Evidence map›Paper›PMID 25023703›Full record

ArticleOncogene2015

Conditional inactivation of the mouse von Hippel-Lindau tumor suppressor gene results in wide-spread hyperplastic, inflammatory and fibrotic lesions in the kidney.

T L Pritchett, H L Bader, J Henderson, T Hsu

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

38 citing papers in PubMed, 54 citations in OpenAlex.

  1. Tumor-Induced PDPNInternational journal of molecular sciences · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Loss of Von Hippel-Lindau (International journal of molecular sciences · 2021
    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

4 authors at 2 institutions in 2 countries.

T L PritchettDepartment of Medicine, Boston University School of Medicine, Boston, MA, USA.
H L BaderDepartment of Medicine, Boston University School of Medicine, Boston, MA, USA.
J Henderson1] Department of Medicine, Boston University School of Medicine, Boston, MA, USA [2] Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
T Hsu1] Department of Medicine, Boston University School of Medicine, Boston, MA, USA [2] Institute of Systems Biology and Bioinformatics, National Central University, Jhongli, Taiwan.
Boston University · USNational Central University · TW

Funding

RESEARCH TRAINING IN BLOOD DISEASES AND RESOURCEST32HL007501 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LERNER, ADAM, STEINBERG, MARTIN H. · 1985 to 2018
$5.4M
VHL tumor suppressor gene and the initiation of renal cell carcinomaR01CA109860 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HSU, TIEN · 2004 to 2015
$3.2M
NCI NIH HHS #R01CA109860NCI NIH HHS R01 CA109860NHLBI NIH HHS #T32HL007501
6 · The paper itself

Abstract

Mutations of the tumor suppressor gene von Hippel-Lindau (VHL) can lead to benign and malignant tumors, including clear-cell renal cell carcinoma (ccRCC). To understand the progression of ccRCC, we generated a novel mouse Vhlh conditional knockout, using Hoxb7-driven Cre that is specific for the collecting ducts and a subset of distal tubules. These mice exhibited wide-spread epithelial disruption and interstitial inflammation as early as 2 months of age with high penetrance. Lesions are cystic, show severe fibrosis and display significant hyperplasia. An abundance of infiltrating macrophages and lymphocytes was detected. Interestingly, the Vhlh mutant lesions could be rescued when Hif-1α, but not Hif-2α, was also knocked out. In addition, administration of a JAK1/2 kinase inhibitor alleviated the Vhlh knockout phenotypes. Taken together, these results suggest that HIF-1α-dependent inflammation and fibrosis may be an early event in the development of ccRCC.

Indexed as

MutationAnimalsCarcinoma, Renal CellFibrosisHumansHyperplasiaHypoxia-Inducible Factor 1, alpha SubunitJanus Kinase 1Janus Kinase 2KidneyKidney NeoplasmsMiceMice, TransgenicVon Hippel-Lindau Tumor Suppressor ProteinHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitJak1 protein, mouseJak2 protein, mouseJanus Kinase 1Janus Kinase 2VHL protein, mouseVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID25023703
OpenAlexW2084998185

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.