Cutaneous melanoma is mostly diagnosed at an early stage of disease and, although its incidence is continuously increasing in the population from western countries, it can be effectively treated by surgical excision [1]. Conversely, a large fraction of advanced stages remains refractory to systemic therapies [2]. Despite the impressive advancements into the treatment of the disease during the recent past years, clinical outcomes are still hardly predictable in melanoma patients due to the marked heterogeneity of the disease from the biological and molecular point of view [3, 4]. Therefore, the need to obtain a classification of the various tumor subtypes with distinct genetic and molecular characteristics becomes mandatory, definitively overcoming the concept according to which melanoma—as for all cancer subtypes—can be considered a single disease. Given the central role of protein kinases in mediating different cell pathways, it is not surprising that aberrant kinase activity is a common feature of cancer cells and that kinase inhibitors are used and researched as anticancer therapies, including melanoma [5]. When constitutively activated, some kinases can be oncogenic and directly drive tumor growth, while other kinases can play an indirect role, acting as regulators of oncogenic intracellular signals or promoting extracellular effects into the tumor microenvironment such as the induction of angiogenesis or mechanisms for invasion and immune escape [6, 7]. From the genetic point of view, the pathogenesis of melanoma—like all other forms of malignant neoplasms—is based on the acquisition of sequential alterations affecting specific chromosome loci and genes involved in metabolic and molecular pathways controlling all such cellular homeostasis mechanisms [8, 9]. In other words, melanoma pathogenesis and, more in general, tumorigenesis may be actually considered as due to a process of sequential accumulation of mutations and changes in specific genes and DNA regions [8, 9].
Molecular landscape profile of melanoma
Colombino M.;Casula M.;Sini M. C.;Manca A.;Pisano M.;
2021
Abstract
Cutaneous melanoma is mostly diagnosed at an early stage of disease and, although its incidence is continuously increasing in the population from western countries, it can be effectively treated by surgical excision [1]. Conversely, a large fraction of advanced stages remains refractory to systemic therapies [2]. Despite the impressive advancements into the treatment of the disease during the recent past years, clinical outcomes are still hardly predictable in melanoma patients due to the marked heterogeneity of the disease from the biological and molecular point of view [3, 4]. Therefore, the need to obtain a classification of the various tumor subtypes with distinct genetic and molecular characteristics becomes mandatory, definitively overcoming the concept according to which melanoma—as for all cancer subtypes—can be considered a single disease. Given the central role of protein kinases in mediating different cell pathways, it is not surprising that aberrant kinase activity is a common feature of cancer cells and that kinase inhibitors are used and researched as anticancer therapies, including melanoma [5]. When constitutively activated, some kinases can be oncogenic and directly drive tumor growth, while other kinases can play an indirect role, acting as regulators of oncogenic intracellular signals or promoting extracellular effects into the tumor microenvironment such as the induction of angiogenesis or mechanisms for invasion and immune escape [6, 7]. From the genetic point of view, the pathogenesis of melanoma—like all other forms of malignant neoplasms—is based on the acquisition of sequential alterations affecting specific chromosome loci and genes involved in metabolic and molecular pathways controlling all such cellular homeostasis mechanisms [8, 9]. In other words, melanoma pathogenesis and, more in general, tumorigenesis may be actually considered as due to a process of sequential accumulation of mutations and changes in specific genes and DNA regions [8, 9].I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
