Evidence map›Paper›PMID 15107820›Full record

ArticleOncogene2004

The topoisomerase I- and p53-binding protein topors is differentially expressed in normal and malignant human tissues and may function as a tumor suppressor.

Ahamed Saleem, Jayeeta Dutta, Diptee Malegaonkar, Farheena Rasheed, Zeshaan Rasheed, Rajeev Rajendra, Henderson Marshall, Minje Luo, Honghua Li, Eric H Rubin

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-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

18 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Regulation of the p53 Family Proteins by the Ubiquitin Proteasomal Pathway.International journal of molecular sciences · 2019
    Review
  6. Article
  7. Review
  8. Epigenetic therapy in gastrointestinal cancer: the right combination.Therapeutic advances in gastroenterology · 2016
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Plk1-mediated phosphorylation of Topors regulates p53 stability.The Journal of biological chemistry · 2009
    Article
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Ahamed SaleemDepartment of Pharmacology, The Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ, USA.
Jayeeta Dutta
Diptee Malegaonkar
Farheena Rasheed
Zeshaan Rasheed
Rajeev Rajendra
Henderson Marshall
Minje Luo
Honghua Li
Eric H Rubin
Rutgers Cancer Institute of New JerseyRutgers, The State University of New Jersey · US

Funding

MECHANISMS OF ACTION IN ANTITUMOR DRUGSR01CA039662 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI LIU, LEROY F · 1985 to 2013
$3.8M
FUNCTIONAL STUDIES OF TOPOISOMERASE IR01GM059170 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI RUBIN, ERIC H. · 1999 to 2002
$623k
NCI NIH HHS CA39662NIGMS NIH HHS GM59170
6 · The paper itself

Abstract

Topors was identified recently as a human protein that binds to topoisomerase I and p53. Topors contains a highly conserved RING domain and localizes in promyelocytic leukemia nuclear bodies. Relatively little is known regarding topors expression patterns or function. We now demonstrate that topors mRNA and protein are widely expressed in normal human tissues. By contrast, topors mRNA and protein levels are decreased or undetectable in colon adenocarcinomas relative to normal colon tissue, and expression of the topors protein is not detectable in several colon cancer cell lines. The human TOPORS gene is located on chromosome 9p21, with loss of heterozygosity in this region frequently observed in several different malignancies. While we were unable to detect loss of heterozygosity of the TOPORS gene in 16 sporadic colon cancer cases, increased methylation of a CpG island in the TOPORS promoter was evident in colon adenocarcinoma specimens relative to matched normal tissues. Additional studies indicate that forced expression of topors inhibits cellular proliferation and is associated with an accumulation of cells in the G(0)/G(1) phase of the cell cycle. This effect is independent of the topors RING domain and maps to a C-terminal region of the protein. These results suggest that topors functions as a negative regulator of cell growth, and possibly as a tumor suppressor.

Indexed as

Genes, Tumor SuppressorNeoplasm ProteinsAdenocarcinomaCarrier ProteinsCell CycleCell DivisionColonColonic NeoplasmsCpG IslandsDNA-Binding ProteinsDNA MethylationFlow CytometryG1 PhaseGreen Fluorescent ProteinsHeLa CellsHumansCarrier ProteinsDNA-Binding ProteinsGreen Fluorescent ProteinsLuminescent ProteinsNeoplasm ProteinsNuclear ProteinsRNA, MessengerThymidineTOPORS protein, humanTranscription FactorsTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID15107820
OpenAlexW2332416849

What OpenQuestion holds

Textmetadata
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.