Evidence map›Paper›PMID 24052708›Full record

ArticleBalkan journal of medical genetics : BJMG2011

Amplification of c-MYC and MLL Genes as a Marker of Clonal Cell Progression in Patients with Myeloid Malignancy and Trisomy of Chromosomes 8 or 11.

S Angelova, M Jordanova, B Spassov, V Shivarov, M Simeonova, I Christov, P Angelova, K Alexandrova, A Stoimenov, V Nikolova and 5 more

Open access · goldAbstract read
In one paragraph

Article in Balkan journal of medical genetics : BJMG, 2011. 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
–field-weighted citation impact, top 87% 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

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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, 5 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

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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

15 authors at 1 institution in 1 country.

S AngelovaLaboratory of Cytogenetics and Molecular Biology, National Specialized Hospital for Active Therapy of Hematological Diseases, Sofia, Bulgaria.
M Jordanova
B Spassov
V Shivarov
M Simeonova
I Christov
P Angelova
K Alexandrova
A Stoimenov
V Nikolova
I Dimova
P Ganeva
N Tzvetkov
E Hadjiev
S Toshkov
National Specialized Hospital for Active Treatment of Hematologic Diseases · BG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene amplification (amp) is one of the basic mechanisms connected with overexpression of oncogenes. The c-MYC (located in 8q24) and MLL (located in 11q23) are the most often over represented genes that lead to a rapid proliferation of the affected cell clone in patients with myeloid neoplasms. Assessment of the level of amp c-MYC or amp MLL in the cases with trisomy 8 (+8) or trisomy 11 (+11) and myeloid malignances is necessary for a more precise estimation of the disease progression. A total of 26 patients with acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) were included in the study: 18 with +8, six with +11 and two with complex karyotypes suspected of the partial trisomy. Routine cytogenetic analysis and fluorescent in situ hybridization (FISH) were applied to indicate the chromosome alterations and genes amp in the bone marrow cells. Amp c-MYC was observed in 12 from 18 (66.7%) patients with +8. All the patients with +11 demonstrated a different level of amp MLL. In most of the cases with MDS (9/10), the coincidence of the +8 or +11 with amp c-MYC or amp MLL, respectively, leads to transformation to AML and/or short overall survival. Our data suggest that amp c-MYC and amp MLL develop in conformity with +8 and +11, especially in cases with progressive deviations in the karyotype as an aggressive expansion of an aberrant cell clone and appearance of additional chromosome anomalies.

Indexed as

Acute myeloid leukemia (AML)c-MYCGene amplification (amp)MLL genesMyelodysplastic syndromes (MDS)Myeloid malignanciesTrisomy chromosomes of 8 or 11

Identifiers

PMID24052708
PMCPMC3776705
OpenAlexW2097586670

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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.