Evidence map›Paper›PMID 27132514›Full record

ArticleOncogene2016

Leukemic survival factor SALL4 contributes to defective DNA damage repair.

F Wang, C Gao, J Lu, H Tatetsu, D A Williams, L U Müller, W Cui, L Chai

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 20% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. SALL4 is a CRL3Cell death and differentiation · 2024
    Article
  3. Article
  4. Review
  5. Review
  6. SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022
    Review
  7. SALL4 Gene Expression in Acute Myeloid Leukemia.Asian Pacific journal of cancer prevention : APJCP · 2019
    Article
  8. Review
  9. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

F WangDepartment of Pathology, Joint Program in Transfusion Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
C GaoDepartment of Pathology, Joint Program in Transfusion Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
J LuDepartment of Pathology, Joint Program in Transfusion Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
H TatetsuDepartment of Pathology, Joint Program in Transfusion Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
D A WilliamsDivision of Hematology/Oncology, Children's Hospital Boston, Harvard Medical School, Boston, MA, USA.
L U MüllerDivision of Hematology/Oncology, Children's Hospital Boston, Harvard Medical School, Boston, MA, USA.
W CuiDepartment of Clinical Laboratory, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
L ChaiDepartment of Pathology, Joint Program in Transfusion Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Harvard University · USBoston Children's Hospital · USPeking Union Medical College Hospital · CNBrigham and Women's Hospital · US

Funding

Transcription regulation in hematopoiesisP01HL095489 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI PARK, SHINYOUNG · 2010 to 2020
$20.1M
Murine Models on SALL4 in Hepatocellular CarcinomaR03CA184531 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI CHAI, LI · 2015 to 2016
$163k
NCI NIH HHS R03 CA184531NHLBI NIH HHS P01 HL095489
6 · The paper itself

Abstract

SALL4 is aberrantly expressed in human myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). We have generated a SALL4 transgenic (SALL4B Tg) mouse model with pre-leukemic MDS-like symptoms that transform to AML over time. This makes our mouse model applicable for studying human MDS/AML diseases. Characterization of the leukemic initiation population in this model leads to the discovery that Fancl (Fanconi anemia, complementation group L) is downregulated in SALL4B Tg leukemic and pre-leukemic cells. Similar to the reported Fanconi anemia (FA) mouse model, chromosomal instability with radial changes can be detected in pre-leukemic SALL4B Tg bone marrow (BM) cells after DNA damage challenge. Results from additional studies using DNA damage repair reporter assays support a role of SALL4 in inhibiting the homologous recombination pathway. Intriguingly, unlike the FA mouse model, after DNA damage challenge, SALL4B Tg BM cells can survive and generate hematopoietic colonies. We further elucidated that the mechanism by which SALL4 promotes cell survival is through Bcl2 activation. Overall, our studies demonstrate for the first time that SALL4 has a negative impact in DNA damage repair, and support the model of dual functional properties of SALL4 in leukemogenesis through inhibiting DNA damage repair and promoting cell survival.

Indexed as

DNA DamageDNA RepairAnimalsBone Marrow CellsBone Marrow TransplantationChromosomal InstabilityCluster AnalysisDisease Models, AnimalDNA-Binding ProteinsDNA End-Joining RepairFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group L ProteinFemaleGene ExpressionGene Expression ProfilingGene Expression RegulationDNA-Binding ProteinsFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group L ProteinMitomycinSALL4 protein, humanSall4 protein, mouseTranscription Factors

Identifiers

PMID27132514
PMCPMC5093088
OpenAlexW2345637395

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.