Evidence map›Paper›PMID 27491826›Full record

ArticleScientific reports2016

Simultaneous targeted activation of Notch1 and Vhl-disruption in the kidney proximal epithelial tubular cells in mice.

Elinn Johansson, Birgitte Rönö, Martin Johansson, David Lindgren, Christina Möller, Håkan Axelson, Emma M K Smith

Open access · goldAbstract read
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Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Elinn JohanssonDivision of Translational Cancer Research, Department of Laboratory Medicine, Medicon Village, Building 404 A3, Scheelevägen 8, 404A3, 223 63 Lund, Sweden.
Birgitte RönöDivision of Translational Cancer Research, Department of Laboratory Medicine, Medicon Village, Building 404 A3, Scheelevägen 8, 404A3, 223 63 Lund, Sweden.
Martin JohanssonCenter for Molecular Pathology, Department of Translational Medicine, Skåne University Hospital, 205 02 Malmö, Sweden.
David LindgrenDivision of Translational Cancer Research, Department of Laboratory Medicine, Medicon Village, Building 404 A3, Scheelevägen 8, 404A3, 223 63 Lund, Sweden.
Christina MöllerDivision of Translational Cancer Research, Department of Laboratory Medicine, Medicon Village, Building 404 A3, Scheelevägen 8, 404A3, 223 63 Lund, Sweden.
Håkan AxelsonDivision of Translational Cancer Research, Department of Laboratory Medicine, Medicon Village, Building 404 A3, Scheelevägen 8, 404A3, 223 63 Lund, Sweden.
Emma M K SmithDivision of Translational Cancer Research, Department of Laboratory Medicine, Medicon Village, Building 404 A3, Scheelevägen 8, 404A3, 223 63 Lund, Sweden.
Medicon Village · SESkåne University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clear cell renal cell carcinoma (ccRCC) is the most common subtype of kidney cancer, representing approximately 75% of all renal neoplasms. ccRCC is known to be strongly associated with silencing of the von Hippel Lindau (VHL) tumor suppressor gene, yet VHL deficiency alone does not seem to be sufficient to drive the oncogenic transformation of normal renal epithelium and induce renal tumorigenesis. We, and others, have previously suggested that constitutive activation of the Notch signaling pathway, alongside with VHL loss, contribute to the oncogenic features of ccRCC. Here we report a prevailing hyperactivation of the Notch1 receptor in human ccRCC relative to the healthy counterpart. To explore the consequences of the elevated Notch1 signaling observed in ccRCC patient material, we made use of a conditional mouse model based on concurrent ectopic expression of constitutively active Notch1 (NICD1) and deletion of the Vhl gene. Histological examination of the kidneys of the conditional mice demonstrate the existence of nests of dysplastic cells with a clear cytoplasm as a consequence of lipid accumulation, thus displaying a one important hallmark of human ccRCC.

Indexed as

AnimalsCarcinoma, Renal CellCell Line, TumorGene Knockout TechniquesHumansKidneyKidney NeoplasmsLipid MetabolismMiceNeoplasms, ExperimentalReceptor, Notch1Signal TransductionVon Hippel-Lindau Tumor Suppressor ProteinNOTCH1 protein, humanReceptor, Notch1VHL protein, humanVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID27491826
PMCPMC4974510
OpenAlexW2476066144

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Registered trials

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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.