Abstract
For the first time new treatments in melanoma have produced significant responses in advanced diseases, but 30-90% of melanoma patients do not respond or eventually relapse after the initial response to the current treatments. The resistance of these melanomas is likely due to tumor heterogeneity, which may be explained by models such as the stochastic, hierarchical, and phenotype-switching models. This review will discuss the recent advancements in targeting BCL-2 family members for cancer treatments, and how this approach can be applied as an alternative option to combat melanoma, and overcome melanoma relapse or resistance in current treatment regimens.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Antineoplastic Agents / administration & dosage
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Apoptosis / drug effects*
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Apoptosis / genetics
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Complementary Therapies / methods
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Drug Resistance, Neoplasm
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Female
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Humans
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Male
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Melanoma / drug therapy*
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Melanoma / genetics
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Melanoma / mortality
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Molecular Targeted Therapy / methods*
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Neoplasm Recurrence, Local / prevention & control
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Neoplastic Stem Cells / drug effects*
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Prognosis
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Proto-Oncogene Proteins c-bcl-2 / drug effects*
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Risk Assessment
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Skin Neoplasms / drug therapy*
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Skin Neoplasms / genetics
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Skin Neoplasms / mortality
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Survival Analysis
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Treatment Outcome
Substances
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Antineoplastic Agents
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Proto-Oncogene Proteins c-bcl-2