Leukemic survival factor SALL4 contributes to defective DNA damage repair
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SALL4 overexpression is associated with poor prognosis and lower survival rate of patients.
“its overexpression is associated with poor prognosis and lower survival rate of patients [64–67]”
From SALL4 is a CRL3REN/KCTD11 substrate that drives Sonic Hedgehog-dependent medulloblastoma (2024) · cites this paper as [66]
The Results section (page unavailable) associates higher SALL4 expression with complex karyotype in MDS/AML patients, and the Introduction reports aberrant expression in high-grade MDS. The paper does not show that patients with higher SALL4 expression had poorer prognosis or lower survival rates; the Discussion's reference to poor prognosis concerns MDS patients who progress to AML generally. (LLM, conf=0.76)
Experimental — accuracy not yet measuredAberrant SALL4 activity has been reported in acute myeloid leukemia, lung adenocarcinoma, breast cancer, and other aggressive malignancies.
“An aberrant SALL4 activity has been reported in acute myeloid leukemia, lung adenocarcinoma, breast cancer, and other aggressive malignancies”
From SALL4 is a CRL3REN/KCTD11 substrate that drives Sonic Hedgehog-dependent medulloblastoma (2024) · cites this paper as [66]
The Introduction (page not provided) says SALL4 is aberrantly expressed in most acute myeloid leukemia patients, supporting the AML portion. The paper does not report aberrant SALL4 activity in lung adenocarcinoma, breast cancer, or other aggressive malignancies; searches for those cancers found no supporting passage. (LLM, conf=0.90)
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- Authors
- Wang, F., Gao, C., Lu, J., Tatetsu, H., Williams, D. A., Müller, L. U., Cui, W., & Chai, L.
- Affiliations
- Brigham and Women's Hospital (US)
- Boston Children's Hospital (US)
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Corresponding author
- Cui, W
- Chai, L
- Venue
- Oncogene
- Published
- 2016-05-02
- Volume
- 35
- Issue
- 47
- Pages
- 6087-6095
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- PMC
- PMC5093088
- OpenAlex
- W2345637395
- Cited by
- 17
- References
- 43
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 1 · 2020: 1 · 2019: 3 · 2018: 4
- FWCI
- 1.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Heart, Lung, and Blood Institute (P01HL095489)
- National Cancer Institute (R03CA184531)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Blood disorders and treatments
- Keywords
- SALL4, DNA repair, Fanconi anemia, FANCL, homologous recombination, myelodysplastic syndrome, acute myeloid leukemia, leukemogenesis, chromosomal instability, Bcl-2, transgenic mouse model, hematopoietic cell survival, bone marrow
- MeSH terms
- Animals, Bone Marrow Cells, Disease Models, Animal, DNA Damage, DNA Repair, DNA-Binding Proteins, Female, Gene Expression Regulation, Hematopoietic Stem Cells, Humans, Male, Mice, Transgenic, Myelodysplastic Syndromes, Transcription Factors, Leukemia, Myeloid, Acute, Gene Expression, Cluster Analysis, Bone Marrow Transplantation, Mitomycin, Genes, bcl-2, Gene Expression Profiling, Chromosomal Instability, Mice, Fanconi Anemia Complementation Group D2 Protein, Fanconi Anemia Complementation Group L Protein, Homologous Recombination, DNA End-Joining Repair, Karyotype
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