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- W2318562854 abstract "Melanoma patients develop resistance to both chemotherapy and targeted-therapy drugs. Promising preclinical and clinical results with immune checkpoint inhibitors using antibodies directed against cytotoxic T-lymphocyte-associated protein 4 and programmed cell death protein 1 have re-energized the field of immune-based therapies in melanoma. However, similar to chemotherapy or targeted therapies, immune checkpoint blockade responds in only subsets of melanoma patients. A number of factors, including gene mutations, altered cell-signaling pathways and tumor heterogeneity can contribute to therapy resistance. Recent studies have highlighted the role of inflammatory tumor microenvironment on therapy resistance of cancer cells. Cancer cells either alone or in conjunction with the tumor stroma can contribute to an inflammatory microenvironment. Multimodal approaches of targeting the tumor microenvironment, in addition to malignant cells, may be necessary for better therapy responses." @default.
- W2318562854 created "2016-06-24" @default.
- W2318562854 creator A5012401963 @default.
- W2318562854 creator A5073284900 @default.
- W2318562854 creator A5087868960 @default.
- W2318562854 date "2016-03-01" @default.
- W2318562854 modified "2023-10-03" @default.
- W2318562854 title "The role of tumor microenvironment in melanoma therapy resistance" @default.
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- W2318562854 doi "https://doi.org/10.2217/mmt.15.37" @default.
- W2318562854 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6094607" @default.
- W2318562854 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30190870" @default.
- W2318562854 hasPublicationYear "2016" @default.
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