Evidence map›Paper›PMID 26325506›Full record

ArticleOncotarget2015

Dissecting tRNA-derived fragment complexities using personalized transcriptomes reveals novel fragment classes and unexpected dependencies.

Aristeidis G Telonis, Phillipe Loher, Shozo Honda, Yi Jing, Juan Palazzo, Yohei Kirino, Isidore Rigoutsos

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

134 citing papers in PubMed, 1 synthesis or guideline pooled it, 194 citations in OpenAlex.

  1. Pooled it
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  11. Unlocking the role of tRNA-derived fragments in shaping breast cancer signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
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74 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Aristeidis G TelonisComputational Medicine Center, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA, USA.
Phillipe LoherComputational Medicine Center, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA, USA.
Shozo HondaComputational Medicine Center, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA, USA.
Yi JingComputational Medicine Center, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA, USA.
Juan PalazzoDepartment of Pathology Anatomy and Cell Biology, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA, USA.
Yohei KirinoComputational Medicine Center, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA, USA.
Isidore RigoutsosComputational Medicine Center, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA, USA.
Thomas Jefferson University · US

Funding

piRNA biogenesis ruled by PIWI-TUDOR interactionR01GM106047 · NIGMS · THOMAS JEFFERSON UNIVERSITY · PI KIRINO, YOHEI · 2013 to 2022
$2.8M
NIGMS NIH HHS GM106047NIGMS NIH HHS R01 GM106047
6 · The paper itself

Abstract

We analyzed transcriptomic data from 452 healthy men and women representing five different human populations and two races, and, 311 breast cancer samples from The Cancer Genome Atlas. Our studies revealed numerous constitutive, distinct fragments with overlapping sequences and quantized lengths that persist across dozens of individuals and arise from the genomic loci of all nuclear and mitochondrial human transfer RNAs (tRNAs). Surprisingly, we discovered that the tRNA fragments' length, starting and ending points, and relative abundance depend on gender, population, race and also on amino acid identity, anticodon, genomic locus, tissue, disease, and disease subtype. Moreover, the length distribution of mitochondrially-encoded tRNAs differs from that of nuclearly-encoded tRNAs, and the specifics of these distributions depend on tissue. Notably, tRNA fragments from the same anticodon do not have correlated abundances. We also report on a novel category of tRNA fragments that significantly contribute to the differences we observe across tissues, genders, populations, and races: these fragments, referred to as i-tRFs, are abundant in human tissues, wholly internal to the respective mature tRNA, and can straddle the anticodon. HITS-CLIP data analysis revealed that tRNA fragments are loaded on Argonaute in a cell-dependent manner, suggesting cell-dependent functional roles through the RNA interference pathway. We validated experimentally two i-tRF molecules: the first was found in 21 of 22 tested breast tumor and adjacent normal samples and was differentially abundant between health and disease whereas the second was found in all eight tested breast cancer cell lines.

Indexed as

Gene Expression RegulationAnticodonBase SequenceBreast NeoplasmsCell LineCell Line, TumorCluster AnalysisFemaleGenetic VariationHumansMaleMCF-7 CellsModels, GeneticMolecular Sequence DataNucleic Acid ConformationRNAAnticodonRNARNA, MitochondrialRNA, TransferArgonautehuman genomemitochondrial tRNAnuclear tRNAtRNA fragment

Identifiers

PMID26325506
PMCPMC4694795
OpenAlexW2117147211

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.