Cited by 88Acute Myeloid Leukemia ResearchRetinoids in leukemia and cellular processesCancer-related Molecular Pathways

Molecular Pathophysiology of Myelodysplastic Syndromes

Open access
Lindsley, R. Coleman, Ebert, Benjamin L.·2013·Annual Review of Pathology: Mechanisms of Disease

Abstract

The clinicopathologic heterogeneity of myelodysplastic syndromes (MDS) is driven by diverse, somatically acquired genetic abnormalities. Recent technological advances have enabled the identification of many new mutations, which have implicated novel pathways in MDS pathogenesis, including RNA splicing and epigenetic regulation of gene expression. Molecular abnormalities, either somatic point mutations or chromosomal lesions, can be identified in the vast majority of MDS cases and underlie specific disease phenotypes. As the full array of molecular abnormalities is characterized, genetic variables are likely to complement standard morphologic evaluation in future MDS classification schemes and risk models.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1146/annurev-pathol-011811-132436

Cites

153 of 153 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In myelodysplastic syndromes, mutations in several components of the core splicing apparatus cause very specific splicing defects in particular transcripts and lead to a highly tissue-specific phenotype.

    “mutations in several components of the core splicing apparatus, such as U2 small nuclear ribonucleoprotein auxiliary factor 2 (U2AF65), splicing factor 3B, subunit 1 (SF3B1) and other proteins, were found to cause very specific splicing defects in particular transcripts and to lead to a highly tissue-specific phenotype185–187.”

    From The neurogenetics of alternative splicing (2016) · cites this paper as [186]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Lindsley, R. C., & Ebert, B. L.
Affiliations
Brigham and Women's Hospital (US)
Venue
Annual Review of Pathology: Mechanisms of Disease
Published
2013-01-24
Volume
8
Issue
1
Pages
21-47
ISSN
  • 1553-4006 (ISSN-L)
  • 1553-4014
OpenAlex
W2157260351
Cited by
88
References
153
Citations by year
2025: 2 · 2024: 1 · 2023: 5 · 2022: 11 · 2021: 2 · 2020: 10 · 2019: 6 · 2018: 6 · 2017: 10 · 2016: 7 · 2015: 5 · 2014: 11 · 2013: 9 · 2012: 2
FWCI
0.93
Type
journal article
Language
en
Open access
Locations
  • Annual Review of Pathology Mechanisms of Disease (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Heart, Lung, and Blood Institute (R01HL082945)
  • National Cancer Institute (T32CA009172)
Topics
  • Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords
myelodysplastic syndrome, somatic mutations, chromosomal abnormalities, RNA splicing, epigenetic regulation, pathogenesis, MDS classification, risk model
MeSH terms
Animals, Humans, Myelodysplastic Syndromes, Phenotype, Point Mutation, Epigenesis, Genetic

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review