Evidence map›Paper›PMID 30292352›Full record

ReviewTrends in cancer2018

Trinucleotide Repeat Expansion Diseases, RNAi, and Cancer.

Andrea E Murmann, Jindan Yu, Puneet Opal, Marcus E Peter

Open access · greenAbstract readReview
In one paragraph

Review in Trends in cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Differential effects of Wnt-β-catenin signaling in Purkinje cells and Bergmann glia in spinocerebellar ataxia type 1.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Article
  8. DISE/6mer seed toxicity-a powerful anti-cancer mechanism with implications for other diseases.Journal of experimental & clinical cancer research : CR · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Huntington disease: Advances in the understanding of its mechanisms.Clinical parkinsonism & related disorders · 2020
    Review
  13. Article
  14. Article
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

4 authors at 1 institution in 1 country.

Andrea E MurmannDepartment of Medicine, Division Hematology/Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Jindan YuDepartment of Medicine, Division Hematology/Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Biochemistry and Molecular Genetics, Northwestern University, Chicago, IL 60611, USA.
Puneet OpalDavee Department of Neurology, Northwestern University, Chicago, IL 60611, USA.
Marcus E PeterDepartment of Medicine, Division Hematology/Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Biochemistry and Molecular Genetics, Northwestern University, Chicago, IL 60611, USA. Electronic address: m-peter@northwestern.edu.
Northwestern University · US

Funding

DISE - a natural cancer surveillance mechanism - a new road to cancer therapyR35CA197450 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PETER, MARCUS E. · 2015 to 2021
$6.2M
NCI NIH HHS R35 CA197450
6 · The paper itself

Abstract

Many neurodegenerative diseases are caused by unstable trinucleotide repeat (TNR) expansions located in disease-associated genes. siRNAs based on CAG repeat expansions effectively kill cancer cell lines in vitro through RNAi. They also cause significant reduction in tumor growth in a human ovarian cancer mouse model with no toxicity to the treated mice. This suggests that cancer cells are particularly sensitive to CAG TNR-derived siRNAs, and explains a reported inverse correlation between the length of CAG TNRs and reduced global cancer incidences in some CAG TNR diseases. This review discusses both mutant proteins and mutant RNAs as a cause of TNR diseases, with a focus on RNAi and its role in contributing to disease pathology and in suppressing cancer.

Indexed as

RNA InterferenceCarcinogenesisComorbidityGenetic TherapyHumansIncidenceMolecular Targeted TherapyNeoplasmsNeurodegenerative DiseasesRNA, Small InterferingTrinucleotide Repeat ExpansionRNA, Small InterferingARcancerHuntington’s diseaseRNASBMATNR

Identifiers

PMID30292352
PMCPMC6613933
OpenAlexW2894310390

What OpenQuestion holds

Textmetadata
LicenceTDM
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.