Evidence map›Paper›PMID 38676926›Full record

ArticleCell reports2024

Loss of LPAR6 and CAB39L dysregulates the basal-to-luminal urothelial differentiation program, contributing to bladder carcinogenesis.

Sangkyou Lee, Jolanta Bondaruk, Yishan Wang, Huiqin Chen, June Goo Lee, Tadeusz Majewski, Rachel D Mullen, David Cogdell, Jiansong Chen, Ziqiao Wang and 15 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

6 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Association ofTranslational cancer research · 2026
    Article
  4. Review
  5. Review
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors at 5 institutions in 2 countries.

Sangkyou LeeDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Jolanta BondarukDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Yishan WangDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Huiqin ChenDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
June Goo LeeDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Tadeusz MajewskiDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Rachel D MullenDepartment of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
David CogdellDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Jiansong ChenDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Ziqiao WangDepartment of Biostatistics, Johns Hopkins University, Baltimore, MD 21218, USA.
Hui YaoDepartment of Bioinformatics & Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Pawel KusDepartment of Systems Biology and Engineering, Silesian University of Technology, Gliwice, Poland.
Joon JeongDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Ilkyun LeeDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Woonyoung ChoiJohns Hopkins Greenberg Bladder Cancer Institute, Johns Hopkins University, Baltimore, MD 21218, USA.
Neema NavaiDepartment of Urology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Charles GuoDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Colin DinneyDepartment of Urology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Keith BaggerlyDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Cathy MendelsohnDepartment of Urology, Genetics & Development and Pathology, Columbia University, New York, NY 10032, USA.
David McConkeyJohns Hopkins Greenberg Bladder Cancer Institute, Johns Hopkins University, Baltimore, MD 21218, USA.
Richard R BehringerDepartment of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Marek KimmelDepartment of Statistics, Rice University, Houston, TX 77005, USA.
Peng WeiDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Bogdan CzerniakDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: bczernia@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USJohns Hopkins University · USCancer Genetics (United States) · USRice University · USSilesian University of Technology · PL

Funding

Targeting Ral GTPases in Bladder CancerP50CA091846 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DINNEY, COLIN P.N., MCCONKEY, DAVID J. · 2001 to 2018
$37.4M
NCI NIH HHS P50 CA091846
6 · The paper itself

Abstract

We describe a strategy that combines histologic and molecular mapping that permits interrogation of the chronology of changes associated with cancer development on a whole-organ scale. Using this approach, we present the sequence of alterations around RB1 in the development of bladder cancer. We show that RB1 is not involved in initial expansion of the preneoplastic clone. Instead, we found a set of contiguous genes that we term "forerunner" genes whose silencing is associated with the development of plaque-like field effects initiating carcinogenesis. Specifically, we identified five candidate forerunner genes (ITM2B, LPAR6, MLNR, CAB39L, and ARL11) mapping near RB1. Two of these genes, LPAR6 and CAB39L, are preferentially downregulated in the luminal and basal subtypes of bladder cancer, respectively. Their loss of function dysregulates urothelial differentiation, sensitizing the urothelium to N-butyl-N-(4-hydroxybutyl)nitrosamine-induced cancers, which recapitulate the luminal and basal subtypes of human bladder cancer.

Indexed as

CarcinogenesisCell DifferentiationUrinary Bladder NeoplasmsUrotheliumAgedAged, 80 and overAnimalsAntigens, NeoplasmApoptosis Regulatory ProteinsFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred C57BLMiddle AgedAntigens, NeoplasmApoptosis Regulatory ProteinsCAB39L protein, humanLPAR6 protein, humanReceptors, Lysophosphatidic Acidbladder cancerCP: Cancerfield carcinogenesisfield effectsforerunner genesmucosal microenvironmenturothelial differentiation

Identifiers

PMID38676926
PMCPMC11265536
OpenAlexW4395478812

What OpenQuestion 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 OpenQuestion graph.