Evidence map›Paper›PMID 20101231›Full record

ArticleOncogene2010

Accelerated hepatocellular carcinoma development in mice expressing the Pim-3 transgene selectively in the liver.

Y Wu, Y Y Wang, Y Nakamoto, Y-Y Li, T Baba, S Kaneko, C Fujii, N Mukaida

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. PIM Kinase as an Executional Target in Cancer.Journal of cancer prevention · 2018
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Pim-3 is a Critical Risk Factor in Development and Prognosis of Prostate Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  15. Article
  16. Review
  17. Differential expression of Pim-3, c-Myc, and p-p27 proteins in adenocarcinomas of the gastric cardia and distal stomach.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  18. Review
  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

8 authors at 3 institutions in 2 countries.

Y WuDepartment of Hematology and Hematology research Laboratory, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan Province, PR China.
Y Y Wang
Y Nakamoto
Y-Y Li
T Baba
S Kaneko
C Fujii
N Mukaida
Kanazawa University · JPShinshu University · JPTakara (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pim-3, a proto-oncogene with serine/threonine kinase activity, was enhanced in hepatocellular carcinoma (HCC) tissues. To address the roles of Pim-3 in HCC development, we prepared transgenic mice that express human Pim-3 selectively in liver. The mice were born at a Mendelian ratio, were fertile and did not exhibit any apparent pathological changes in the liver until 1 year after birth. Pim-3-transgenic mouse-derived hepatocytes exhibited accelerated cell cycle progression. The administration of a potent hepatocarcinogen, diethylnitrosamine (DEN), induced accelerated proliferation of liver cells in Pim-3 transgenic mice in the early phase, compared with that observed for wild-type mice. Treatment with DEN induced lipid droplet accumulation with increased proliferating cell numbers 6 months after the treatment. Eventually, wild-type mice developed HCC with a frequency of 40% until 10 month after the treatment. Lipid accumulation was accelerated in Pim-3 transgenic mice with higher proliferating cell numbers, compared with that observed for wild-type mice. Pim-3 transgenic mice developed HCC with a higher incidence (80%) and a heavier burden, together with enhanced intratumoral CD31-positive vascular areas, compared with that observed for wild-type mice. These observations indicate that Pim-3 alone cannot cause, but can accelerate HCC development when induced by a hepatocarcinogen, such as DEN.

Indexed as

Gene Expression Regulation, NeoplasticAlbuminsAnimalsCarcinoma, HepatocellularCell ProliferationHumansLiverLiver NeoplasmsMaleMiceMice, TransgenicOrgan SpecificityPromoter Regions, GeneticProtein Serine-Threonine KinasesProto-Oncogene MasProto-Oncogene ProteinsAlbuminsMAS1 protein, humanPIM3 protein, humanProtein Serine-Threonine KinasesProto-Oncogene MasProto-Oncogene Proteins

Identifiers

PMID20101231
OpenAlexW2043776462

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.