Molecular alterations at chromosome 9p21 in melanocytic nevi and melanoma
| Autor: | Paolo A. Ascierto, P. Baldinu, Antonio Muggiano, Annalisa Cossu, Gerardo Botti, Giuseppe Palmieri, Stefania D'Atri, Antonella Manca, Francesco Cremona, Milena Casula, Maria Cristina Sini, Amelia Lissia, Grazia Palomba, Marilena Budroni, Francesco Tanda |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2008 |
| Předmět: |
Adult
Male Pathology medicine.medical_specialty Skin Neoplasms Loss of Heterozygosity p16CDKN2A protein expression Locus (genetics) Dermatology Biology medicine.disease_cause chromosome 9p21 Loss of heterozygosity CDKN2A medicine Humans Nevus Melanoma neoplasms In Situ Hybridization Fluorescence Aged Aged 80 and over Nevus Pigmented medicine.diagnostic_test melanomagenesis Genes p16 Middle Aged Melanocytic nevus medicine.disease Italy Cancer research Female Chromosomes Human Pair 9 Carcinogenesis FISH analysis Fluorescence in situ hybridization |
| Zdroj: | British journal of dermatology (1951. Print) 158 (2008): 243–250. doi:10.1111/j.1365-2133.2007.08310.x info:cnr-pdr/source/autori:Sini MC; Manca A; Cossu A; Budroni M; Botti G; Ascierto PA; Cremona F; Muggiano A; D'Atri S; Casula M; Baldinu P; Palomba G; Lissia A; Tanda F; Palmieri G./titolo:Molecular alterations at chromosome 9p21 in melanocytic nevi and melanoma./doi:10.1111%2Fj.1365-2133.2007.08310.x/rivista:British journal of dermatology (1951. Print)/anno:2008/pagina_da:243/pagina_a:250/intervallo_pagine:243–250/volume:158 |
| Popis: | Summary Background The chromosome 9p21 and its CDKN locus, with the p16 tumour suppressor gene (CDKN2A), are recognized as the genomic regions involved in the pathogenesis of melanoma. Objectives To elucidate further the role of such regions during the different phases of melanocytic tumorigenesis. Methods Tissue sections from naevi, primary and metastatic melanomas were investigated by fluorescence in situ hybridization for allelic loss at the 9p21 chromosome and by immunochemistry for p16CDKN2A expression. Results Dysplastic naevi and primary or secondary melanomas were found to carry hemizygous deletions within the entire 9p21 region at similar frequencies (varying from 55% to 62%). Allelic deletion spanning the CDKN locus was observed at significantly increased rates moving from early (7%) to advanced (28%) primary melanomas and to secondary melanoma lesions (37%) (P = 0·018). Also, inactivation of the p16 gene (CDKN2A) was absent in naevi and present at steadily increasing rates moving from primary melanomas (7% early lesions to 17% advanced lesions) to melanoma metastases (62%) (P = 0·004). Conclusions Our findings indicate that, in a model of sequential accumulation of genetic alterations, 9p21 deletions may play a role in melanocytic transformation and tumour initiation whereas rearrangements at the CDKN locus, and p16 gene (CDKN2A) inactivation may contribute to tumour progression. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|