Evidence map›Paper›PMID 35794567›Full record

ArticleJournal of translational medicine2022

Molecular dissection of a hyper-aggressive CBFB-MYH11/FLT3-ITD-positive acute myeloid leukemia.

Gabriele Lo Iudice, Eleonora De Bellis, Arianna Savi, Luca Guarnera, Alice Massacci, Francesca De Nicola, Frauke Goeman, Tiziana Ottone, Mariadomenica Divona, Matteo Pallocca and 3 more

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

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. The Fusion Genes and Their Relation with Genetic Variants in Egyptian AML Patients.Asian Pacific journal of cancer prevention : APJCP · 2025
    Article
  2. Review
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

13 authors at 3 institutions in 2 countries.

Gabriele Lo Iudice *SAFU Unit, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Eleonora De Bellis *Department of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
Arianna SaviDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
Luca GuarneraDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
Alice MassacciBiostatistics, Bioinformatics and Clinical Trial Center, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Francesca De NicolaSAFU Unit, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Frauke GoemanSAFU Unit, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Tiziana OttoneDepartment of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
Mariadomenica DivonaLaboratory of Advanced Diagnostics in Oncohematology, Hematology Department, Tor Vergata Hospital, Rome, Italy.
Matteo PalloccaBiostatistics, Bioinformatics and Clinical Trial Center, IRCCS Regina Elena National Cancer Institute, Rome, Italy. matteo.pallocca@ifo.it.ORCID 0000-0002-7756-3579
Maurizio FanciulliSAFU Unit, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Maria Teresa Voso *Department of Biomedicine and Prevention, Tor Vergata University, Rome, Italy.
Gennaro Ciliberto *Scientific Direction, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Istituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Rome Tor Vergata · ITNational Cancer Institute · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute Myeloid Leukaemia (AML) is a haematological malignancy showing a hypervariable landscape of clinical outcomes and phenotypic differences, explainable by heterogeneity at the cellular and molecular level. Among the most common genomic alterations, CBFB-MYH11 rearrangement and FLT3-ITD gene mutations, have opposite clinical significance and are unfrequently associated. We present here a Molecular Case Report in which these two events co-exist an ultra-aggressive phenotype resulting in death in 4 days from hospital admittance. Somatic and germline Whole Exome Sequencing analysis was performed to uncover other putative driver mutations, de-novo genomic structural events or germline clusters increasing cancer insurgence. Only three mutations in LTK, BCAS2 and LGAS9 were found, unlikely causative of the exhibited phenotype, prompting to additional investigation of the rare CBFB-MYH11/ FLT3-ITD scenario.

Indexed as

Leukemia, Myeloid, AcuteCore Binding Factor beta Subunitfms-Like Tyrosine Kinase 3HumansMutationMyosin Heavy ChainsPhenotypeCBFB protein, humanCore Binding Factor beta SubunitFLT3 protein, humanfms-Like Tyrosine Kinase 3MYH11 protein, humanMyosin Heavy Chains

Identifiers

PMID35794567
PMCPMC9258203
OpenAlexW4283831969

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.