Evidence map›Paper›PMID 36115690›Full record

ReviewSeminars in hematology2022

Clonality in immune aplastic anemia: Mechanisms of immune escape or malignant transformation.

Jibran Durrani, Emma M Groarke

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Seminars in hematology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
2.4field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Jibran DurraniHematology Branch, National Heart, Lung and Blood Institute, National Institutes of Health. Electronic address: jibran.durrani@nih.gov.
Emma M GroarkeHematology Branch, National Heart, Lung and Blood Institute, National Institutes of Health.
National Institutes of Health · US

Funding

Intramural NIH HHS Z99 HL999999
6 · The paper itself

Abstract

Aplastic anemia (AA) is the prototypic bone marrow failure syndrome and can be classified as either acquired or inherited. Inherited forms are due to the effects of germline mutations, while acquired AA is suspected to result from cytotoxic T-cell mediated immune attack on hematopoietic stem and progenitor cells. Once thought to be a purely "benign" condition, clonality in the form of chromosomal abnormalities and single nucleotide variants is now well recognized in AA. Mechanisms underpinning this clonality likely relate to selection of clones that allow immune evasion or increased cell survival the marrow environment under immune attack. Widespread use and availability of next generation and other genetic sequencing techniques has enabled us to better understand the genomic landscape of aplastic anemia. This review focuses on the current concepts associated with clonality, in particular somatic mutations and their impact on diagnosis and clinical outcomes in immune aplastic anemia.

Indexed as

Anemia, AplasticMyelodysplastic SyndromesBone MarrowGerm-Line MutationHumansNucleotidesNucleotidesAcquired/immune aplastic anemiaBone marrow failureClonal hematopoiesisHematopoietic stem cellsImmunosuppressive therapy

Identifiers

PMID36115690
PMCPMC9938528
OpenAlexW4291155706

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.