Evidence map›Paper›PMID 11021751›Full record

ArticleLeukemia2000

Elevated MLF1 expression correlates with malignant progression from myelodysplastic syndrome.

N Matsumoto, N Yoneda-Kato, T Iguchi, Y Kishimoto, T Kyo, H Sawada, E Tatsumi, S Fukuhara

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.5field-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

26 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Myeloid leukemia factor is a conserved regulator of RUNX transcription factor activity involved in hematopoiesis.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

8 authors at 4 institutions in 1 country.

N MatsumotoFirst Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
N Yoneda-Kato
T Iguchi
Y Kishimoto
T Kyo
H Sawada
E Tatsumi
S Fukuhara
Kansai Medical University · JPJapanese Red Cross Hiroshima College of Nursing · JPKobe University · JPTenri Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MLF1 is a novel protein identified as the NPM-MLF1 chimeric protein produced by a t(3;5)(q25.1;q34) chromosomal translocation, which is associated with myelodysplastic syndrome (MDS), often prior to acute myeloid leukemia (AML), except for M3. The clinical features of t(3;5)-positive myeloid disorders suggest that this chimeric protein is involved in dysregulation of progenitor cells with the capability to differentiate into multiple lineages. So far, involvement of wild-type MLF1 in hematopoiesis or in leukemogenesis has not been fully investigated. In the present study, 65 patients with AML and 44 patients with MDS were tested for the expression of MLF1 using the quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method. A significantly higher level of MLF1 expression (ratio of MLF1/beta-actin mRNA >0.4) was readily detected in seven of 65 patients with de novo AML, three of 12 with post-MDS AML and seven of 44 with MDS, but not in any patients with ALL (n = 18). According to the FAB classification, high levels of MLF1 were found in patients with relatively immature subtypes of AML (M1, M2, M6 and M7) and high risk MDS (RAEB and RAEB-T). These findings indicate that the pattern of MLF1 expression is identical to the clinical morphology appearing in the t(3;5)-positive myeloid disorders and is correlated to the MDS-associated AML and transformation phase of MDS in t(3;5)-negative myeloid disorders. A CD34+ population of normal bone marrow cells preferentially expressed MLF1 with obviously decreasing levels of expression during maturation. Therefore, MLF1 normally functions in multi-potent progenitor cells and its dysregulation may take part in leukemogenesis from MDS.

Indexed as

Acute DiseaseAnimalsBase SequenceBlotting, NorthernCell Cycle ProteinsChromosomes, Human, Pair 3Chromosomes, Human, Pair 5Disease ProgressionDNA-Binding ProteinsDNA PrimersHumansLeukemia, MyeloidMiceMice, Inbred BALB CMyelodysplastic SyndromesPrognosisCell Cycle ProteinsDNA-Binding ProteinsDNA PrimersMLF1 protein, humanMlf1 protein, mouseProteins

Identifiers

PMID11021751
OpenAlexW2056473907

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.