Evidence map›Paper›PMID 41193273›Full record

ArticleEuropean urology oncology2025

Genomic and Epigenomic Signatures Can Distinguish Aggressive Chromophobe Renal Cell Carcinoma from Indolent Renal Oncocytic Tumors in Clinical-grade Samples.

Roberto Ruiz-Cordero, Qi Wang, Gayatri Kumar, Mahmut Akgul, Chad J Creighton, Priya Rao, Pheroze Tamboli, Lan Zheng, Jianping Zhao, Paari Murugan and 13 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European urology oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

23 authors.

Roberto Ruiz-CorderoDepartment of Pathology, Jackson Memorial Hospital/University of Hospital, Miami, FL, USA.
Qi WangDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Gayatri KumarDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Mahmut AkgulAlbany Medical Center, Albany, NY, USA.
Chad J CreightonDepartment of Medicine and the Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, USA.
Priya RaoDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Pheroze TamboliDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Lan ZhengDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Jianping ZhaoDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Paari MuruganUniversity of Minnesota, Minneapolis, MN, USA.
Steven ShenHouston Methodist Hospital, Houston, TX, USA.
Fadi BrimoMcGill University, Montreal, Quebec, Canada.
Ravesanker EzhilarasanDepartment of Radiation Oncology, NYU Langone Health, New York, NY, USA.
Erik SulmanDepartment of Radiation Oncology, NYU Langone Health, New York, NY, USA.
Khalida WaniDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Alexander J LazarDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Taebeom KimDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Ken ChenDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Krishna P L BhatDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Kasthuri KannanDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Jing WangDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Jose A KaramDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Department of Urology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Kanishka SircarDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: ksircar@mdanderson.org.

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Michael M Ittmann · 2007 to 2026
$73.9M
NCI NIH HHS P30 CA016672NCI NIH HHS P30 CA125123
6 · The paper itself

Abstract

BACKGROUND AND

objectiveOnly a minority of renal oncocytic tumors are aggressive. These tumors' behavior is difficult to predict by histopathological evaluation; consequently, many patients experience anxiety upon diagnosis and may undergo unnecessary treatment. Our aim was to derive genomic and epigenomic signatures to distinguish clinically indolent renal oncocytic tumors from aggressive chromophobe renal cell carcinoma (ChRCC).

methodsWe performed molecular profiling of nephrectomies from 68 patients: 44 with indolent renal oncocytic tumors (19 renal oncocytoma, two oncocytic renal neoplasm of low malignant potential, and 23 indolent ChRCC) and 24 with aggressive ChRCC. We performed targeted exome sequencing, gene expression profiling, and whole-genome methylation sequencing of formalin-fixed, paraffin-embedded (FFPE) samples. We also analyzed The Cancer Genome Atlas Kidney Chromophobe data from 66 ChRCC patients in silico. Genomic and epigenomic signatures linked to aggressive ChRCC-obtained from sampling morphologically nonsarcomatoid foci-from both cohorts were derived using the least absolute shrinkage and selection operator method. KEY FINDINGS AND LIMITATIONS: Aggressive ChRCC was distinguished from indolent ChRCC and other indolent renal oncocytic tumors using a focused seven- to 11-gene expression signature (ten-fold cross-validation [CV] area under the curve [AUC] = 0.77-0.85) with an external validation AUC of 0.88, and an eight-CpG methylation signature (ten-fold CV AUC = 0.86) with an external validation AUC of 0.91. TP53 and PTEN mutations substantially increased the probability of aggressive ChRCC. Limitations include the small sample size. CONCLUSIONS AND CLINICAL IMPLICATIONS: Focused genomic and epigenomic signatures from routinely processed FFPE tumor tissues can help distinguish aggressive ChRCC from indolent renal oncocytic tumors, including indolent ChRCC. This forms the basis for replication studies to inform appropriate patient management, provide reassurance, and guide follow-up.

Indexed as

Adenoma, OxyphilicCarcinoma, Renal CellKidney NeoplasmsAdultAgedDiagnosis, DifferentialDNA MethylationEpigenomicsFemaleGene Expression ProfilingGenomicsHumansMaleMiddle AgedNeoplasm GradingChromophobe renal cell carcinomaGene expressionMethylationMutationOncocytoma

Identifiers

PMID41193273
PMCPMC13633056

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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.