Multiple genetic alterations in malignant metastatic insulinomas (CROSBI ID 113943)
Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija
Podaci o odgovornosti
Pavelić, Krešimir ; Hrašćan, Reno ; Kapitanović, Sanja ; Karapandža, Nikola ; Vraneš, S. ; Belicza, Mladen ; Krušlin, Božidar ; Čabrijan, Tomislav
engleski
Multiple genetic alterations in malignant metastatic insulinomas
Proto-oncogenes, growth factors/receptors, and tumour suppressor genes were analysed in malignant metastatic insulinomas. Normal pancreas showed only a moderate immunoreaction for c-myc proto-oncogene and a strong reaction for insulin. Benign insulinomas were slightly or moderately positive for transforming growth factor a (TGF alpha), weakly positive for epidermal growth factor receptor (EGF-R), and strongly positive for c-myc and insulin. In malignant insulinomas, besides a strong immunoreaction for c-myc and TGF alpha, activation of c-K-ras and overexpression of p53 protein were found. Insulin reaction was moderate or strong. Three out of six malignant insulinomas displayed a c-g-ras point mutation at codon 12. All mutations were guanine to cytosine transversion, resulting in amino acid substitution, glycine to arginine. Mutations were present in metastatic insulinomas only. Patients with mutated c-g-ras oncogene had overexpression of p53 protein as well as c-myc and TGF alpha overexpression. Our results support the view that malignant progression is a consequence of more than one genetic lesion and suggest that activation of myc, TGF alpha, and ras genes plays a role in a multistep process of tumour progression, perhaps serving as an initiating event.
insulinoma ; genetic alterations ; oncogenes
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
Podaci o izdanju
Povezanost rada
Temeljne medicinske znanosti, Kliničke medicinske znanosti