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Prognostic Significance of iNOS in Human Melanoma

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Nitric Oxide (NO) and Cancer

Part of the book series: Cancer Drug Discovery and Development ((CDD&D))

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Abstract

Melanoma is the leading cause of death from skin cancer, particularly in young adults. Precise staging of melanoma progression is highly critical as even relatively small melanomas can metastasize and it is extremely difficult to treat once the tumor has metastasized beyond the locoregional area. Clinical and histological variables such as primary tumor invasion, ulceration, and lymph node status might be unsuccessful to identify early stage that will eventually progress to further stages of disease. Therefore, there is an urgent need to develop biomarkers that might help to identify patients with early-stage melanoma who are likely to develop advanced disease and would benefit from additional therapies. In recent years, molecular biology and the identification of molecular markers in melanoma have been a major focus for cancer researchers. Thus, for human melanoma, a growing number of molecular markers, including transcription factors, oncogene products, and loss of tumor suppressor molecules, have been proposed. Most human melanoma tumor cells are known to express the enzyme, inducible nitric oxide synthase (iNOS), which is responsible for cytokine-induced nitric oxide (NO) production in macrophages during immune responses. This constitutive expression of iNOS in many patients’ tumor cells, as well as its strong association with poor patient survival, has led to the consideration of iNOS as a molecular marker of poor prognosis, as well as a possible target for therapy. The mechanisms underlying the expression of iNOS expression and the molecular pathways affected by NO are currently active areas of research.

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Ekmekcioglu, S., Grimm, E.A. (2010). Prognostic Significance of iNOS in Human Melanoma. In: Bonavida, B. (eds) Nitric Oxide (NO) and Cancer. Cancer Drug Discovery and Development. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-1432-3_16

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