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• W2058261521 startingPage "1036" @default.
• W2058261521 abstract "We among others have recently demonstrated that normal cells produce “fusion mRNAs”. These fusion mRNAs do not derive from rearranged genomic loci, but rather they are derived from “early-terminated transcripts” (ETTs). Premature transcriptional termination takes place in intronic sequences that belong to “breakpoint cluster regions”. One important property of ETTs is that they exhibit an unsaturated splice donor site. This results in: (1) splicing to “cryptic exons” present in the final intron; (2) Splicing to another transcript of the same gene (intragenic trans-splicing), resulting in “exon repetitions”; (3) splicing to a transcript of another gene (intergenic trans-splicing), leading to “non-genomically encoded fusion transcripts” (NGEFTs). These NGEFTs bear the potential risk to influence DNA repair processes, since they share identical nucleotides with their DNA of origin, and thus, could be used as “guidance RNA” for DNA repair processes. Here, we present experimental data about four other genes. Three of them are associated with hemato-malignancies (ETV6, NUP98 and RUNX1), while one is associated with solid tumors (EWSR1). Our results demonstrate that all genes investigated so far (MLL, AF4, AF9, ENL, ELL, ETV6, NUP98, RUNX1 and EWSR1) display ETTs and produce transpliced mRNA species, indicating that this is a genuine property of translocating genes." @default.
• W2058261521 created "2016-06-24" @default.
• W2058261521 creator A5035899357 @default.
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• W2058261521 date "2012-10-18" @default.
• W2058261521 modified "2023-10-06" @default.
• W2058261521 title "Do Non-Genomically Encoded Fusion Transcripts Cause Recurrent Chromosomal Translocations?" @default.
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• W2058261521 doi "https://doi.org/10.3390/cancers4041036" @default.
• W2058261521 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3712730" @default.
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