Evidence map›Paper›PMID 31456164›Full record

ArticleJournal of applied genetics2019

MLPA as a complementary tool for diagnosis of chromosome 21 aberrations in childhood BCP-ALL.

Ewa Wrona, Marcin Braun, Agata Pastorczak, Joanna Taha, Monika Lejman, Jerzy Kowalczyk, Wojciech Fendler, Wojciech Młynarski

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

Article in Journal of applied genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 37% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Genetics of B-Cell Acute Lymphoblastic Leukemia (B-ALL): Recent Updates and Indian Perspective.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025
    Review
  3. Article
  4. 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

8 authors at 3 institutions in 2 countries.

Ewa WronaDepartment of Pediatrics, Oncology and Hematology, Medical University of Lodz, Lodz, Poland. ewawrona00@gmail.com.ORCID http://orcid.org/0000-0003-3247-924X
Marcin BraunDepartment of Pathology, Chair of Oncology, Medical University of Lodz, Lodz, Poland.
Agata PastorczakDepartment of Pediatrics, Oncology and Hematology, Medical University of Lodz, Lodz, Poland.
Joanna TahaDepartment of Pediatrics, Oncology and Hematology, Medical University of Lodz, Lodz, Poland.
Monika LejmanDepartment of Pediatric Hematology and Oncology, Medical University of Lublin, Lublin, Poland.
Jerzy KowalczykDepartment of Pediatric Hematology and Oncology, Medical University of Lublin, Lublin, Poland.
Wojciech FendlerDepartment of Biostatistics & Translational Medicine, Medical University of Lodz, Lodz, Poland.
Wojciech MłynarskiDepartment of Pediatrics, Oncology and Hematology, Medical University of Lodz, Lodz, Poland.
Medical University of Lodz · PLMedical University of Lublin · PLDana-Farber Cancer Institute · US

Funding

National Center of Research and Development STRATEGMED3/304586/5/2017National Science Centre 2014/13/N/NZ5/03660
6 · The paper itself

Abstract

Chromosome 21 abnormalities are the most frequent genetic findings in childhood B cell precursor acute lymphoblastic leukemia (BCP-ALL) cases. Majority of patients are effectively diagnosed with fluorescence in situ hybridization (FISH) and karyotyping; however, some cases may require additional tools to be used. Bone marrow samples of 373 childhood BCP-ALL patients were tested for chromosome 21 copy number variations (CNVs) with Multiplex Ligation-dependent Probe Amplification (MLPA) P327 array. Results from MLPA and cytogenetics were compared between groups according to the type of abnormality found on chromosome 21. Out the group of 235 patients, chromosome 21 multiplication was found by FISH assay in 56 cases (23.81%), ETV6-RUNX1 fusion in 34 (14.47%) and iAMP21 in 3 (1.28%) children, remaining 142 (60.43%) patients had no known chromosome 21 aberration. Median peak ratios of all tested probes in MLPA in aforementioned groups were 1.47 (IQR 1.28-1.77) vs. 1.00 (IQR 1.00-1.09) vs. 2.79 (IQR 1.97-2.83) vs. 1.00 (1.00-1.11), respectively. Aforementioned peak ratio of ETV6-RUNX1 fusion group was similar with patients of no known chromosome 21 aberration (p = 0.71). Interestingly, both groups differed from patients with chromosome 21 multiplication (p < 10

Indexed as

Chromosome AberrationsChildChild, PreschoolChromosomes, Human, Pair 21Core Binding Factor Alpha 2 SubunitCytodiagnosisDNA Copy Number VariationsETS Translocation Variant 6 ProteinFemaleHumansIn Situ Hybridization, FluorescenceKaryotypingMalePrecursor B-Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene Proteins c-etsRepressor ProteinsCore Binding Factor Alpha 2 SubunitETS Translocation Variant 6 ProteinProto-Oncogene Proteins c-etsRepressor ProteinsRUNX1 protein, humanChildhood BCP-ALLCNVsETV6-RUNX1 fusionFISH assayIntrachromosomal amplification of chromosome 21 (iAMP21)MLPA

Identifiers

PMID31456164
PMCPMC6803575
OpenAlexW2970521766

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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.