ArticlePloS one2018
Very long intergenic non-coding RNA transcripts and expression profiles are associated to specific childhood acute lymphoblastic leukemia subtypes.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 24 citations in OpenAlex.
- Epigenetic control of chromosome-associated lncRNA genes essential for replication and stability.Nature communications · 2022Article
- Linear and Circular Long Non-Coding RNAs in Acute Lymphoblastic Leukemia: From Pathogenesis to Classification and Treatment.International journal of molecular sciences · 2022Review
- Mammalian DNA Replication Timing.Cold Spring Harbor perspectives in biology · 2021Review
- Very long intergenic non-coding (vlinc) RNAs directly regulate multiple genes in cis and trans.BMC biology · 2021Article
- Complex Age- and Cancer-Related Changes in Human Blood Transcriptome-Implications for Pan-Cancer Diagnostics.Frontiers in genetics · 2021Article
- Reciprocal monoallelic expression of ASAR lncRNA genes controls replication timing of human chromosome 6.RNA (New York, N.Y.) · 2020Article
- A CRISPR/Cas13-based approach demonstrates biological relevance of vlinc class of long non-coding RNAs in anticancer drug response.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Very long intergenic non-coding RNAs (vlincRNAs) are a novel class of long transcripts (~50 kb to 1 Mb) with cell type- or cancer-specific expression. We report the discovery and characterization of 256 vlincRNAs from a cohort of 64 primary childhood pre-B and pre-T acute lymphoblastic leukemia (cALL) samples, of which 61% are novel and specifically expressed in cALL. Validation was performed in 35 pre-B and pre-T cALL primary samples. We show that their expression is cALL immunophenotype and molecular subtype-specific and correlated with epigenetic modifications on their promoters, much like protein-coding genes. While the biological functions of these vlincRNAs are still unknown, our results suggest they could play a role in cALL etiology or progression.
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Registered trials
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