Recent advances in melanoma research.
At the end of the last decade, sporadic melanomas were still considered a genetic black box. Fortunately, in the last few years the box has been opened bringing to light melanoma-relevant oncogenes, aberrant signal transduction pathways, critical alterations in the melanoma cell cycle that go beyond p16INK4a, and melanoma- microenvironment interactions that are essential for tumor progression. This review will discuss some of the latest findings in melanoma research including the critical role of the MAPK pathway in the genesis of melanoma and senescence of nevi, the paradoxical tumor suppressor and oncogenic activities of the transcription factor MITF, and the unexpected oncogenic activities of the low molecular weight forms of cyclin E.
Reed
Jon A
JA
Department of Pathology, Baylor College of Medicine, Houston, TX 77030, USA.
Medrano
Estela E
EE
D002453:Cell Cycle; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000502:physiology; D044127:Epigenesis, Genetic; D052138:Genes, Neoplasm; D005838:Genotype; D006801:Humans; D008545:Melanoma / Q000201:enzymology* / Q000235:genetics / Q000503:physiopathology*; D051739:Microphthalmia-Associated Transcription Factor / Q000502:physiology*; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism*; D009154:Mutation; D010641:Phenotype; D015398:Signal Transduction; D012878:Skin Neoplasms / Q000201:enzymology* / Q000235:genetics / Q000503:physiopathology*
D019941:Cyclin-Dependent Kinase Inhibitor p16; D051739:Microphthalmia-Associated Transcription Factor; D020929:Mitogen-Activated Protein Kinase Kinases