Evidence map›Paper›PMID 22654601›Full record

ArticleTheScientificWorldJournal2012

Altered expression of cellular Bcl-2 in the progression of hamster cholangiocarcinogenesis.

Byung-Suk Jeon, Byung-Il Yoon

Open access · goldAbstract read
In one paragraph

Article in TheScientificWorldJournal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Therapeutic mechanism of treating SMMC-7721 liver cancer cells with magnetic fluid hyperthermia using Fe₂O₃ nanoparticles.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014
    Article
  3. 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

2 authors at 1 institution in 1 country.

Byung-Suk JeonLaboratory of Histology and Molecular Pathogenesis, College of Veterinary Medicine and Institute of Veterinary Science, Kangwon National University, Chuncheon 200-701, Republic of Korea.
Byung-Il Yoon
Kangwon National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bcl-2 is an intracytoplasmic and membrane-associated apoptosis suppressor, and its overexpression is closely associated with survival of malignant tumors, in particular their aggressive behavior and poor prognosis. The role of Bcl-2 is, however, still controversial in cholangiocarcinogenesis because of the discrepancies in the expression of the protein. In the present study, alteration in the expression of Bcl-2 in cholangiocarcinogenesis was investigated by studying the immunoreactivities of this protein in normal, hyperplastic bile ducts with or without dysplastic changes, and neoplastic bile duct cells from a hamster cholangiocarcinoma (ChC) model. Cytoplasmic staining, which reflects high-Bcl-2 immunoreactivity, was negative to very weak in normal and hyperplastic bile ducts without dysplastic changes, while hyperplastic bile ducts with dysplasia indicated heterogeneously strong expression. On the other hand, most of the neoplastic cells of invasive cholangiocarcinomas were negative to weak as much as the level of normal bile ducts. The results suggest that the antiapoptotic factor Bcl-2 plays a limited role in the survival of highly proliferative, potentially dysplastic bile duct cells. However, the role of Bcl-2 in biliary cancer cells was not significant.

Indexed as

AnimalsBile Duct NeoplasmsBlotting, WesternCholangiocarcinomaCricetinaeDisease ProgressionImmunohistochemistryLiverProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-bcl-2

Identifiers

PMID22654601
PMCPMC3361260
OpenAlexW2108014571

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.