Evidence map›Paper›PMID 39368485›Full record

ArticleCell reports. Medicine2024

Modeling high-risk Wilms tumors enables the discovery of therapeutic vulnerability.

Gui Ma, Ang Gao, Jiani Chen, Peng Liu, Rakesh Sarda, Jessica Gulliver, Yidan Wang, Carstyn Joiner, Mingshan Hu, Eui-Jun Kim and 5 more

Abstract read
In one paragraph

Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
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

15 authors.

Gui MaMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA; Carbone Comprehensive Cancer Center, University of Wisconsin, Madison, WI 53706, USA.
Ang GaoMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA; Carbone Comprehensive Cancer Center, University of Wisconsin, Madison, WI 53706, USA.
Jiani ChenDepartment of Computational Biology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
Peng LiuDepartment of Biostatistics and Medical Informatics, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53706, USA; Carbone Comprehensive Cancer Center, University of Wisconsin, Madison, WI 53706, USA.
Rakesh SardaDepartment of Pathology and Laboratory Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Jessica GulliverDepartment of Pathology and Laboratory Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Yidan WangMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA; Carbone Comprehensive Cancer Center, University of Wisconsin, Madison, WI 53706, USA.
Carstyn JoinerMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA; Carbone Comprehensive Cancer Center, University of Wisconsin, Madison, WI 53706, USA.
Mingshan HuMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA; Carbone Comprehensive Cancer Center, University of Wisconsin, Madison, WI 53706, USA.
Eui-Jun KimMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA; Carbone Comprehensive Cancer Center, University of Wisconsin, Madison, WI 53706, USA.
Herman YegerProgram in Developmental and Stem Cell Biology, Peter Gilgan Centre for Research and Learning, SickKids, Toronto, ON M5G 0A4, Canada.
Hau D LeDepartment of Surgery, Division of Pediatric Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Xiang ChenDepartment of Computational Biology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
Wan-Ju LiDepartment of Orthopedics and Rehabilitation, University of Wisconsin-Madison, Madison, WI, USA.
Wei XuMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA; Carbone Comprehensive Cancer Center, University of Wisconsin, Madison, WI 53706, USA. Electronic address: wxu@oncology.wisc.edu.

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Justine Yang Bruce · 1985 to 2026
$142.6M
Training in Cancer Biology Training GrantT32CA009135 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SUGDEN, WILLIAM M. · 1985 to 2024
$10.4M
Protein Arginine Methylation in Breast CancerR01CA236356 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Wei Xu · 2019 to 2026
$2.9M
Ctr9 as a Predictive Biomarker for EZH2 Inhibitor SensitivityR01CA268183 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Wei Xu · 2022 to 2026
$2.0M
Functions of BRD8 in HR+/HER2+ breast cancerR01CA281024 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Wei Xu · 2023 to 2026
$1.6M
Mechanism and treatment of Wilms Tumors caused by CTR9 mutationsR21CA295443 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Wei Xu · 2025 to 2026
$400k
A New Strategy for Screening Effective Therapies for Metastatic Wilms TumorsR21CA288336 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI XU, WEI · 2024 to 2025
$396k
NCI NIH HHS P30 CA014520NCI NIH HHS R01 CA236356NCI NIH HHS R01 CA268183NCI NIH HHS R01 CA281024NCI NIH HHS R21 CA288336NCI NIH HHS R21 CA295443NCI NIH HHS T32 CA009135
6 · The paper itself

Abstract

Wilms tumor (WT) is the most common pediatric kidney cancer treated with standard chemotherapy. However, less-differentiated blastemal type of WT often relapses. To model the high-risk WT for therapeutic intervention, we introduce pluripotency factors into WiT49, a mixed-type WT cell line, to generate partially reprogrammed cells, namely WiT49-PRCs. When implanted into the kidney capsule in mice, WiT49-PRCs form kidney tumors and develop both liver and lung metastases, whereas WiT49 tumors do not metastasize. Histological characterization and gene expression signatures demonstrate that WiT49-PRCs recapitulate blastemal-predominant WTs. Moreover, drug screening in isogeneic WiT49 and WiT49-PRCs leads to the identification of epithelial- or blastemal-predominant WT-sensitive drugs, whose selectivity is validated in patient-derived xenografts (PDXs). Histone deacetylase (HDAC) inhibitors (e.g., panobinostat and romidepsin) are found universally effective across different WT and more potent than doxorubicin in PDXs. Taken together, WiT49-PRCs serve as a blastemal-predominant WT model for therapeutic intervention to treat patients with high-risk WT.

Indexed as

Histone Deacetylase InhibitorsKidney NeoplasmsWilms TumorAnimalsAntineoplastic AgentsCell Line, TumorDisease Models, AnimalHumansMiceXenograft Model Antitumor AssaysAntineoplastic AgentsHistone Deacetylase InhibitorsHDAC inhibitorsiPSCPanobinostatRomedipsinWilms tumor modelWIT49

Identifiers

PMID39368485
PMCPMC11513831

What Socratic 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 Socratic graph.