Evidence map›Paper›PMID 23273547›Full record

ArticleMolecular oncology2013

Promoter methylation of the SALL2 tumor suppressor gene in ovarian cancers.

Chang K Sung, Dawei Li, Erik Andrews, Ronny Drapkin, Thomas Benjamin

Open access · bronzeAbstract read
In one paragraph

Article in Molecular oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. International journal of molecular sciences · 2025
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  8. Transcriptomic analysis reveals that BMP4 sensitizes glioblastoma tumor-initiating cells to mechanical cues.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Article
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  13. Epigenetic modification ofJournal of Cancer · 2018
    Article
  14. Article
  15. Article
  16. Article
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  20. The tumor suppressor protein p150(Sal2) in carcinogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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

5 authors at 2 institutions in 1 country.

Chang K SungDepartment of Microbiology and Immunobiology, Harvard Medical School, Boston, MA, USA.
Dawei Li
Erik Andrews
Ronny Drapkin
Thomas Benjamin
Harvard University · USBrigham and Women's Hospital · US

Funding

Novel Serum, Plasma, and Urine Biomarkers of Ovarian CanP50CA105009 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI CRAMER, DANIEL WILLIAM · 2004 to 2010
$13.3M
Proteomic, Genomic, and Longitudinal Pathways to Ovarian Cancer Biomarker DiscoveryU01CA152990 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI BIRRER, MICHAEL, SKATES, STEVEN J · 2010 to 2021
$8.9M
Tumor Host Range Mutants of Polyoma and Their TargetsR01CA092520 · NCI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BENJAMIN, THOMAS LIVINGSTON · 2001 to 2010
$6.0M
NCI NIH HHS P50 CA105009NCI NIH HHS R01 CA-092520NCI NIH HHS U01 CA152990
6 · The paper itself

Abstract

The SALL2 gene product and transcription factor p150 were first identified in a search for tumor suppressors targeted for inactivation by the oncogenic mouse polyoma virus. SALL2 has also been identified as a cellular quiescence factor, essential for cells to enter and remain in a state of growth arrest under conditions of serum deprivation. p150 is a transcriptional activator of p21(Cip1/Waf1) and BAX, sharing important growth arrest and proapoptotic properties with p53. It also acts as a repressor of c-myc. Restoration of SALL2 expression in cells derived from a human ovarian carcinoma (OVCA) suppresses growth of the cells in immunodeficient mice. Here we examine the pattern of p150 expression in the normal human ovary, in OVCA-derived cell lines and in primary ovarian carcinomas. Immunohistochemical staining showed that p150 is highly expressed in surface epithelial cells of the normal human ovary. Expression is exclusively from the P2 promoter governing the E1A splice variant of p150. The P2 promoter is CpG-rich and susceptible to methylation silencing. p150 expression was restored in OVCA cell lines following growth in the presence of 5-azacytidine. In a survey of 210 cases of OVCA, roughly 90% across major and minor histological types failed to show expression of the protein. Immunological and biochemical approaches were used to show hypermethylation of the SALL2 P2 promoter in OVCA-derived cell lines and in a majority of primary tumors. These results bring together molecular biological and clinical evidence in support of a role of SALL2 as a suppressor of ovarian cancers.

Indexed as

DNA MethylationPromoter Regions, GeneticBase SequenceCell Line, TransformedCell Line, TumorCpG IslandsDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticHumansMolecular Sequence DataOvarian NeoplasmsOvaryProtein IsoformsTranscription FactorsDNA-Binding ProteinsProtein IsoformsSALL2 protein, humanTranscription Factors

Identifiers

PMID23273547
PMCPMC5528472
OpenAlexW2165027982

What OpenQuestion holds

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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.