3′ tRNA‐derived fragments (3′ tRFs) are important epigenetic regulators in normal and pathological conditions. In this study, we aimed to explore the potential value of a 3′ tRF as a prognostic and/or screening biomarker for B‐cell chronic l...
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https://www.riss.kr/link?id=O106690230
2021년
-
0902-4441
1600-0609
SCI;SCIE;SCOPUS
학술저널
821-830 [※수록면이 p5 이하이면, Review, Columns, Editor's Note, Abstract 등일 경우가 있습니다.]
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
3′ tRNA‐derived fragments (3′ tRFs) are important epigenetic regulators in normal and pathological conditions. In this study, we aimed to explore the potential value of a 3′ tRF as a prognostic and/or screening biomarker for B‐cell chronic l...
3′ tRNA‐derived fragments (3′ tRFs) are important epigenetic regulators in normal and pathological conditions. In this study, we aimed to explore the potential value of a 3′ tRF as a prognostic and/or screening biomarker for B‐cell chronic lymphocytic leukemia (B‐CLL).
Publicly available next‐generation sequencing data from 20 B‐CLL cases were analyzed, followed by prediction of targets of the most abundantly and ubiquitously expressed 3′ tRFs, leading to selection of tRF‐LeuAAG/TAG. PBMCs were isolated from blood samples of 91 B‐CLL patients and 43 non‐leukemic donors, followed by total RNA extraction, in‐vitro polyadenylation, and first‐strand cDNA synthesis. Next, a real‐time quantitative PCR (qPCR) assay was developed for the accurate quantification of tRF‐LeuAAG/TAG and applied in all samples, prior to biostatistical analysis.
High tRF‐LeuAAG/TAG levels are associated with inferior overall survival (OS) of B‐CLL patients. The unfavorable significance of tRF‐LeuAAG/TAG was independent of established prognostic factors in B‐CLL. Stratified Kaplan‐Meier OS analysis uncovered the unfavorable prognostic role of high tRF‐LeuAAG/TAG levels for patients in Binet A or Rai I stage, negative CD38 expression, mutated, or unmutated IGHV genomic locus.
Our approach revealed the independent prognostic value of a particular 3′ tRF, derived from tRNALeuAAG and tRNALeuTAG (tRF‐LeuAAG/TAG) in B‐CLL.
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