Evidence map›Paper›PMID 15467739›Full record

ArticleOncogene2004

Inactivating mutations of the Siah-1 gene in gastric cancer.

Chang Jae Kim, Yong Gu Cho, Cho Hyun Park, Seong Whan Jeong, Suk Woo Nam, Su Young Kim, Sug Hyung Lee, Nam Jin Yoo, Jung Young Lee, Won Sang Park

Abstract 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. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 13% 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, 46 citations in OpenAlex.

  1. Article
  2. The roles of E3 ligases in Hepatocellular carcinoma.American journal of cancer research · 2022
    Review
  3. Tumor reversion: a dream or a reality.Biomarker research · 2021
    Review
  4. Review
  5. MUTYH: Not just polyposis.World journal of clinical oncology · 2020
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Regulators and effectors of Siah ubiquitin ligases.Cell biochemistry and biophysics · 2013
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

10 authors at 1 institution in 1 country.

Chang Jae KimDepartment of Pathology, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Yong Gu Cho
Cho Hyun Park
Seong Whan Jeong
Suk Woo Nam
Su Young Kim
Sug Hyung Lee
Nam Jin Yoo
Jung Young Lee
Won Sang Park
Catholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SIAH-1: is the mammalian homolog of Drosophila seven in absentia (sina) and has been identified as a p53-inducible gene. Siah-1 can induce cell cycle arrests, tumor suppression, and apoptosis through a novel beta-catenin degradation pathway. To determine whether genetic alterations of Siah-1 gene are involved in the development and/or progression of gastric cancer, we searched for mutation of the Siah-1 gene in 95 gastric cancers by single-strand conformational polymorphism and sequencing. The effect of Siah-1 on beta-catenin degradation was further examined in wild- and mutant-type Siah-1-transfected HEK 293T cells. We found two missense mutations of the Siah-1 gene. The cases with Siah-1 mutation showed nuclear translocation and cytoplasmic staining of beta-catenin. Interestingly, two mutants of Siah-1 stabilized cytoplasmic levels of beta-catenin, even after treatment of adriamycin. Furthermore, both mutants failed to suppress cyclin D1 expression and to induce apoptosis. These data suggest that inactivating mutations of the Siah-1 may contribute to the development of gastric cancer through beta-catenin stabilization and apoptosis block.

Indexed as

Apoptosisbeta CateninCell Line, TumorCyclin D1Cytoskeletal ProteinsGene Expression RegulationHumansImmunohistochemistryMutationNuclear ProteinsProtein TransportSeven in Absentia ProteinsStomach NeoplasmsTrans-ActivatorsTumor Suppressor Protein p53Ubiquitin-Protein Ligasesbeta CateninCTNNB1 protein, humanCyclin D1Cytoskeletal ProteinsNuclear ProteinsSeven in Absentia ProteinsTrans-ActivatorsTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID15467739
OpenAlexW2051486745

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.