Evidence map›Paper›PMID 42786155›Full record

ArticleNature communications2026

Fusion-driven oncogenic programs shape the immune landscape in translocation renal cell carcinoma.

Prathyusha Konda, Alexandra J Wakolbinger, Yantong Cui, Gabriel Roberti de Oliveira, Yasmin L Nabil, Cary N Weiss, Maxwell D Seager, Riva Deodhar, Jiao Li, Sayed Matar and 14 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors.

Prathyusha KondaDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.ORCID http://orcid.org/0000-0002-6861-4442
Alexandra J Wakolbinger *Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.ORCID http://orcid.org/0009-0000-6049-5090
Yantong Cui *Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Gabriel Roberti de OliveiraDepartment of Pathology, Brigham and Women's Hospital, Boston, MA, USA.
Yasmin L NabilDepartment of Pathology, Brigham and Women's Hospital, Boston, MA, USA.ORCID http://orcid.org/0000-0003-0848-9843
Cary N WeissDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Maxwell D SeagerDepartment of Pathology, Brigham and Women's Hospital, Boston, MA, USA.ORCID http://orcid.org/0009-0009-1111-6854
Riva DeodharDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Jiao LiDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.ORCID http://orcid.org/0000-0002-8027-5877
Sayed MatarDepartment of Pathology, Brigham and Women's Hospital, Boston, MA, USA.
Jinyu WangDepartment of Biomedical Informatics, Dana-Farber Cancer Institute, Boston, MA, USA.ORCID http://orcid.org/0000-0002-5081-8850
Jack HorstDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Sabrina Y CampDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Aseman B SheshdehDivision of Hematology/Oncology, Boston Children's Hospital; Harvard Medical School, Boston, MA, USA.
Jonathan L HechtDepartment of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
David J EinsteinDivision of Medical Oncology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Yashika RustagiDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Anwesha NagDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Aaron R ThornerDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Cheng-Zhong ZhangDepartment of Biomedical Informatics, Dana-Farber Cancer Institute, Boston, MA, USA.ORCID http://orcid.org/0000-0001-8825-7158
Eliezer M Van AllenDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.ORCID http://orcid.org/0000-0002-0201-4444
Sabina SignorettiDepartment of Pathology, Brigham and Women's Hospital, Boston, MA, USA.ORCID http://orcid.org/0000-0002-5000-9105
Toni K ChoueiriDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA. toni_choueiri@dfci.harvard.edu.ORCID http://orcid.org/0000-0002-9201-3217
Srinivas R ViswanathanDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA. srinivas_viswanathan@dfci.harvard.edu.ORCID http://orcid.org/0000-0003-1856-3023

Funding

Probing the role of somatic X-chromosome alterations in shaping cancer sex differencesR01CA286652 · NCI · DANA-FARBER CANCER INST · PI VISWANATHAN, SRINIVAS RAGHAVAN, ZHANG, CHENG-ZHONG · 2023 to 2025
$2.7M
Molecular mechanisms and therapeutic targeting of activated NRF2 signaling in MiT/TFE translocation renal cell carcinomaR01CA279044 · NCI · DANA-FARBER CANCER INST · PI Srinivas Raghavan Viswanathan · 2023 to 2026
$2.0M
Damon Runyon Cancer Research Foundation (Cancer Research Fund of the Damon Runyon-Walter Winchell Foundation) 71-22Doris Duke Charitable Foundation (DDCF) 2020101NCI NIH HHS R01 CA279044NCI NIH HHS R01 CA286652United States Department of Defense | United States Army | Army Medical Command | Congressionally Directed Medical Research Programs (CDMRP) W81XWH-22-1-016U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA279044U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA286652
6 · The paper itself

Abstract

Renal cell carcinomas (RCC) comprise multiple molecularly distinct cancers but most are treated empirically with therapies designed for clear cell RCC (ccRCC), the most common subtype, due to incomplete understanding of subtype-specific biology. We analyzed single-cell transcriptomes and chromatin accessibility profiles from translocation renal cell carcinoma (tRCC), an aggressive RCC defined by oncogenic TFE3 gene fusions. We show that, despite arising from a proximal tubule cell of origin similar to ccRCC, tRCCs display distinct oncogenic programs and an immunosuppressive tumor microenvironment (TME). tRCCs exhibit six conserved tumor meta-programs, including epithelial-mesenchymal transition (EMT) and proximal tubule identity programs whose balance is regulated by TFE3 fusion activity. The fusion-driven EMT program drives a suppressive TME marked by progenitor-exhausted CD8 + T cells, anti-inflammatory SPP1+ macrophages, and matrix-associated fibroblasts. Our findings highlight unique TFE3 fusion-driven biology in tRCC, explaining its reduced immunotherapy responsiveness relative to ccRCC, and suggesting strategies for targeting fusion-driven oncogenic programs and TME reprogramming.

Indexed as

Basic Helix-Loop-Helix Leucine Zipper Transcription FactorsCarcinoma, Renal CellKidney NeoplasmsOncogene Proteins, FusionAnimalsCD8-Positive T-LymphocytesCell Line, TumorEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansKidney Tubules, ProximalMacrophagesSingle-Cell AnalysisTranslocation, GeneticTumor MicroenvironmentBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsOncogene Proteins, FusionTFE3 protein, human

Identifiers

PMID42786155
PMCPMC13612822

What Socratic 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 Socratic graph.