Evidence map›Paper›PMID 30623437›Full record

ArticleJournal of cellular physiology2019

Increased autocrine interleukin-6 production is significantly associated with worse clinical outcome in patients with chronic lymphocytic leukemia.

Hua-Qing Wang, Li Jia, Yu-Ting Li, Timothy Farren, Samir G Agrawal, Feng-Ting Liu

Expression of concernOpen access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.3field-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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Hua-Qing WangDepartment of Hematology and Oncology, Tianjin Union Medial Center of Nankai University, Tianjin, China.
Li JiaCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom.ORCID 0000-0002-6076-8455
Yu-Ting LiKey Laboratory of Cancer Prevention and Therapy, National Clinical Research Centre for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Timothy FarrenPathology Group, Blizard Institute, Queen Mary University of London, London, United Kingdom.
Samir G AgrawalDivision of Haemato-Oncology, St Bartholomew's Hospital, Barts Health NHS Trust and Queen Mary University of London, London, United Kingdom.
Feng-Ting LiuDepartment of Hematology and Oncology, Tianjin Union Medial Center of Nankai University, Tianjin, China.ORCID 0000-0002-0332-257X
Queen Mary University of London · GBSt Bartholomew's Hospital · GBNankai University · CNTianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic lymphocytic leukemia (CLL) remains incurable with current standard therapy. We have previously reported that an increased expression of interleukin-6 (IL-6) receptor CD126 leads to resistance of CLL cells to chemotherapy and worse prognosis for patients with CLL. In this study, we determine whether autocrine IL-6 production by CLL B cells is associated with poor clinical outcome and explore IL-6-mediated survival mechanism in primary CLL cells. Our results demonstrate that higher levels of autocrine IL-6 are significantly associated with shorter absolute lymphocyte doubling time, patients received treatment, without complete remission, advanced Binet stages, 17p/11q deletion, and shorter time to first time treatment and progression-free survival. IL-6 activated both STAT3 and nuclear factor kappa B (NF-κB) in primary CLL cells. Blocking IL-6 receptor and JAK2 inhibited IL-6-mediated activation of STAT3 and NF-κB. Our study demonstrates that an increased autocrine IL-6 production by CLL B-cells are associated with worse clinical outcome for patients with CLL. IL-6 promotes CLL cell survival by activating both STAT3 and NF-κB through diverse signaling cascades. Neutralizing IL-6 or blocking IL-6 receptor might contribute overcoming the resistance of CLL cells to chemotherapy. We propose that the measurement of autocrine IL-6 could be a useful approach to predict clinical outcome.

Indexed as

Autocrine CommunicationApoptosisDisease-Free SurvivalHumansInterleukin-6Leukemia, Lymphocytic, Chronic, B-CellMitochondriaMultivariate AnalysisNF-kappa BSignal TransductionSTAT3 Transcription FactorTreatment OutcomeTumor Cells, CulturedInterleukin-6NF-kappa BSTAT3 Transcription Factorautocrine IL-6chronic lymphocytic leukemiaclinical outcometumor microenvironment

Identifiers

PMID30623437
PMCPMC6590298
OpenAlexW2909765484

What OpenQuestion holds

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LicenceCC BY-NC
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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.