Evidence map›Paper›PMID 27272942›Full record

ArticleInternational journal of hematology2016

High IL-7 levels in the bone marrow microenvironment mediate imatinib resistance and predict disease progression in chronic myeloid leukemia.

Xiaoyan Zhang, Huaijun Tu, Yazhi Yang, Qian Wan, Lijun Fang, Qiong Wu, Jian Li

Abstract read
PubMed Publisher
In one paragraph

Article in International journal of hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Trial
  2. Article
  3. Biology and Therapeutic Properties of Mesenchymal Stem Cells in Leukemia.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Interleukin (IL)-7 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. 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

7 authors at 2 institutions in 1 country.

Xiaoyan ZhangThe Key Laboratory of Hematology of Jiangxi Province, The Department of Hematology, The Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, 330006, Jiangxi, P.R. China.
Huaijun TuThe Department of Neurology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, P.R. China.
Yazhi YangThe Key Laboratory of Hematology of Jiangxi Province, The Department of Hematology, The Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, 330006, Jiangxi, P.R. China.
Qian WanThe Key Laboratory of Hematology of Jiangxi Province, The Department of Hematology, The Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, 330006, Jiangxi, P.R. China.
Lijun FangThe Key Laboratory of Hematology of Jiangxi Province, The Department of Hematology, The Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, 330006, Jiangxi, P.R. China.
Qiong WuThe Key Laboratory of Hematology of Jiangxi Province, The Department of Hematology, The Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, 330006, Jiangxi, P.R. China.
Jian LiThe Key Laboratory of Hematology of Jiangxi Province, The Department of Hematology, The Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, 330006, Jiangxi, P.R. China. thj127900@163.com.
Nanchang University · CNSecond Affiliated Hospital of Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is a three-stage myeloproliferative disease caused by translocation between chromosomes 9 and 22. Although tyrosine kinase inhibitors (TKI) are highly effective in the treatment of CML, numerous clinical trials have shown that many patients become refractory or drug resistance, especially those in the blastic crisis of CML. The molecular mechanisms underlying CML, however, remain poorly understood. In the present study, we used a coculture model to address possible mechanisms underlying the involvement of bone marrow microenvironment in the drug resistance of CML. Our data show that interleukin-7(IL-7) levels in the bone marrow of CML patients in blastic crisis are significantly higher than those of both healthy persons and CML patients in chronic and accelerated phases. The increased IL-7 was secreted by mesenchymal stem cells (MSC) in the bone marrow, which may protect leukemic cells from apoptosis induced by imatinib through JAK1/STAT5 signaling pathway. Our findings suggest that therapeutic strategies IL-7 signaling pathway may represent a promising approach for improving CML therapy, especially for patients in blastic crisis.

Indexed as

Disease ProgressionDrug Resistance, NeoplasmApoptosisBlast CrisisBone MarrowCells, CulturedCoculture TechniquesHumansImatinib MesylateInterleukin-7Leukemia, Myelogenous, Chronic, BCR-ABL PositiveMesenchymal Stem CellsSignal TransductionIL7 protein, humanImatinib MesylateInterleukin-7Chronic myeloid leukemiaIL-7ImatinibMesenchymal stem cells

Identifiers

PMID27272942
OpenAlexW2412984672

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.