Evidence map›Paper›PMID 24402164›Full record

ArticleLeukemia2014

High number of additional genetic lesions in acute myeloid leukemia with t(8;21)/RUNX1-RUNX1T1: frequency and impact on clinical outcome.

M-T Krauth, C Eder, T Alpermann, U Bacher, N Nadarajah, W Kern, C Haferlach, T Haferlach, S Schnittger

Abstract read
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In one paragraph

Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
8.1field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  19. Therapy-related core binding factor acute myeloid leukemia.International journal of hematologic oncology · 2023
    Review
  20. Review

14 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

M-T Krauth1] MLL Munich Leukemia Laboratory, Munich, Germany [2] Department of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University Vienna, Vienna, Austria.
C EderMLL Munich Leukemia Laboratory, Munich, Germany.
T AlpermannMLL Munich Leukemia Laboratory, Munich, Germany.
U BacherMLL Munich Leukemia Laboratory, Munich, Germany.
N NadarajahMLL Munich Leukemia Laboratory, Munich, Germany.
W KernMLL Munich Leukemia Laboratory, Munich, Germany.
C HaferlachMLL Munich Leukemia Laboratory, Munich, Germany.
T HaferlachMLL Munich Leukemia Laboratory, Munich, Germany.
S SchnittgerMLL Munich Leukemia Laboratory, Munich, Germany.
Munich Leukemia Laboratory (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

t(8;21)/RUNX1-RUNX1T1-positive acute myeloid leukemia (AML) is prognostically favorable; however, outcome is heterogeneous. We analyzed 139 patients with t(8;21)/RUNX1-RUNX1T1-positive AML (de novo: n=117; therapy-related: n=22) to determine frequency and prognostic impact of additional genetic abnormalities. All patients were investigated for mutations (mut) in ASXL1, FLT3, KIT, NPM1, MLL, IDH1, IDH2, KRAS, NRAS, CBL and JAK2. Sixty-nine of 139 cases (49.6%) had 1 mutation in addition to RUNX1-RUNX1T1, and 23/139 (16.5%) had ⩾2 additional mutations. Most common were KITmut (23/139; 16.5%), NRASmut (18/139; 12.9%) and ASXL1mut (16/139; 11.5%). FLT3-ITD, FLT3-TKDmut, CBLmut, KRASmut, IDH2mut and JAK2mut were found in 2.9-5.0%. Additional chromosomal abnormalities (ACAs) were found in 97/139 (69.8%). Two-year overall survival (OS) was 73.4% in 111 intensively treated patients. KITD816mut negatively impacted on OS in de novo AML (2-year OS: 59.1% vs 82.0%, P=0.03), ASXL1mut on EFS (de novo AML: 20% vs 59.1%, P=0.011; total cohort: 28.6% vs 56.7%, P=0.021). Sex chromosome loss was favorable (2-year EFS: 66.9% vs 43.0%, P=0.031), whereas +8 was adverse on EFS (2-year EFS: 26.7% vs 55.9%, P=0.02). In conclusion, t(8;21)/RUNX1-RUNX1T1-positive AML shows a high frequency of additional genetic alterations. Investigation for KITD816 and ASXL1mut combined with investigation of ACAs is recommended in t(8;21)/RUNX1-RUNX1T1-positive AML because of the prognostic significance of these parameters.

Indexed as

Chromosomes, Human, Pair 21Chromosomes, Human, Pair 8Translocation, GeneticAdolescentAdultAgedAged, 80 and overChromosome AberrationsCore Binding Factor Alpha 2 SubunitFemaleGene Expression Regulation, LeukemicGene FrequencyGenetic Association StudiesHumansLeukemia, Myeloid, AcuteMaleAML1-ETO fusion protein, humanCore Binding Factor Alpha 2 SubunitNPM1 protein, humanNucleophosminOncogene Proteins, FusionRUNX1 Translocation Partner 1 Protein

Identifiers

PMID24402164
OpenAlexW2036318424

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.