Evidence map›Paper›PMID 21527527›Full record

ArticleBlood2011

SNP array-based karyotyping: differences and similarities between aplastic anemia and hypocellular myelodysplastic syndromes.

Manuel G Afable, Marcin Wlodarski, Hideki Makishima, Mohammed Shaik, Mikkael A Sekeres, Ramon V Tiu, Matt Kalaycio, Christine L O'Keefe, Jaroslaw P Maciejewski

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 128 citations in OpenAlex.

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  16. Clinical and Molecular Determinants of Clonal Evolution in Aplastic Anemia and Paroxysmal Nocturnal Hemoglobinuria.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023
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6 more citing papers are in PubMed but not listed here.

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 1 institution in 2 countries.

Manuel G AfableDepartment of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.
Marcin Wlodarski
Hideki Makishima
Mohammed Shaik
Mikkael A Sekeres
Ramon V Tiu
Matt Kalaycio
Christine L O'Keefe
Jaroslaw P Maciejewski
Cleveland Clinic · US

Funding

Predisposition to chromosomal alterations in MDSR01HL082983 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI MACIEJEWSKI, JAROSLAW P. · 2005 to 2008
$1.5M
Training/Research Center-Bone Marrow Failure SyndromesK24HL077522 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI MACIEJEWSKI, JAROSLAW P. · 2005 to 2014
$1.2M
NHLBI NIH HHS K24 HL-077522NHLBI NIH HHS K24 HL077522NHLBI NIH HHS R01 HL082983NHLBI NIH HHS R01HL-082983
6 · The paper itself

Abstract

In aplastic anemia (AA), contraction of the stem cell pool may result in oligoclonality, while in myelodysplastic syndromes (MDS) a single hematopoietic clone often characterized by chromosomal aberrations expands and outcompetes normal stem cells. We analyzed patients with AA (N = 93) and hypocellular MDS (hMDS, N = 24) using single nucleotide polymorphism arrays (SNP-A) complementing routine cytogenetics. We hypothesized that clinically important cryptic clonal aberrations may exist in some patients with BM failure. Combined metaphase and SNP-A karyotyping improved detection of chromosomal lesions: 19% and 54% of AA and hMDS cases harbored clonal abnormalities including copy-neutral loss of heterozygosity (UPD, 7%). Remarkably, lesions involving the HLA locus suggestive of clonal immune escape were found in 3 of 93 patients with AA. In hMDS, additional clonal lesions were detected in 5 (36%) of 14 patients with normal/noninformative routine cytogenetics. In a subset of AA patients studied at presentation, persistent chromosomal genomic lesions were found in 10 of 33, suggesting that the initial diagnosis may have been hMDS. Similarly, using SNP-A, earlier clonal evolution was found in 4 of 7 AA patients followed serially. In sum, our results indicate that SNP-A identify cryptic clonal genomic aberrations in AA and hMDS leading to improved distinction of these disease entities.

Indexed as

Oligonucleotide Array Sequence AnalysisPolymorphism, Single NucleotideAdultAgedAged, 80 and overAnemia, AplasticChromosome AberrationsCytogenetic AnalysisFemaleHumansKaryotypingMaleMiddle AgedMyelodysplastic Syndromes

Identifiers

PMID21527527
PMCPMC3128479
OpenAlexW2076506261

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.