Evidence map›Paper›PMID 32259323›Full record

ArticleGenes, chromosomes & cancer2020

Novel renal medullary carcinoma cell lines, UOK353 and UOK360, provide preclinical tools to identify new therapeutic treatments.

Darmood Wei, Youfeng Yang, Christopher J Ricketts, Cathy D Vocke, Mark W Ball, Carole Sourbier, Darawalee Wangsa, Danny Wangsa, Rajarshi Guha, Xiaohu Zhang and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. New developments in existing WHO entities and evolving molecular concepts: The Genitourinary Pathology Society (GUPS) update on renal neoplasia.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021
    Guideline
  2. Panitumumab-Based EGFR Blockade in SMARCB1-Deficient Renal Medullary Carcinoma: Preclinical Basis and Prospective Clinical Activity.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. CA-125 as a Biomarker in Renal Medullary Carcinoma: Integrated Molecular Profiling, Functional Characterization, and Prospective Clinical Validation.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Recent Advances in Renal Medullary Carcinoma.International journal of molecular sciences · 2022
    Review
  11. Article
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

17 authors at 1 institution in 1 country.

Darmood WeiUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Youfeng YangUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Christopher J RickettsUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Cathy D VockeUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Mark W BallUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Carole SourbierUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Darawalee WangsaGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Danny WangsaGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Rajarshi GuhaDivision of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, Maryland, United States.
Xiaohu ZhangDivision of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, Maryland, United States.
Kelli WilsonDivision of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, Maryland, United States.
Lu ChenDivision of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, Maryland, United States.
Paul S MeltzerGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Thomas RiedGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.ORCID 0000-0002-0767-6009
Craig J ThomasDivision of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, Maryland, United States.
Maria J MerinoLaboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
W Marston LinehanUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.ORCID 0000-0001-7983-3109
National Institutes of Health · US

Funding

Molecular Therapeutics of Kidney Cancer: VHL Gene and Fumarate Hydratase GeneZIABC011038 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LINEHAN, WILLIAM MARSTON · 2009 to 2025
$29.8M
Clinical Studies of the Molecular Genetic Basis of Kidney CancerZIABC011028 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LINEHAN, WILLIAM MARSTON · 2009 to 2025
$17.9M
Clinical Nursing and Data Management CoreZIDBC011089 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LINEHAN, WILLIAM MARSTON · 2009 to 2025
$17.4M
Cancer Genomics Technology DevelopmentZIABC011091 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MELTZER, PAUL S. · 2009 to 2025
$16.9M
Tissue ProcessingSequencing FacilityZICBC011044 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI VOCKE, CATHY D · 2009 to 2025
$13.5M
Intratumor heterogeneity and tumor evolutionZIABC010834 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2023
$12.2M
Clinical Nursing and Data Management CoreZ01BC011089 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LINEHAN, WILLIAM MARSTON · 2008 to 2008
$855k
Intramural NIH HHS Z01 BC011089Intramural NIH HHS ZIA BC011028Intramural NIH HHS ZIA BC011038Intramural NIH HHS ZIC BC011044Intramural Research Program of the NIH, National Cancer Institute, Center for Cancer Research ZIA BC011089
6 · The paper itself

Abstract

Renal medullary carcinoma (RMC) is a rare, aggressive disease that predominantly afflicts individuals of African or Mediterranean descent with sickle cell trait. RMC comprises 1% of all renal cell carcinoma diagnoses with a median overall survival of 13 months. Patients are typically young (median age-22) and male (male:female ratio of 2:1) and tumors are characterized by complete loss of expression of the SMARCB1 tumor suppressor protein. Due to the low incidence of RMC and the disease's aggressiveness, treatment decisions are often based on case reports. Thus, it is critical to develop preclinical models of RMC to better understand the pathogenesis of this disease and to identify effective forms of therapy. Two novel cell line models, UOK353 and UOK360, were derived from primary RMCs that both demonstrated the characteristic SMARCB1 loss. Both cell lines overexpressed EZH2 and other members of the polycomb repressive complex and EZH2 inhibition in RMC tumor spheroids resulted in decreased viability. High throughput drug screening of both cell lines revealed several additional candidate compounds, including bortezomib that had both in vitro and in vivo antitumor activity. The activity of bortezomib was shown to be partially dependent on increased oxidative stress as addition of the N-acetyl cysteine antioxidant reduced the effect on cell proliferation. Combining bortezomib and cisplatin further decreased cell viability both in vitro and in vivo that single agent bortezomib treatment. The UOK353 and UOK360 cell lines represent novel preclinical models for the development of effective forms of therapy for RMC patients.

Indexed as

AnimalsAntineoplastic AgentsBortezomibCarcinoma, MedullaryCell Line AuthenticationCell Line, TumorCell ProliferationCisplatinEnhancer of Zeste Homolog 2 ProteinHumansKidney NeoplasmsMiceMice, NudePrimary Cell CultureSMARCB1 ProteinTumor Cells, CulturedAntineoplastic AgentsBortezomibCisplatinEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanSMARCB1 ProteinSMARCB1 protein, humanBortezomibEZH2 inhibitorINI1renal medullary carcinomaRMCSMARCB1SWI/SNF complexUOK353UOK360

Identifiers

PMID32259323
PMCPMC7383978
OpenAlexW3014736130

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.