Hypermethylation of RAD9A intron 2 in childhood cancer patients, leukemia and tumor cell lines suggest a role for oncogenic transformation

Abstract: Most childhood cancers occur sporadically and cannot be explained by an inherited mutation or an unhealthy lifestyle. However, risk factors might trigger the oncogenic transformation of cells. Among other regulatory signals, hypermethylation of RAD9A intron 2 is responsible for the increased expression of RAD9A protein, which may play a role in oncogenic transformation. Here, we analyzed the RAD9A intron 2 methylation in primary fibroblasts of 20 patients with primary cancer in childhood and second primary cancer (2N) later in life, 20 matched patients with only one primary cancer in childhood (1N) and 20 matched cancer-free controls (0N), using bisulfite pyrosequencing and deep bisulfite sequencing (DBS). Four 1N patients and one 2N patient displayed elevated mean methylation levels (³10 %) of RAD9A. DBS revealed ³2 % hypermethylated alleles of RAD9A, indicative for constitutive mosaic epimutations. Bone marrow samples of NHL and AML tumor patients (n=74), EBV (Epstein Barr Virus).... https://www.excli.de/index.php/excli/article/view/4482

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• Standort: Deutsche Nationalbibliothek Frankfurt am Main
• Umfang: Online-Ressource
• Sprache: Englisch

Verweise und Beziehungen

• Erschienen in: Hypermethylation of RAD9A intron 2 in childhood cancer patients, leukemia and tumor cell lines suggest a role for oncogenic transformation ; volume:21 ; day:07 ; month:01 ; year:2022 ; EXCLI journal ; 21 (07.01.2022)

Beteiligte, Orts- und Zeitangaben

• Urheber: Galetzka, Danuta ; Böck, Julia ; Wagner, Lukas ; Dittrich, Marcus ; Sinizyn , Olesja ; Ludwig, Marco ; Rossmann, Heidi ; Spix, Claudia ; Radsak, Markus ; Scholz-Kreisel, Peter ; Mirsch, Johanna ; Linke, Matthias ; Brenner, Walburgis ; Marron, Manuela ; Poplawski, Alicia ; Haaf, Thomas ; Schmidberger, Heinz ; Prawitt, Dirk

Weitere Informationen

• DOI: 10.17179/excli2021-4482
• URN: urn:nbn:de:101:1-2022020402131164050523
• Rechteinformation: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.