Evidence map›Paper›PMID 33144689›Full record

ReviewNature reviews. Nephrology2021

Clear cell renal cell carcinoma ontogeny and mechanisms of lethality.

Eric Jonasch, Cheryl Lyn Walker, W Kimryn Rathmell

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 438 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
438citing papers in PubMed, 1 pooled it
44.7field-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

438 citing papers in PubMed, 1 synthesis or guideline pooled it, 662 citations in OpenAlex.

  1. Pooled it
  2. Diagnostic efficacy of [European journal of nuclear medicine and molecular imaging · 2024
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  5. Integrative omics profiling of CRELD2 in ccRCC: a nexus of genetics, prognosis, and tumor microenvironment.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  7. Review
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378 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 1 country.

Eric JonaschDepartment of Genitourinary Medical Oncology, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. ejonasch@mdanderson.org.ORCID http://orcid.org/0000-0003-0943-2806
Cheryl Lyn WalkerCenter for Precision Environmental Health, Baylor College of Medicine, Houston, TX, USA.
W Kimryn RathmellDepartment of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.ORCID http://orcid.org/0000-0002-4984-0225
Baylor College of Medicine · USThe University of Texas MD Anderson Cancer Center · USVanderbilt University Medical Center · US

Funding

A New Target for Chromatin Remodeler Defects in CancerR35CA231993 · NCI · BAYLOR COLLEGE OF MEDICINE · PI WALKER, CHERYL L. · 2018 to 2024
$6.2M
Methyltransferase Contributions to Genomic Stability and CancerR01CA203012 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RATHMELL, WENDY KIMRYN, WALKER, CHERYL L. · 2016 to 2020
$2.2M
NCI NIH HHS R01 CA203012NCI NIH HHS R35 CA231993
6 · The paper itself

Abstract

The molecular features that define clear cell renal cell carcinoma (ccRCC) initiation and progression are being increasingly defined. The TRACERx Renal studies and others that have described the interaction between tumour genomics and remodelling of the tumour microenvironment provide important new insights into the molecular drivers underlying ccRCC ontogeny and progression. Our understanding of common genomic and chromosomal copy number abnormalities in ccRCC, including chromosome 3p loss, provides a mechanistic framework with which to organize these abnormalities into those that drive tumour initiation events, those that drive tumour progression and those that confer lethality. Truncal mutations in ccRCC, including those in VHL, SET2, PBRM1 and BAP1, may engender genomic instability and promote defects in DNA repair pathways. The molecular features that arise from these defects enable categorization of ccRCC into clinically and therapeutically relevant subtypes. Consideration of the interaction of these subtypes with the tumour microenvironment reveals that specific mutations seem to modulate immune cell populations in ccRCC tumours. These findings present opportunities for disease prevention, early detection, prognostication and treatment.

Indexed as

Gene Expression Regulation, NeoplasticBiomarkers, TumorCarcinoma, Renal CellDisease ProgressionHumansKidney NeoplasmsMutationPrognosisTumor MicroenvironmentBiomarkers, Tumor

Identifiers

PMID33144689
PMCPMC8172121
OpenAlexW3095456389

What OpenQuestion holds

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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.