Evidence map›Paper›PMID 19458628›Full record

ArticleLeukemia2009

AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) acute myeloid leukemia-M2.

B Jiao, C-F Wu, Y Liang, H-M Chen, S-M Xiong, B Chen, J-Y Shi, Y-Y Wang, J-H Wang, Y Chen and 8 more

Abstract read
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In one paragraph

Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. DNA Repair Genes Polymorphisms: Impact on Acute Myeloid Leukemia Patients Outcome.Asian Pacific journal of cancer prevention : APJCP · 2022
    Article
  8. Acute myeloid leukemia with variant t(8;10;21).Leukemia research reports · 2022
    Article
  9. Clinical significance of CD34Frontiers of medicine · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. A novel epigeneticEMBO molecular medicine · 2017
    Article
  19. Article
  20. Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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

18 authors at 4 institutions in 1 country.

B JiaoState Key Laboratory of Medical Genomics, Institute of Health Sciences, Shanghai Institutes for Biological Sciences and Graduate School, Chinese Academy of Sciences and Shanghai Institute of Hematology, Rui Jin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
C-F Wu
Y Liang
H-M Chen
S-M Xiong
B Chen
J-Y Shi
Y-Y Wang
J-H Wang
Y Chen
J-M Li
L-J Gu
J-Y Tang
Z-X Shen
B-W Gu
W-L Zhao
Z Chen
S-J Chen
Shanghai Jiao Tong University · CNShanghai Institutes for Biological Sciences · CNShanghai Institute of Hematology · CNShanghai Children's Medical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AML1-ETO fusion gene is generated from chromosomal translocation t(8;21) mainly in acute myeloid leukemia M2 subtype (AML-M2). Its spliced variant transcript, AML1-ETO9a, rapidly induces leukemia in murine model. To evaluate its clinical significance, AML1-ETO9a expression was assessed in 118 patients with t(8;21) AML-M2, using qualitative and nested quantitative reverse transcriptase (RT)-PCR methods. These cases were accordingly divided into the AML1-ETO9a-H group (n=86, positive for qualitative RT-PCR, with higher level of AML1-ETO9a by quantitative RT-PCR) and the AML1-ETO9a-L group (n=32, negative for qualitative RT-PCR, with lower but still detectable level of AML1-ETO9a by quantitative RT-PCR). C-KIT expression was significantly increased in the AML1-ETO9a-H group, as compared with the AML1-ETO9a-L group. Of the 36 patients harboring C-KIT mutations, 32 patients overexpressed AML1-ETO9a (P=0.0209). Clinically, AML1-ETO9a-H patients exhibited significantly elevated white blood cells count, less bone marrow aberrant myelocytes, increased CD56 but decreased CD19 expression (P=0.0451, P=0.0479, P=0.0149 and P=0.0298, respectively). Moreover, AML1-ETO9a overexpression was related to short event-free and overall survival time (P=0.0072 and P=0.0076, respectively). Taken together, these data suggest that AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) AML-M2.

Indexed as

Chromosomes, Human, Pair 21Chromosomes, Human, Pair 8MutationTranslocation, GeneticAdolescentAdultAgedChildChild, PreschoolCore Binding Factor Alpha 2 SubunitFemaleHumansLeukemia, Myeloid, AcuteMaleMiddle AgedOncogene Proteins, FusionAML1-ETO fusion protein, humanCore Binding Factor Alpha 2 SubunitOncogene Proteins, FusionProto-Oncogene Proteins c-kitRUNX1 Translocation Partner 1 Protein

Identifiers

PMID19458628
OpenAlexW2066499145

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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.