ArticleCancer letters2023
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Article in Cancer letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- PKA signaling modulates PRMT5/hnRNP A1-mediated IRES translation and dictates responses to mTOR inhibition in glioblastoma.Journal of neuro-oncology · 2026Article
- Integrated Analysis of the mTOR Signaling Pathway Mediated by the ORF3 Protein of Swine Hepatitis E Virus in HepG2 Cells via a circRNA-miRNA Network.Veterinary sciences · 2026Article
- Mechanisms and therapeutic potential of YTHDF readers: Linking epitranscriptomics to cancer.Journal of pharmaceutical analysis · 2026Review
- Epitranscriptomic analysis reveals clinical and molecular signatures in glioblastoma.Acta neuropathologica communications · 2025Article
- Exploring m6A modifications in gastric cancer: from molecular mechanisms to clinical applications.European journal of medical research · 2025Review
- The role of RNA methylation in glioma progression: mechanisms, diagnostic implications, and therapeutic value.Frontiers in immunology · 2025Review
- Spliceosomal vulnerability of MYCN-amplified neuroblastoma is contingent on PRMT5-mediated regulation of epitranscriptomic and metabolomic pathways.Cancer letters · 2024Article
- Decoding the epitranscriptome: a new frontier for cancer therapy and drug resistance.Cell communication and signaling : CCS · 2024Review
- Non-canonical translation in cancer: significance and therapeutic potential of non-canonical ORFs, mCell death discovery · 2024Review
- Small molecule inhibitors targeting mJournal of hematology & oncology · 2024Review
- Emerging Roles and Mechanisms of RNA Modifications in Neurodegenerative Diseases and Glioma.Cells · 2024Review
- SINEUPs to boost translation.Molecular therapy. Nucleic acids · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
A major mechanism conferring resistance to mTOR inhibitors is activation of a salvage pathway stimulating internal ribosome entry site (IRES)-mediated mRNA translation, driving the synthesis of proteins promoting resistance of glioblastoma (GBM). Previously, we found this pathway is stimulated by the requisite IRES-trans-acting factor (ITAF) hnRNP A1, which itself is subject to phosphorylation and methylation events regulating cyclin D1 and c-myc IRES activity. Here we describe the requirement for m
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.