Evidence map›Paper›PMID 24747439›Full record

ArticleNature cell biology2014

Cellular origin of bladder neoplasia and tissue dynamics of its progression to invasive carcinoma.

Kunyoo Shin, Agnes Lim, Justin I Odegaard, Jared D Honeycutt, Sally Kawano, Michael H Hsieh, Philip A Beachy

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Nature cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 120 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 1 pooled it
22.3field-weighted citation impact, top 1% 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

120 citing papers in PubMed, 1 synthesis or guideline pooled it, 195 citations in OpenAlex.

  1. Pooled it
  2. NOTCH pathway inactivation promotes bladder cancer progression.The Journal of clinical investigation · 2015
    Trial
  3. Review
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  5. Article
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  13. KRT5Stem cell research & therapy · 2025
    Article
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  17. Article
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  19. Review
  20. Gold nanorod-assisted theranostic solution for nonvisible residual disease in bladder cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article

60 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Kunyoo ShinInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.
Agnes LimDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305, USA.
Justin I OdegaardDepartment of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA.
Jared D HoneycuttStanford Immunology, Stanford University School of Medicine, Stanford, California 94305, USA.
Sally KawanoInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.
Michael H HsiehDepartment of Urology, Stanford University School of Medicine, Stanford, California 94305, USA.
Philip A Beachy1] Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA [2] Department of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305, USA [3] Department of Biochemistry, Stanford University School of Medicine, Stanford, California 94305, USA [4] Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305, USA.
Stanford University · US

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Proliferation and Differentiation of Bladder Epithelial Cells in Regeneration and MalignancyR01CA157877 · NCI · STANFORD UNIVERSITY · PI BEACHY, PHILIP A · 2011 to 2022
$4.2M
Common Mechanisms of Stem Cell Regulation in Bladder Cancer and RegenerationR00CA166232 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI SHIN, KUNYOO · 2014 to 2015
$490k
Howard Hughes Medical Institute K99/R00NCI NIH HHS R00 CA166232NCI NIH HHS R01 CA157877NIAID NIH HHS T32 AI007290
6 · The paper itself

Abstract

Understanding how malignancies arise within normal tissues requires identification of the cancer cell of origin and knowledge of the cellular and tissue dynamics of tumour progression. Here we examine bladder cancer in a chemical carcinogenesis model that mimics muscle-invasive human bladder cancer. With no prior bias regarding genetic pathways or cell types, we prospectively mark or ablate cells to show that muscle-invasive bladder carcinomas arise exclusively from Sonic hedgehog (Shh)-expressing stem cells in basal urothelium. These carcinomas arise clonally from a single cell whose progeny aggressively colonize a major portion of the urothelium to generate a lesion with histological features identical to human carcinoma in situ. Shh-expressing basal cells within this precursor lesion become tumour-initiating cells, although Shh expression is lost in subsequent carcinomas. We thus find that invasive carcinoma is initiated from basal urothelial stem cells but that tumour cell phenotype can diverge significantly from that of the cancer cell of origin.

Indexed as

Cell LineageAnimalsButylhydroxybutylnitrosamineCarcinomaCell ProliferationCell Transformation, NeoplasticDisease Models, AnimalGenotypeHedgehog ProteinsHumansMaleMiceMice, TransgenicNeoplasm InvasivenessNeoplastic Stem CellsPhenotypeButylhydroxybutylnitrosamineHedgehog ProteinsRecombinant Fusion ProteinsShh protein, mouse

Identifiers

PMID24747439
PMCPMC4196946
OpenAlexW2033800456

What OpenQuestion holds

Textmetadata
LicenceTDM
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.