Evidence map›Paper›PMID 10980120›Full record

ArticleThe American journal of pathology2000

Highly invasive transitional cell carcinoma of the bladder in a simian virus 40 T-antigen transgenic mouse model.

P J Grippo, E P Sandgren

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 73 citations in OpenAlex.

  1. Bioprinted research models of urological malignancy.Exploration (Beijing, China) · 2024
    Review
  2. Perspective: Humanized Pig Models of Bladder Cancer.Frontiers in molecular biosciences · 2021
    Article
  3. Article
  4. Review
  5. Modeling human bladder cancer.World journal of urology · 2018
    Review
  6. Polyoma virus-associated carcinomas of the urologic tract: a clinicopathologic and molecular study.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. MALAT1 -- a paradigm for long noncoding RNA function in cancer.Journal of molecular medicine (Berlin, Germany) · 2013
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  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

2 authors at 1 institution in 1 country.

P J GrippoDepartment of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA.
E P Sandgren
University of Wisconsin–Madison · US

Funding

GENETIC MECHANISMS IN EXPERIMENTAL PANCREATIC CANCERR01CA076361 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SANDGREN, ERIC P · 1998 to 2009
$2.2M
NCI NIH HHS R01 CA076361NCI NIH HHS R01-CA76361
6 · The paper itself

Abstract

Transitional cell carcinoma (TCC), a neoplasm of urinary bladder urothelial cells, generally appears in either of two forms, papillary non-invasive or invasive TCC, although intermediate forms can occur. Each has a distinctive morphology and clinical course. Altered expression of the p53 and pRb genes has been associated with the more serious invasive TCC, suggesting that the loss of activity of these tumor suppressor proteins may have a causal role in this disease. To test this hypothesis directly, transgenic mice were developed that expressed the simian virus 40 large T antigen (TAg) in urothelial cells under the control of the cytokeratin 19 gene (CK19) regulatory elements. In one CK19-TAg lineage, all transgenic mice developed highly invasive bladder neoplasms that resembled invasive human bladder TCCs. Stages of disease progression included development of carcinoma in situ, stromal invasion, muscle invasion, rapid growth, and, in 20% of affected mice, intravascular lung metastasis. Papillary lesions never were observed. Western blot analysis indicated that TAg was bound to both p53 and pRb, which has been shown to cause inactivation of these proteins. Our findings support suggestions that (i) inactivation of p53 and/or pRb constitutes a causal step in the etiology of invasive TCC, (ii) papillary and invasive TCC may have different molecular causes, and (iii) carcinoma in situ can represent an early stage in the progression to invasive TCC.

Indexed as

Alkaline PhosphataseAnimalsAntigens, Polyomavirus TransformingBlotting, WesternCarcinoma in SituCarcinoma, Transitional CellCell LineageDisease Models, AnimalDisease ProgressionHumansImmunoenzyme TechniquesKeratinsLung NeoplasmsMiceMice, TransgenicNeoplasm InvasivenessAlkaline PhosphataseAntigens, Polyomavirus TransformingKeratinsRetinoblastoma ProteinTumor Suppressor Protein p53

Identifiers

PMID10980120
PMCPMC1885716
OpenAlexW2059044738

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.