Evidence map›Paper›PMID 32630050›Full record

ReviewInternational journal of molecular sciences2020

Nonsense Suppression Therapy: New Hypothesis for the Treatment of Inherited Bone Marrow Failure Syndromes.

Valentino Bezzerri, Martina Api, Marisole Allegri, Benedetta Fabrizzi, Seth J Corey, Marco Cipolli

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Molecular Approaches Fighting Nonsense.International journal of molecular sciences · 2021
    Article
  7. Nonsense suppression therapies in human genetic diseases.Cellular and molecular life sciences : CMLS · 2021
    Review
  8. 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

6 authors at 3 institutions in 2 countries.

Valentino BezzerriCystic Fibrosis Center, Azienda Ospedaliero Universitaria Ospedali Riuniti, Via Conca 71, 60126 Ancona, Italy.ORCID 0000-0002-6849-4487
Martina ApiCystic Fibrosis Center, Azienda Ospedaliero Universitaria Ospedali Riuniti, Via Conca 71, 60126 Ancona, Italy.ORCID 0000-0003-2636-2969
Marisole AllegriCystic Fibrosis Center, Azienda Ospedaliero Universitaria Ospedali Riuniti, Via Conca 71, 60126 Ancona, Italy.
Benedetta FabrizziCystic Fibrosis Center, Azienda Ospedaliero Universitaria Ospedali Riuniti, Via Conca 71, 60126 Ancona, Italy.
Seth J CoreyDepartment of Pediatric Hematology/Oncology and Stem Cell Transplantation, Cleveland Clinic, Cleveland, OH 44195, USA.
Marco CipolliCystic Fibrosis Center, Azienda Ospedaliera Universitaria Integrata, P.le A. Stefani 1, 37126 Verona, Italy.
Azienda Ospedaliero Universitaria Ospedali Riuniti · ITAzienda Ospedaliera Universitaria Integrata Verona · ITCleveland Clinic · US

Funding

Associazione Italiana Sindrome di Shwachman-Diamond (AISS) 9/2017Ministero della Salute GR-2016-02363570
6 · The paper itself

Abstract

Inherited bone marrow failure syndromes (IBMFS) are a group of cancer-prone genetic diseases characterized by hypocellular bone marrow with impairment in one or more hematopoietic lineages. The pathogenesis of IBMFS involves mutations in several genes which encode for proteins involved in DNA repair, telomere biology and ribosome biogenesis. The classical IBMFS include Shwachman-Diamond syndrome (SDS), Diamond-Blackfan anemia (DBA), Fanconi anemia (FA), dyskeratosis congenita (DC), and severe congenital neutropenia (SCN). IBMFS are associated with high risk of myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), and solid tumors. Unfortunately, no specific pharmacological therapies have been highly effective for IBMFS. Hematopoietic stem cell transplantation provides a cure for aplastic or myeloid neoplastic complications. However, it does not affect the risk of solid tumors. Since approximately 28% of FA, 24% of SCN, 21% of DBA, 20% of SDS, and 17% of DC patients harbor nonsense mutations in the respective IBMFS-related genes, we discuss the use of the nonsense suppression therapy in these diseases. We recently described the beneficial effect of ataluren, a nonsense suppressor drug, in SDS bone marrow hematopoietic cells ex vivo. A similar approach could be therefore designed for treating other IBMFS. In this review we explain in detail the new generation of nonsense suppressor molecules and their mechanistic roles. Furthermore, we will discuss strengths and limitations of these molecules which are emerging from preclinical and clinical studies. Finally we discuss the state-of-the-art of preclinical and clinical therapeutic studies carried out for IBMFS.

Indexed as

AminoglycosidesCodon, NonsenseCongenital Bone Marrow Failure SyndromesHumansNonsense Mediated mRNA DecayOxadiazolesAminoglycosidesatalurenCodon, NonsenseOxadiazolesatalureninherited bone marrow failure syndromesnonsense mediated decaynonsense suppression therapy

Identifiers

PMID32630050
PMCPMC7369780
OpenAlexW3038906953

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.