ArticleBlood2006
SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 2 of them syntheses that pooled 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.
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
126 citing papers in PubMed, 2 syntheses or guidelines pooled it, 217 citations in OpenAlex.
- The Coming of Age of Preclinical Models of MDS.Frontiers in oncology · 2022Pooled it
- Higher expression of SALL4 predicts poor cancer prognosis: A meta-analysis.Cancer biomarkers : section A of Disease markers · 2017Pooled it
- Aberrant expression of SALL4 in acute B cell lymphoblastic leukemia: mechanism, function, and implication for a potential novel therapeutic target.Experimental hematology · 2014Trial
- ADT increases prostate cancer cell invasion via altering AR/SALL4/SOX2-OCT4 stem cell signaling.Cell biology and toxicology · 2025Article
- Cytoplasmic SALL4-A isoform expression as a diagnostic marker of less aggressive tumor behavior in gastric cancer.World journal of surgical oncology · 2025Article
- Review
- SALL4 in gastrointestinal tract cancers: upstream and downstream regulatory mechanisms.Molecular medicine (Cambridge, Mass.) · 2024Review
- SALL4 is a CRL3Cell death and differentiation · 2024Article
- Acute lymphoblastic leukemia in children and SALL4 and BMI-1 gene expression.Pediatric research · 2023Article
- Dissecting the cell of origin of aberrant SALL4 expression in myelodysplastic syndrome.Clinical and translational medicine · 2023Article
- SALL4 correlates with proliferation, metastasis, and poor prognosis in prostate cancer by affecting MAPK pathway.Cancer medicine · 2023Article
- The new advance of SALL4 in cancer: Function, regulation, and implication.Journal of clinical laboratory analysis · 2023Review
- Dual-Regulated Mechanism of EZH2 and KDM6A on SALL4 Modulates Tumor Progression via Wnt/β-Catenin Pathway in Gastric Cancer.Digestive diseases and sciences · 2023Article
- Review
- Curse and blessing: upregulation of oncogenes upon treatment with hypomethylating agents in myelodysplastic syndrome.Signal transduction and targeted therapy · 2022Article
- Demethylation and Up-Regulation of an Oncogene after Hypomethylating Therapy.The New England journal of medicine · 2022Article
- SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022Review
- Pluripotency Stemness and Cancer: More Questions than Answers.Advances in experimental medicine and biology · 2022Article
- SALL Proteins; Common and Antagonistic Roles in Cancer.Cancers · 2021Review
- Pseudogene-mediated DNA demethylation leads to oncogene activation.Science advances · 2021Article
66 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
10 authors at 2 institutions in 1 country.
Funding
Abstract
SALL4, a human homolog to Drosophila spalt, is a novel zinc finger transcriptional factor essential for development. We cloned SALL4 and its isoforms (SALL4A and SALL4B). Through immunohistochemistry and real-time reverse-transcription-polymerase chain reaction (RT-PCR), we demonstrated that SALL4 was constitutively expressed in human primary acute myeloid leukemia (AML, n = 81), and directly tested the leukemogenic potential of constitutive expression of SALL4 in a murine model. SALL4B transgenic mice developed myelodysplastic syndrome (MDS)-like features and subsequently AML that was transplantable. Increased apoptosis associated with dysmyelopoiesis was evident in transgenic mouse marrow and colony-formation (CFU) assays. Both isoforms could bind to beta-catenin and synergistically enhanced the Wnt/beta-catenin signaling pathway. Our data suggest that the constitutive expression of SALL4 causes MDS/AML, most likely through the Wnt/beta-catenin pathway. Our murine model provides a useful platform to study human MDS/AML transformation, as well as the Wnt/beta-catenin pathway's role in the pathogenesis of leukemia stem cells.
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.