Evidence map›Paper›PMID 35799207›Full record

ArticleMolecular cytogenetics2022

21q22 amplification detection in three patients with acute myeloid leukemia: cytogenomic profiling and literature review.

Emily M Kudalkar, Changlee Pang, Mary M Haag, Daniel A Pollyea, Manali Kamdar, Gang Xu, Meng Su, Billie Carstens, Karen Swisshelm, Liming Bao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cytogenetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

10 authors at 3 institutions in 1 country.

Emily M KudalkarColorado Genetics Laboratory, Department of Pathology, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Changlee PangDepartment of Pathology, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Mary M HaagColorado Genetics Laboratory, Department of Pathology, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Daniel A PollyeaDivision of Hematology, Department of Medicine, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Manali KamdarDivision of Hematology, Department of Medicine, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Gang XuDepartment of Pathology, Presbyterian St. Luke Medical Center, Denver, CO, USA.
Meng SuColorado Genetics Laboratory, Department of Pathology, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Billie CarstensColorado Genetics Laboratory, Department of Pathology, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Karen SwisshelmColorado Genetics Laboratory, Department of Pathology, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Liming BaoColorado Genetics Laboratory, Department of Pathology, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, USA. Liming.Bao@cuanschutz.edu.
University of Colorado Anschutz Medical Campus · USPresbyterian St. Luke's Medical Center · USSema4 (United States) · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
NCI NIH HHS P30 CA046934NCI NIH HHS P30CA046934
6 · The paper itself

Abstract

background21q22 amplification is a rare cytogenetic aberration in acute myeloid leukemia (AML). So far, the cytogenomic and molecular features and clinical correlation of 21q22 amplification in AML have not been well-characterized. CASE PRESENTATION: Here, we describe a case series of three AML patients with amplified 21q22 identified by fluorescence in situ hybridization using a RUNX1 probe. Two of these patients presented with therapy-related AML (t-AML) secondary to chemotherapy, while the third had de novo AML. There was one case each of FAB M0, M1 and M4. Morphologic evidence of dysplasia was identified in both t-AML cases. Phenotypic abnormalities of the myeloblasts were frequently observed. Extra copies of 21q22 were present on chromosome 21 and at least one other chromosome in two cases. Two showed a highly complex karyotype. Microarray analysis of 21q22 amplification in one case demonstrated alternating levels of high copy number gain split within the RUNX1 locus at 21q22. The same patient also had mutated TP53. Two patients died at 1.5 and 11 months post-treatment, while the third elected palliative care and died within 2 weeks.

conclusionsOur results provide further evidence that 21q22 amplification in AML is associated with complex karyotypes, TP53 aberrations, and poor outcomes. Furthermore, we demonstrate that 21q22 amplification is not always intrachromosomally localized to chromosome 21 and could be a result of structural aberrations involving 21q22 and other chromosomes.

Indexed as

Acute myeloid leukemiaAmplificationChromosome 21q22CytogenomicOutcomes

Identifiers

PMID35799207
PMCPMC9264596
OpenAlexW4284879381

What OpenQuestion holds

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Registered trials

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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.