title: Main roads to melanoma.
abstract: The characterization of the molecular mechanisms involved in development and progression of melanoma could be helpful to identify the molecular profiles underlying aggressiveness, clinical behavior, and response to therapy as well as to better classify the subsets of melanoma patients with different prognosis and/or clinical outcome. Actually, some aspects regarding the main molecular changes responsible for the onset as well as the progression of melanoma toward a more aggressive phenotype have been described. Genes and molecules which control either cell proliferation, apoptosis, or cell senescence have been implicated. Here we provided an overview of the main molecular changes underlying the pathogenesis of melanoma. All evidence clearly indicates the existence of a complex molecular machinery that provides checks and balances in normal melanocytes. Progression from normal melanocytes to malignant metastatic cells in melanoma patients is the result of a combination of down- or up-regulation of various effectors acting on different molecular pathways.
authors.affiliation: Istituto di Chimica Biomolecolare, Consiglio Nazionale delle Ricerche (CNR), Sassari, Italy. gpalmieri@yahoo.com
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Palmieri
authors.forename: Mariaelena
authors.initials: M
authors.lastname: Capone
authors.forename: Maria Libera
authors.initials: ML
authors.lastname: Ascierto
authors.forename: Giusy
authors.initials: G
authors.lastname: Gentilcore
authors.forename: David F
authors.initials: DF
authors.lastname: Stroncek
authors.forename: Milena
authors.initials: M
authors.lastname: Casula
authors.forename: Maria Cristina
authors.initials: MC
authors.lastname: Sini
authors.forename: Marco
authors.initials: M
authors.lastname: Palla
authors.forename: Nicola
authors.initials: N
authors.lastname: Mozzillo
authors.forename: Paolo A
authors.initials: PA
authors.lastname: Ascierto
mesh_terms: D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000473:pathology; D051358:Cyclin-Dependent Kinase 4 / Q000235:genetics / Q000378:metabolism; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics / Q000378:metabolism; D018450:Disease Progression; D006801:Humans; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism; D008545:Melanoma / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D051739:Microphthalmia-Associated Transcription Factor / Q000235:genetics / Q000378:metabolism; D009362:Neoplasm Metastasis; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000378:metabolism; D051059:PTEN Phosphohydrolase / Q000235:genetics / Q000378:metabolism; D048493:Proto-Oncogene Proteins B-raf / Q000235:genetics / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D012878:Skin Neoplasms / Q000209:etiology / Q000473:pathology / Q000503:physiopathology
chemical_list: D019941:Cyclin-Dependent Kinase Inhibitor p16; D007527:Isoenzymes; C497234:MITF protein, human; D051739:Microphthalmia-Associated Transcription Factor; D019001:Nitric Oxide Synthase; C482119:BRAF protein, human; D048493:Proto-Oncogene Proteins B-raf; D051057:Proto-Oncogene Proteins c-akt; C495900:CDK4 protein, human; D051358:Cyclin-Dependent Kinase 4; D051059:PTEN Phosphohydrolase