ArticleThe Journal of clinical investigation1989
Participation of the cytokines interleukin 6, tumor necrosis factor-alpha, and interleukin 1-beta secreted by acute myelogenous leukemia blasts in autocrine and paracrine leukemia growth control.
Article in The Journal of clinical investigation, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 34 papers.
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.
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.
Who cites it
34 citing papers in PubMed, 179 citations in OpenAlex.
- Innate immune-inflammatory signaling milieu in myeloid leukemia and aging-associated clonal hematopoiesis pathologies.Frontiers in immunology · 2025Review
- Cytokine levels in patients with non-M3 myeloid leukemia are key indicators of how well the disease responds to chemotherapy.Clinical and experimental medicine · 2023Article
- Volatile Phases Derived from Serum, DC, or MLC Culture Supernatants to Deduce a VOC-Based Diagnostic Profiling Strategy for Leukemic Diseases.Biomolecules · 2023Article
- The cytokine network in acute myeloid leukemia.Frontiers in immunology · 2022Review
- Data-Driven Math Model of FLT3-ITD Acute Myeloid Leukemia Reveals Potential Therapeutic Targets.Journal of personalized medicine · 2021Article
- IL-37 Was Involved in Progress of Acute Myeloid Leukemia Through Regulating IL-6 Expression.Cancer management and research · 2021Article
- Article
- Review
- IL-32θ: a recently identified anti-inflammatory variant of IL-32 and its preventive role in various disorders and tumor suppressor activity.American journal of translational research · 2017Review
- Article
- Performance status in elderly patients with acute myeloid leukemia: exploring gene expression signatures of cytokines and chemokines.The journals of gerontology. Series A, Biological sciences and medical sciences · 2015Article
- Normal and leukemic stem cell niches: insights and therapeutic opportunities.Cell stem cell · 2015Review
- Cardiopulmonary Failure Requiring ECMO Bypass Resulting from Leukemia Cell Lysis in a Patient with Childhood Acute Myelomonocytic Leukemia.Case reports in hematology · 2015Article
- Assessment of cytokine expression profile in acute myeloid leukemia patients before and after chemotherapy.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2014Article
- TNF-α signaling in Fanconi anemia.Blood cells, molecules & diseases · 2014Review
- A VEGFR-3 antagonist increases IFN-γ expression on low functioning NK cells in acute myeloid leukemia.Journal of clinical immunology · 2013Article
- Inflammatory ROS promote and cooperate with the Fanconi anemia mutation for hematopoietic senescence.Journal of cell science · 2007Article
- Article
- Tumor necrosis factor alpha induces senescence and chromosomal instability in human leukemic cells.Oncogene · 2004Article
- Cytogenetic subgroups in acute myeloid leukemia differ in proliferative activity and response to GM-CSF.Leukemia · 2001Article
Corrections and comments
- Retraction · 2003-10-15Falsification/Fabrication of Data · Investigation by Company/Institution · Investigation by Third Party ·
- RetractedRetraction.2003
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autonomous in vitro growth of myeloid leukemic colony-forming cells may in part result from autocrine production of colony-stimulating factors (CSF). Some acute myeloid leukemia (AML) samples, however, fail to synthesize CSF despite growing autonomously in agar, and are therefore believed to bypass CSF requirements. Cytokines such as IL-6, tumor necrosis factor (TNF)-alpha, and IL-1, products of cells of the myeloid lineage, are known to be involved in growth control of myeloid progenitor cells. Since these molecules may also contribute to autocrine and paracrine growth regulation of myeloid leukemias, we screened a series of AML for cytokine production. In addition, possible roles of IL-6, TNF-alpha, and IL-1 in growth control of AML were investigated in vitro. We show that a substantial proportion of AML cells produce IL-6, TNF-alpha, and IL-1-beta and use these mediators to stimulate their growth by disparate mechanisms: IL-6 acts as a costimulator to enhance CSF-induced clonogenicity of AML blasts. TNF-alpha induces CSF production by endothelial cells and may therefore provide a paracrine loop to support leukemia growth.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.