Promoter hypermethylation of multiple genes in astrocytic gliomas.

摘要: Promoter hypermethylation represents a primary mechanism in the inactivation of tumor suppressor genes during tumorigenesis. To determine frequency and timing carcinogenesis astrocytic tumors, we analysed promoter methylation status ten tumor-associated (MGMT, GSTPI, DAPK, p14 ARF , THBS1, TIMP-3, p73, p16 INK4A RBI TP53) series 88 gliomas, including 24 diffuse astrocytomas; 21 anaplastic astrocytomas, 43 glioblastomas (33 10 secondary), as well two non-neoplastic brain samples, by methylation-specific PCR. Aberrant CpG island was detected all analysed, but one sample displayed anomalies at least gene. The index (number methylated genes/total analysed) 0.3, 0.38, 0.33 0.29 for astrocytomas secondary glioblastomas, respectively. Some differences may be established regarding profiles specific types: MGMT, THBSI, appear hypermethylated low-grade tumors (at 45% cases), whereas GSTP1, are mostly changed 15-50% higher grade forms versus <10% tumors. variation also exists values p73 (10-40% cases) among groups. TP53 presented rates subtypes. Our findings thus suggest that common contributes to inactivating cancer-related neoplasms. This epigenetic change is, general, an early event development neoplasms this gene silencing late involving some loci.