ReviewOncogene2000
The role of STATs in myeloid differentiation and leukemia.
Review in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 227 citations in OpenAlex.
- Preliminary Effects of Benralizumab in an AML Cell Model with Promyelocytic Features Expressing IL-5R: An Exploratory Proof-of-Concept Study.Biomedicines · 2026Article
- NDRG1 enhances the sensitivity to Cetuximab by promoting Stat1 ubiquitylation in colorectal cancer.Journal of advanced research · 2025Article
- The JAK-STAT pathway: from structural biology to cytokine engineering.Signal transduction and targeted therapy · 2024Review
- Inflammation as a driver of hematological malignancies.Frontiers in oncology · 2024Review
- Targeting of STAT5 using the small molecule topotecan hydrochloride suppresses acute myeloid leukemia progression.Oncology reports · 2023Article
- Article
- Human cytomegalovirus UL138 interaction with USP1 activates STAT1 in infection.PLoS pathogens · 2023Article
- Human Cytomegalovirus UL138 Interaction with USP1 Activates STAT1 in infection.bioRxiv : the preprint server for biology · 2023Article
- Article
- Targeting cancer cell plasticity by HDAC inhibition to reverse EBV-induced dedifferentiation in nasopharyngeal carcinoma.Signal transduction and targeted therapy · 2021Article
- STAT3 phosphorylation in central leptin resistance.Nutrition & metabolism · 2021Review
- The Role of Janus Kinase/STAT3 Pathway in Hematologic Malignancies With an Emphasis on Epigenetics.Frontiers in genetics · 2021Review
- Shwachman-Diamond Syndrome: Molecular Mechanisms and Current Perspectives.Molecular diagnosis & therapy · 2019Review
- BCR-ABL Independent Mechanisms of Resistance in Chronic Myeloid Leukemia.Frontiers in oncology · 2019Review
- Signal Transducer and Activator of Transcription (STATs) Proteins in Cancer and Inflammation: Functions and Therapeutic Implication.Frontiers in oncology · 2019Review
- The phosphatase PPM1A controls monocyte-to-macrophage differentiation.Scientific reports · 2018Article
- Transcriptional Regulation of Emergency Granulopoiesis in Leukemia.Frontiers in immunology · 2018Review
- Automatic identification of informative regions with epigenomic changes associated to hematopoiesis.Nucleic acids research · 2017Article
- Phloridzin docosahexaenoate, a novel flavonoid derivative, suppresses growth and induces apoptosis in T-cell acute lymphoblastic leukemia cells.American journal of cancer research · 2017Article
- Phosphorylated STAT5 regulates p53 expression via BRCA1/BARD1-NPM1 and MDM2.Cell death & disease · 2016Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myeloid differentiation is a highly regulated process governed by various cytokines, such as EPO, TPO, G-CSF, IL-3, IL-5 and GM-CSF. These cytokines act in part through activation of the STAT transcription factor family. In particular, various isoforms of STAT3 and STAT5 are activated during myeloid differentiation in a cell-type and maturation-state dependent fashion. In vitro studies have shown that STAT proteins are essential for cytokine-regulated processes such as cellular proliferation, differentiation as well as survival. Similarly, various STAT knock-outs have highlighted the role of STATs in myeloid differentiation in vivo. STATs also appear to play an important role in various myeloid malignancies, which are characterized by arrested maturation and cytokine-independent proliferation of myeloid progenitors. Constitutive activation of STAT3 and/or STAT5 resulting in enhanced transcription of anti-apoptotic- cell-cycle progression genes is likely to contribute to the pathogenesis of various myeloid leukemia's. Oncogene (2000).
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.