Evidence map›Paper›PMID 35072947›Full record

ArticleThe Journal of pathology2022

GPNMB expression identifies TSC1/2/mTOR-associated and MiT family translocation-driven renal neoplasms.

Daniela C Salles, Kaushal Asrani, Juhyung Woo, Thiago Vidotto, Hans B Liu, Igor Vidal, Andres Matoso, George J Netto, Pedram Argani, Tamara L Lotan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
12.9field-weighted citation impact, top 1% 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

44 citing papers in PubMed, 95 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

10 authors at 2 institutions in 1 country.

Daniela C Salles *Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0003-1904-185X
Kaushal Asrani *Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Juhyung WooDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Thiago VidottoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Hans B LiuDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Igor VidalDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Andres MatosoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
George J NettoDepartment of Pathology, University of Alabama, Birmingham, AL, USA.
Pedram ArganiDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Tamara L LotanDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-0494-9067
Johns Hopkins University · USUniversity of Alabama at Birmingham · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI WILLIAM George NELSON · 1985 to 2026
$208.6M
BIOCHEMISTRY, CELLULAR AND MOLECULAR BIOLOGY PROGRAMT32GM007445 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI GREEN, RACHEL · 1985 to 2021
$24.1M
NCI Cancer Center Support 5P30CA006973-52NCI NIH HHS P30 CA006973NIGMS NIH HHS T32 GM007445
6 · The paper itself

Abstract

GPNMB (glycoprotein nonmetastatic B) and other TFE3/TFEB transcriptional targets have been proposed as markers for microphthalmia (MiT) translocation renal cell carcinomas (tRCCs). We recently demonstrated that constitutive mTORC1 activation via TSC1/2 loss leads to increased activity of TFE3/TFEB, suggesting that the pathogenesis and molecular markers for tRCCs and TSC1/2-associated tumors may be overlapping. We examined GPNMB expression in human kidney and angiomyolipoma (AML) cell lines with TSC2 and/or TFE3/TFEB loss produced using CRISPR-Cas9 genome editing as well as in a mouse model of Tsc2 inactivation-driven renal tumorigenesis. Using an automated immunohistochemistry (IHC) assay for GPNMB, digital image analysis was employed to quantitatively score expression in clear cell RCC (ccRCC, n = 87), papillary RCC (papRCC, n = 53), chromophobe RCC (chRCC, n = 34), oncocytoma (n = 4), TFE3- or TFEB-driven tRCC (n = 56), eosinophilic solid and cystic RCC (ESC, n = 6), eosinophilic vacuolated tumor (EVT, n = 4), and low-grade oncocytic tumor (LOT, n = 3), as well as AML (n = 29) and perivascular epithelioid cell tumors (PEComas, n = 8). In cell lines, GPNMB was upregulated following TSC2 loss in a MiT/TFE- and mTORC1-dependent fashion. Renal tumors in Tsc2

Indexed as

Carcinoma, Renal CellKidney NeoplasmsLeukemia, Myeloid, AcuteMicrophthalmosPerivascular Epithelioid Cell NeoplasmsAnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBiomarkers, TumorEye ProteinsFemaleHumansMaleMechanistic Target of Rapamycin Complex 1Membrane GlycoproteinsMiceTOR Serine-Threonine KinasesBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBiomarkers, TumorEye ProteinsGPNMB protein, humanGpnmb protein, mouseMechanistic Target of Rapamycin Complex 1Membrane GlycoproteinsMTOR protein, humanTOR Serine-Threonine KinasesTranscription FactorsangiomyolipomaGPNMBrenal cell carcinomaTFE3TFEBtranslocation renal cell carcinomaTSC1/2

Identifiers

PMID35072947
PMCPMC9310781
OpenAlexW4206899650

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.