Evidence map›Paper›PMID 35299281›Full record

ArticleEuropean journal of haematology2022

Multistep pathogenesis of chronic myelomonocytic leukemia in patients.

Klaus Geissler, Eva Jäger, Agnes Barna, Michael Gurbisz, Renate Marschon, Temeida Graf, Thomas Nösslinger, Michael Pfeilstöcker, Sigrid Machherndl-Spandl, Reinhard Stauder and 6 more

Abstract read
In one paragraph

Article in European journal of haematology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
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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

16 authors.

Klaus GeisslerMedical School, Sigmund Freud University, Vienna, Austria.ORCID https://orcid.org/0000-0003-1921-7034
Eva JägerDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Agnes BarnaBlood Transfusion Service, Blood Transfusion Service for Upper Austria, Austrian Red Cross, Linz, Austria.
Michael GurbiszDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Renate MarschonLaboratory for Molecular and Genetic Diagnostics, Ordensklinikum Linz, Linz, Austria.
Temeida GrafDepartment of Internal Medicine V with Hematology, Oncology and Palliative Medicine, Hospital Hietzing, Vienna, Austria.
Thomas NösslingerDepartment of Internal Medicine III, Hanusch Hospital, Vienna, Austria.
Michael PfeilstöckerDepartment of Internal Medicine III, Hanusch Hospital, Vienna, Austria.
Sigrid Machherndl-SpandlDepartment of Internal Medicine I with Hematology with Stem Cell Transplantation, Hemostaseology and Medical Oncology, Ordensklinikum Linz Barmherzige Schwestern - Elisabethinen, Linz, Austria.
Reinhard StauderInternal Medicine V with Hematology and Oncology, Medical University of Innsbruck, Innsbruck, Austria.ORCID https://orcid.org/0000-0002-8993-9561
Armin ZebischDepartment of Internal Medicine, Division of Hematology, Medical University of Graz, Graz, Austria.
Heinz SillDepartment of Internal Medicine, Division of Hematology, Medical University of Graz, Graz, Austria.
Leopold ÖhlerDepartment of Internal Medicine/Oncology, St. Josef Hospital, Vienna, Austria.
Rajko KusecSchool of Medicine, University of Zagreb, University Hospital Dubrava, Zagreb, Croatia.
Gregor HoermannMLL Munich Leukemia Laboratory, Munich, Germany.
Peter ValentLudwig Boltzmann Institute for Hematology and Oncology (LBI HO), Medical University of Vienna, Vienna, Austria.

Funding

Gesellschaft zur Erforschung der Biologie und Therapie von Tumorkrankheiten ABCMML-112015
6 · The paper itself

Abstract

backgroundA multistep pathogenesis of myeloid leukemia including mutations in epigenetic, spliceosome, and signaling genes has been recently demonstrated in a preclinical model but is poorly validated in patients.

methodsClinical, phenotypic, and biologic features were compared between three distinct molecularly defined CMML cohorts including TET2 monomutated patients (T, n = 10), TET2/SRSF2 bimutated patients (TS, n = 19), and patients who had NRAS mutations in addition to TET2/SRSF2 comutations (TSN, n = 14).

resultsMedian survival was 90, 45, and 9 months, respectively (p = .001). Whereas no patient in the T and TS group transformed into acute myeloid leukemia (AML), 6/14 patients in the TSN group had AML at study entry or transformed during follow-up. Leukocyte counts, blast cell counts, and LDH levels were significantly higher in TSN vs. TS and T, respectively, whereas hemoglobin and platelet values were not significantly different. Increased growth factor-independent myeloid colony formation was restricted to TSN but not found in T and TS, respectively. The proportion of patients showing in vitro myelomonocytic skewing in T, TS, and TSN was 0%, 56%, and 100%, respectively (p = .010).

conclusionOur results demonstrate that the model of multistep pathogenesis in CMML can be recapitulated in patients regarding clinical, phenotypic, and biologic features.

Indexed as

Biological ProductsLeukemia, Myeloid, AcuteLeukemia, Myelomonocytic, ChronicHumansMutationPrognosisBiological ProductsCMMLNRASpathogenesisSRSF2TET2

Identifiers

PMID35299281
PMCPMC9310570

What Socratic 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 Socratic graph.