Evidence map›Paper›PMID 32721124›Full record

ArticleCancer reports (Hoboken, N.J.)2019

The RS4;11 cell line as a model for leukaemia with t(4;11)(q21;q23): Revised characterisation of cytogenetic features.

Denise Ragusa, Evgeny M Makarov, Oliver Britten, Daniela Moralli, Catherine M Green, Sabrina Tosi

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

Article in Cancer reports (Hoboken, N.J.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 7 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

6 authors at 2 institutions in 1 country.

Denise RagusaDivision of Biosciences, College of Health and Life Sciences, Institute of Environment, Health and Societies, Brunel University London, Uxbridge, UK.ORCID 0000-0002-0303-8683
Evgeny M MakarovDivision of Biosciences, College of Health and Life Sciences, Institute of Environment, Health and Societies, Brunel University London, Uxbridge, UK.
Oliver BrittenDivision of Biosciences, College of Health and Life Sciences, Institute of Environment, Health and Societies, Brunel University London, Uxbridge, UK.
Daniela MoralliChromosome Dynamics, Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Catherine M GreenChromosome Dynamics, Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Sabrina TosiDivision of Biosciences, College of Health and Life Sciences, Institute of Environment, Health and Societies, Brunel University London, Uxbridge, UK.ORCID 0000-0002-0036-0191
Brunel University of London · GBCentre for Human Genetics · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHaematological malignancies harbouring rearrangements of the KMT2A gene represent a unique subtype of leukaemia, with biphenotypic clinical manifestations, a rapid and aggressive onset, and a generally poor prognosis. Chromosomal translocations involving KMT2A often cause the formation of oncogenic fusion genes, such as the most common translocation t(4;11)(q21;q23) producing the KMT2A-AFF1 chimera.

aimThe aim of this study was to confirm and review the cytogenetic and molecular features of the KMT2A-rearranged RS4;11 cell line and put those in context with other reports of cell lines also harbouring a t(4;11) rearrangement. METHODS AND

resultsThe main chromosomal rearrangements t(4;11)(q21;q23) and i(7q), described when the cell line was first established, were confirmed by fluorescence in situ hybridisation (FISH) and 24-colour karyotyping by M-FISH. Additional cytogenetic abnormalities were investigated by further FISH experiments, including the presence of trisomy 18 as a clonal abnormality and the discovery of one chromosome 8 being an i(8q), which indicates a duplication of the oncogene MYC. A homozygous deletion of 9p21 containing the tumour-suppressor genes CDKN2A and CDKN2B was also revealed by FISH. The production of the fusion transcript KMT2A-AFF1 arising from the der(11)t(4;11) was confirmed by RT-PCR, but sequencing of the amplified fragment revealed the presence of multiple isoforms. Two transcript variants, resulting from alternative splicing, were identified differing in one glutamine residue in the translated protein.

conclusionAs karyotype evolution is a common issue in cell lines, we highlight the need to monitor cell lines in order to re-confirm their characteristics over time. We also reviewed the literature to provide a comparison of key features of several cell lines harbouring a t(4;11). This would guide scientists in selecting the most suitable research model for this particular type of KMT2A-leukaemia.

Indexed as

Cell Line, TumorChromosomes, Human, Pair 11Chromosomes, Human, Pair 4DNA-Binding ProteinsHistone-Lysine N-MethyltransferaseHumansKaryotypingLeukemiaMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionSequence DeletionTranscriptional Elongation FactorsTranslocation, GeneticAFF1 protein, humanDNA-Binding ProteinsHistone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionTranscriptional Elongation Factorsclonal evolutionKMT2AleukaemiaMLLRS4;11t(4;11)(q23;q21)

Identifiers

PMID32721124
PMCPMC7941496
OpenAlexW2953482514

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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.