Evidence map›Paper›PMID 15855651›Full record

ArticleThe American journal of pathology2005

Deletion of Bid impedes cell proliferation and hepatic carcinogenesis.

Li Bai, Hong-Min Ni, Xiaoyun Chen, Daniell DiFrancesca, Xiao-Ming Yin

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Cancer's Achilles' Heel: Apoptosis and Necroptosis to the Rescue.International journal of molecular sciences · 2016
    Review
  6. The Paradox of p53: What, How, and Why?Cold Spring Harbor perspectives in medicine · 2016
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Rejuvenating Bi(d)ology.Oncogene · 2013
    Review
  14. Bid-ding for mercy: twisted killer in action.Cell death and differentiation · 2013
    Article
  15. Article
  16. Article
  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

5 authors at 1 institution in 1 country.

Li BaiDepartment of Pathology, University of Pittsburgh School of Medicine, Scaife Hall, 7th Floor, Room S739, 3550 Terrace Street, Pittsburgh, Pennsylvania 15261, USA.
Hong-Min Ni
Xiaoyun Chen
Daniell DiFrancesca
Xiao-Ming Yin
University of Pittsburgh · US

Funding

Signal integration of the death receptor pathwaysR01CA083817 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI YIN, XIAO-MING · 2000 to 2010
$2.1M
DEATH AGONIST, BID, AND DEVELOPMENT AND NEOPLASIAK01CA074885 · NCI · WASHINGTON UNIVERSITY · PI YIN, XIAO-MING · 1997 to 2001
$305k
NCI NIH HHS K01 CA 74885NCI NIH HHS R01 CA083817NCI NIH HHS R01 CA 83817
6 · The paper itself

Abstract

Mechanisms that control the proliferation capability of the initiated cells during hepatocarcinogenesis are still largely unclear. We investigated the role of a pro-death Bcl-2 family protein, Bid, in liver tumor development using a neonatal diethylnitrosamine model. Diethylnitrosamine was administrated to 15-day-old wild-type and bid-null mice. The development of microfoci at the early stage and of gross tumors at the later stage was compared between the two groups of mice. Both microfoci and gross tumor development were significantly retarded in the bid-null mice, despite reduced cell death as measured by TUNEL staining. Further studies indicated that there were significantly less proliferating cells in diethylnitrosamine-treated bid-null livers. The regulation of cell proliferation by Bid was confirmed in two other systems not involving carcinogenesis. Hepatocyte proliferation following partial hepatectomy and T lymphocyte proliferation following anti-CD3 stimulation were both retarded in bid-null mice. Thus, these studies revealed a previously undisclosed function of Bid in regulating cell proliferation, which can be important to tumor development. Furthermore, the role of Bid in promoting hepatocarcinogenesis is in contrast to its reported role in suppressing myeloid leukemia and thus suggests an organ- and/or etiology-specific role of the Bcl-2 family proteins in regulating oncogenesis.

Indexed as

AnimalsBH3 Interacting Domain Death Agonist ProteinCarrier ProteinsCell CycleCell DeathCell ProliferationDiethylnitrosamineHepatectomyHepatocytesLiver Neoplasms, ExperimentalMaleMiceMice, Inbred C57BLMice, KnockoutBH3 Interacting Domain Death Agonist ProteinBid protein, mouseCarrier ProteinsDiethylnitrosamine

Identifiers

PMID15855651
PMCPMC1606404
OpenAlexW1994462266

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.