Intercellular crosstalk in human malignant melanoma
Jazyk angličtina Země Rakousko Médium print-electronic
Typ dokumentu časopisecké články, přehledy
PubMed
27807664
DOI
10.1007/s00709-016-1038-z
PII: 10.1007/s00709-016-1038-z
Knihovny.cz E-zdroje
- Klíčová slova
- Cancer-associated fibroblast, Cytokine, Keratinocyte, Melanocyte, Melanoma cells, Melanoma ecosystem,
- MeSH
- antitumorózní látky terapeutické užití MeSH
- časná detekce nádoru metody MeSH
- crista neuralis cytologie patologie MeSH
- indoly terapeutické užití MeSH
- keratinocyty MeSH
- lidé MeSH
- maligní melanom kůže MeSH
- melanocyty patologie MeSH
- melanom farmakoterapie epidemiologie patologie MeSH
- nádorové mikroprostředí fyziologie MeSH
- nádory kůže MeSH
- sulfonamidy terapeutické užití MeSH
- ultrafialové záření škodlivé účinky MeSH
- vemurafenib MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- antitumorózní látky MeSH
- indoly MeSH
- sulfonamidy MeSH
- vemurafenib MeSH
Incidence of malignant melanoma is increasing globally. While the initial stages of tumors can be easily treated by a simple surgery, the therapy of advanced stages is rather limited. Melanoma cells spread rapidly through the body of a patient to form multiple metastases. Consequently, the survival rate is poor. Therefore, emphasis in melanoma research is given on early diagnosis and development of novel and more potent therapeutic options. The malignant melanoma is arising from melanocytes, cells protecting mitotically active keratinocytes against damage caused by UV light irradiation. The melanocytes originate in the neural crest and consequently migrate to the epidermis. The relationship between the melanoma cells, the melanocytes, and neural crest stem cells manifests when the melanoma cells are implanted to an early embryo: they use similar migratory routes as the normal neural crest cells. Moreover, malignant potential of these melanoma cells is overdriven in this experimental model, probably due to microenvironmental reprogramming. This observation demonstrates the crucial role of the microenvironment in melanoma biology. Indeed, malignant tumors in general represent complex ecosystems, where multiple cell types influence the growth of genetically mutated cancer cells. This concept is directly applicable to the malignant melanoma. Our review article focuses on possible strategies to modify the intercellular crosstalk in melanoma that can be employed for therapeutic purposes.
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