Trial reportExperimental hematology2014
Aberrant expression of SALL4 in acute B cell lymphoblastic leukemia: mechanism, function, and implication for a potential novel therapeutic target.
Trial report in Experimental hematology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed, 31 citations in OpenAlex.
- SALL4 in gastrointestinal tract cancers: upstream and downstream regulatory mechanisms.Molecular medicine (Cambridge, Mass.) · 2024Review
- Aberrant stem cell and developmental programs in pediatric leukemia.Frontiers in cell and developmental biology · 2024Review
- Acute lymphoblastic leukemia in children and SALL4 and BMI-1 gene expression.Pediatric research · 2023Article
- The new advance of SALL4 in cancer: Function, regulation, and implication.Journal of clinical laboratory analysis · 2023Review
- Review
- SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022Review
- Targeting an Inducible SALL4-Mediated Cancer Vulnerability with Sequential Therapy.Cancer research · 2021Article
- Epigenetic Control of Infant B Cell Precursor Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2021Review
- Identification of Clinical Relevant Molecular Subtypes of Pheochromocytoma.Frontiers in endocrinology · 2021Article
- Novel prognostic prediction model constructed through machine learning on the basis of methylation-driven genes in kidney renal clear cell carcinoma.Bioscience reports · 2020Article
- Sal-Like Protein 4 Transcription Factor: A Significant Diagnostic Biomarker Involved in Childhood ALL Resistance and Relapse.Cancer management and research · 2020Article
- SALL4 promotes gastric cancer progression via hexokinase II mediated glycolysis.Cancer cell international · 2020Article
- Drug Resistance Biomarkers and Their Clinical Applications in Childhood Acute Lymphoblastic Leukemia.Frontiers in oncology · 2019Review
- miR-103/miR-195/miR-15b Regulate SALL4 and Inhibit Proliferation and Migration in Glioma.Molecules (Basel, Switzerland) · 2018Article
- ETS1 and SP1 drive DHX15 expression in acute lymphoblastic leukaemia.Journal of cellular and molecular medicine · 2018Article
- A New Indole Derivative Decreased SALL4 Gene Expression in Acute Promyelocytic Leukemia Cell Line (NB4)Iranian biomedical journal · 2018Article
- SALL4 as a transcriptional and epigenetic regulator in normal and leukemic hematopoiesis.Biomarker research · 2018Review
- Upregulation of the proto-oncogene Bmi-1 predicts a poor prognosis in pediatric acute lymphoblastic leukemia.BMC cancer · 2017Article
- Targeting SALL4 by entinostat in lung cancer.Oncotarget · 2016Article
- Functional and clinical significance of SALL4 in breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Treatment for high-risk pediatric and adult acute B cell lymphoblastic leukemia (B-ALL) remains challenging. Exploring novel pathways in B-ALL could lead to new therapy. Our previous study has shown that stem cell factor SALL4 is aberrantly expressed in B-ALL, but its functional roles and the mechanism that accounts for its upregulation in B-ALL remain unexplored. To address this question, we first surveyed the existing B-ALL cell lines and primary patient samples for SALL4 expression. We then selected the B-ALL cell lines with the highest SALL4 expression for functional studies. RNA interference was used to downregulate SALL4 expression in these cell lines. When compared with control cells, SALL4 knockdown cells exhibited decreased cell proliferation, increased apoptosis in vitro, and decreased engraftment in a xenotransplant model in vivo. Gene expression analysis showed that in SALL4 knockdown B-ALL cells, multiple caspase members involved in cell apoptosis pathway were upregulated. Next, we explored the mechanisms of aberrant SALL4 expression in B-ALL. We found that hypomethylation of the SALL4 CpG islands was correlated with its high expression. Furthermore, treatment of low SALL4-expressing B-ALL cell lines with DNA methylation inhibitor led to demethylation of the SALL4 CpG and increased SALL4 expression. In summary, to our knowledge, we are the first to show that the aberrant expression of SALL4 in B-ALL is associated with hypomethylation, and that SALL4 plays a key role in B-ALL cell survival and could be a potential novel target in B-ALL treatment.
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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.