume 21, Issue 1, Pages 39-55Publisher
WILEY
DOI: 10.1111/j.1755-148X.2007.00427.x
Keywords
melanoma; cancer stem cells; tumorigenicity; self-renewal; differentiation; progression; chemoresistance
Categories
Funding
- NCI NIH HHS [R01 CA113796-03, P50 CA093683-06A2, P50 CA093683, R01 CA113796-02, P50 CA093683-08, R01 CA113796-05, R01 CA113796-01A1, R01 CA113796-04, 1R01CA113796-01A1, 2P50CA093683-05S2, P50 CA093683-07, R01 CA113796] Funding Source: Medline
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Cancer stem cells (CSC) have been identified in hematological malignancies and several solid cancers. Similar to physiological stem cells, CSC are capable of self-renewal and differentiation and have the potential for indefinite proliferation, a function through which they may cause tumor growth. Although conventional anti-cancer treatments might eradicate most malignant cells in a tumor, they are potentially ineffective against chemoresistant CSC, which may ultimately be responsible for recurrence and progression. Human malignant melanoma is a highly aggressive and drug-resistant cancer. Detection of tumor heterogeneity, undifferentiated molecular signatures, and increased tumorigenicity of melanoma subsets with embryonic-like differentiation plasticity strongly suggest the presence and involvement of malignant melanoma stem cells (MMSC) in the initiation and propagation of this malignancy. Here, we review these findings in the context of functional properties ascribed to melanocyte stem cells and CSC in other cancers. We discuss the association of deregulated signaling pathways, genomic instability, and vasculogenic mimicry phenomena observed in melanoma sub-populations in light of the CSC concept. We propose that a subset of MMSC may be responsible for melanoma therapy-resistance, tumor invasiveness, and neoplastic progression and that targeted abrogation of a MMSC compartment could therefore ultimately lead to stable remissions and perhaps cures of metastatic melanoma.
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