Evidence map›Paper›PMID 21793975›Full record

ArticleBrain pathology (Zurich, Switzerland)2012

Genetic alterations in microRNAs in medulloblastomas.

Sheng-Qing Lv, Young-Ho Kim, Fiaschetti Giulio, Tarek Shalaby, Sumihito Nobusawa, Hui Yang, Zheng Zhou, Michael Grotzer, Hiroko Ohgaki

Open access · greenAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. The Non-coding Side of Medulloblastoma.Frontiers in cell and developmental biology · 2020
    Review
  7. Review
  8. MicroRNA-186 suppresses lung cancer progression by targeting SIRT6.Cancer biomarkers : section A of Disease markers · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Role of MYC in Medulloblastoma.Cold Spring Harbor perspectives in medicine · 2013
    Review
  18. From small to big: microRNAs as new players in medulloblastomas.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Review
  19. Article
  20. Signaling pathway and molecular subgroups of medulloblastoma.International journal of clinical and experimental pathology · 2013
    Review
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

9 authors at 3 institutions in 4 countries.

Sheng-Qing LvInternational Agency for Research on Cancer (IARC), Lyon, France Neuro-Oncology Program, University Children's Hospital of Zurich, Switzerland.
Young-Ho Kim
Fiaschetti Giulio
Tarek Shalaby
Sumihito Nobusawa
Hui Yang
Zheng Zhou
Michael Grotzer
Hiroko Ohgaki
Boston Children's Hospital · USCentre International de Recherche sur le Cancer · FRArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) regulate a variety of cellular processes via the regulation of multiple target genes. We screened 48 medulloblastomas for mutation, deletion and amplification of nine miRNA genes that were selected on the basis of the presence of potential target sequences within the 3'-untranslated region of the MYCC mRNA. Differential PCR revealed deletions in miR-186 (15%), miR-135a-1 (33%), miR-548d-1 (42%), miR-548d-2 (21%) and miR-512-2 (33%) genes, whereas deletion or amplification was detected in miR-135b (23%) and miR-135a-2 (15%). In miR-33b, deletion, amplification or a mutation at the precursor miRNA were detected in 10% of medulloblastomas. Overall, 35/48 (73%) medulloblastomas had at least one alteration. Real-time RT-PCR revealed MYCC overexpression in 11 of 37 (30%) medulloblastomas, and there was a correlation between MYCC overexpression and miR-512-2 gene deletion (P = 0.0084). Antisense-based knockdown of miR-512-5p (mature sequence of miR-512-2) resulted in significant upregulation of MYCC expression in HeLa and A549 cells, while forced overexpression of miR-512-2 in medulloblastoma/PNET cell lines DAOY, UW-228-2, PFSK resulted in the downregulation of MYCC protein. Furthermore, the results of luciferase reporter assays suggested that miR-512-2 targets the MYCC gene. These results suggest that alterations in the miRNA genes may be an alternative mechanism leading to MYCC overexpression in medulloblastomas.

Indexed as

AdolescentAdultCerebellar NeoplasmsChildChild, PreschoolFemaleGene AmplificationGene DeletionGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseGenetic TestingHEK293 CellsHeLa CellsHumansInfantLung NeoplasmsMicroRNAsMYC protein, humanProto-Oncogene Proteins c-myc

Identifiers

PMID21793975
PMCPMC8029025
OpenAlexW1947478323

What OpenQuestion holds

Textmetadata
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.