Abstract
The discovery of cancer stem cells (CSCs) in human solid tumors has allowed a better understanding of the biology and neoplastic transformation of normal melanocytes, and the possible mechanisms by which melanoma cells acquire tumorigenicity. In this review I summarize the literature findings on the potential biomarkers of melanoma CSCs, their presence in the melanoma cell populations, the interaction with the immune system (with both T and NK cells) and the role of melanoma CSCs in the clinics. Given the extraordinary progress in the therapy of melanoma caused by immune checkpoint antibodies blockade, I discuss how these antibodies can work by the activation of melanoma infiltrating T cells specifically recognizing neo-antigens expressed even by melanoma CSCs. This is the mechanism that can induce a regression of the metastatic melanomas.
Highlights
Melanoma cancer stem cells (CSCs)Between 1995–2010 many studies reported the presence of a particular subpopulation of cancer cells characterized by self-renewability and the capacity to initiate, replenish and expand human tumors
Italian Network for Bioimmunotherapy of Tumors, Division of Medical Oncology and Immunotherapy, Academic Editor: Vita Golubovskaya
Our group and that of other investigators demonstrated that cancer stem cells (CSCs) from melanoma and from other human solid tumors can activate several mechanisms that allow them to survive in a hostile micro-environment and escape the patient’s immune reactions as it may occur with other tumors like glioblastoma and colorectal cancer [23,24]
Summary
Between 1995–2010 many studies reported the presence of a particular subpopulation of cancer cells characterized by self-renewability and the capacity to initiate, replenish and expand human tumors. Like CSCs of other neoplasms, melanoma CSCs have been shown to express a variety of antigens (including differentiation and cancer testis antigens) known to be recognized by T cells (e.g., MelanA/Mart, HMB45, tyrosinase, gp100, NYESO1) [18,19]. Our group and that of other investigators demonstrated that CSCs from melanoma and from other human solid tumors can activate several mechanisms that allow them to survive in a hostile micro-environment and escape the patient’s immune reactions as it may occur with other tumors like glioblastoma and colorectal cancer [23,24]. NK cells according to the differential expression of some markers (e.g., CD133, CD117, CD271) [23,24,25,26]
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