Pregledni rad
The Role of Apoptosis in the Pathogenesis of Malignant Melanoma
Liborija Lugović Mihić
; Department of Dermatology and Venereology, University Hospital »Sestre Milosrdnice«, Zagreb, Croatia
Vedrana Bulat
; Department of Dermatology and Venereology, University Hospital »Sestre Milosrdnice«, Zagreb, Croatia
Mirna Šitum
; Department of Dermatology and Venereology, University Hospital »Sestre Milosrdnice«, Zagreb, Croatia
Iva Krolo
; Department of Dermatology and Venereology, University Hospital »Sestre Milosrdnice«, Zagreb, Croatia
Ana Šešerko
; Department of Dermatology and Venereology, University Hospital »Sestre Milosrdnice«, Zagreb, Croatia
Sažetak
Malignant melanoma genesis is a very complex process that involves a sequence of pathogenetic cellular events. Mutation of various genes and numerous other cellular mechanisms play an important role in the course of malignant melanocyte alteration and their malignant transformation from naevi into melanoma. Apoptosis is an active, genetically controlled process of programmed cell death, which leads to cell destruction and cell death without involvement of surrounding cells or inflammatory response. In this process, disrupted mechanisms of cell regulation and apoptosis take place in malignant melanoma cells, thus leading to their uncontrolled proliferation and melanocyte growth. Apoptosis is a process that involves two major pathways, the intrinsic and extrinsic apoptotic pathway, which interlace at certain points and ultimately result in apoptosis. It can be said that molecular events regulating cell survival, nomal growth arrest, apoptosis and cell differentiation, contribute to the overall pathogenesis of malignant cell growth. It is presumed that in the future, understanding of molecular aberrations and cellular processes, such as cell signaling, cell cycle regulation and cell apoptosis, will be essential for better patient monitoring and rational design of effective treatment.
Ključne riječi
apoptosis; melanoma; pathogenesis; caspase; oncogene
Hrčak ID:
51681
URI
Datum izdavanja:
20.4.2010.
Posjeta: 1.086 *