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DNA methylation status predicts survival in metastasis free clear cell renal cell carcinoma

ABSTRACT: DNA methylation status predicts survival in metastasis free clear cell renal cell carcinoma

PROVIDER: PRJNA453379 | ENA |

REPOSITORIES: ENA

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DNA methylation status predicts survival in metastasis free clear cell renal cell carcinoma

Project description:Background: Clear cell renal cell carcinomas (ccRCCs) display divergent clinical phenotypes. Up to one third of patients with local disease at diagnosis will progress. Therefore, it is a need to identify patients at risk for recurrence. In the present study, we analyzed genome-wide promoter DNA methylation at diagnosis in relation to clinicopathological parameters, in order to identify DNA methylation profiles associated with risk for progress. Method: DNA methylation status in 155,931 CpGs located in gene promoter regions was analyzed by Illumina HumanMethylation450K arrays in diagnostic tissue samples from 115 ccRCC patients. Methylation profiles were compared with genetic aberrations and clinicopathological parameters. Results: The tumors separated into two clusters based on genome-wide promoter methylation status. The tumors in these clusters differed in tumor diameter (p < 0.001), TNM stage (p < 0.001), morphological grade (p < 0.001), and patients outcome (5 year cancer specific survival (pCSS5yr) 72 % in cluster A vs 26 % in cluster B, p < 0.001). When metastasis-status (M0/M1) and cluster A/B status at diagnosis were combined, we found poor survival in M1 patients regardless of cluster A/B status (pCSS5yr 9 % vs 6 %). In M0 patients, the cluster status clearly separated in survival (pCSS5yr 81 % vs 17 %; p < 0.001). We identified a methylation profile of 398 CpGs that was associated with progress of disease, which included differently methylated CpG sites in the SMAD6, SOCS3 and MX2 genes. An integrated genomic and epigenomic analysis revealed significant correlations between the total number of genetic aberrations and hypermethylated CpGs (R = 0.435, p > 0.001), and predicted mitotic age (R = 0.407, p < 0.001). Conclusion: DNA methylation analysis at diagnosis in ccRCC has the potential to improve outcome-prediction and therapy stratification.

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Epigenetic signature predicts overall survival clear cell renal cell carcinoma.

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Genomic aberrations predicts survival in clear cell renal cell carcinoma

Project description:Detailed genetic profiling of clear cell Renal Cell Carcinoma (ccRCC) has shown that these tumors are characterized by large genetic heterogeneity with some genomic regions commonly affected by structural changes. Loss on chromosomes 3p and 14q, and gain on 5q and 7 are examples of alterations commonly reported in ccRCC. However, there is no consensus regarding the potential prognostic information carried by the identified alterations. We report on poorer outcome for patients with gain on 5q and 7, and loss on 9p, 9q and 14q. These aberrations were in addition found more frequently in metastasized tumors, suggesting that they are markers for advanced disease. Furthermore, the presence of M-bM-^IM-% 4 common aberrations was associated with decreased survival time. Shorter relative telomere length (RTL) has been associated with loss of chromosomal regions in ccRCC tumors, but we found no significant associations between tumor RTL and chromosomal deletions. However, significantly lower tumor-to-nontumor (T/N) RTL ratio was detected for patients with loss on 4q and 9p. Finally, we found a minimum region (MR) of genetic loss of 1.4 Mbp on chromosome 9p and this region contains only one gene, the tumor suppressor candidate 1 gene (TUSC1). TUSC1 has been implicated in lung carcinogenesis and our result further strengthens its role in tumorigenesis. Seventy-four ccRCC tumors and 22 paired normal kidney cortex and blood samples were genotyped on Illuminas HumanCytoSNP-12 bead chips.

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Genomic aberrations predicts survival in clear cell renal cell carcinoma

Project description:Detailed genetic profiling of clear cell Renal Cell Carcinoma (ccRCC) has shown that these tumors are characterized by large genetic heterogeneity with some genomic regions commonly affected by structural changes. Loss on chromosomes 3p and 14q, and gain on 5q and 7 are examples of alterations commonly reported in ccRCC. However, there is no consensus regarding the potential prognostic information carried by the identified alterations. We report on poorer outcome for patients with gain on 5q and 7, and loss on 9p, 9q and 14q. These aberrations were in addition found more frequently in metastasized tumors, suggesting that they are markers for advanced disease. Furthermore, the presence of ≥ 4 common aberrations was associated with decreased survival time. Shorter relative telomere length (RTL) has been associated with loss of chromosomal regions in ccRCC tumors, but we found no significant associations between tumor RTL and chromosomal deletions. However, significantly lower tumor-to-nontumor (T/N) RTL ratio was detected for patients with loss on 4q and 9p. Finally, we found a minimum region (MR) of genetic loss of 1.4 Mbp on chromosome 9p and this region contains only one gene, the tumor suppressor candidate 1 gene (TUSC1). TUSC1 has been implicated in lung carcinogenesis and our result further strengthens its role in tumorigenesis.

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