Evidence map›Paper›PMID 24276242›Full record

ArticleOncogene2014

Distinct cellular origin and genetic requirement of Hedgehog-Gli in postnatal rhabdomyosarcoma genesis.

M Rajurkar, H Huang, J L Cotton, J K Brooks, J Sicklick, A P McMahon, J Mao

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

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 24% 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, 17 citations in OpenAlex.

  1. Article
  2. Hedgehog Signaling: Implications in Cancers and Viral Infections.International journal of molecular sciences · 2021
    Review
  3. Article
  4. Article
  5. Article
  6. Review
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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

7 authors at 3 institutions in 1 country.

M RajurkarDepartment of Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA.
H Huang1] Department of Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA [2] Department of Histology & Embryology, Xiangya School of Medicine, Central South University, Changsha, PR China.
J L CottonDepartment of Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA.
J K BrooksDepartment of Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA.
J SicklickDivision of Surgical Oncology, Moores Cancer Center, University of California, San Diego, La Jolla, CA, USA.
A P McMahonDepartment of Stem Cell Biology and Regenerative Medicine, Broad-CIRM Center for Regenerative Medicine and Stem Cell Research, WM Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA.
J MaoDepartment of Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA.
University of Massachusetts Chan Medical School · USUniversity of California, San Diego · USUniversity of Southern California · US

Funding

Regulation of polarity by Sonic hedgehog morphogen signalingR01NS033642 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MCMAHON, ANDREW P. · 1995 to 2016
$5.7M
Regulation of CNS and Limb Polarity by Sonic HedgehogR37NS033642 · NINDS · HARVARD UNIVERSITY · PI MCMAHON, ANDREW P. · 2005 to 2011
$5.6M
NINDS NIH HHS NS033642NINDS NIH HHS R01 NS033642NINDS NIH HHS R37 NS033642
6 · The paper itself

Abstract

Dysregulation of the Hedgehog (Hh)-Gli signaling pathway is implicated in a variety of human cancers, including basal cell carcinoma (BCC), medulloblastoma (MB) and embryonal rhabdhomyosarcoma (eRMS), three principle tumors associated with human Gorlin syndrome. However, the cells of origin of these tumors, including eRMS, remain poorly understood. In this study, we explore the cell populations that give rise to Hh-related tumors by specifically activating Smoothened (Smo) in both Hh-producing and -responsive cell lineages in postnatal mice. Interestingly, we find that unlike BCC and MB, eRMS originates from the stem/progenitor populations that do not normally receive active Hh signaling. Furthermore, we find that the myogenic lineage in postnatal mice is largely Hh quiescent and that Pax7-expressing muscle satellite cells are not able to give rise to eRMS upon Smo or Gli1/2 overactivation in vivo, suggesting that Hh-induced skeletal muscle eRMS arises from Hh/Gli quiescent non-myogenic cells. In addition, using the Gli1 null allele and a Gli3 repressor allele, we reveal a specific genetic requirement for Gli proteins in Hh-induced eRMS formation and provide molecular evidence for the involvement of Sox4/11 in eRMS cell survival and differentiation.

Indexed as

AnimalsCell LineageCells, CulturedGene Expression Regulation, NeoplasticHedgehog ProteinsHumansImmunoblottingKruppel-Like Transcription FactorsMice, 129 StrainMice, KnockoutNerve Tissue ProteinsPAX7 Transcription FactorReceptors, G-Protein-CoupledReverse Transcriptase Polymerase Chain ReactionRhabdomyosarcomaRNA InterferenceGli1 protein, mouseGli2 protein, mouseGli3 protein, mouseHedgehog ProteinsKruppel-Like Transcription FactorsNerve Tissue ProteinsPax7 protein, mousePAX7 Transcription FactorReceptors, G-Protein-CoupledSmoothened ReceptorSmo protein, mouseSox11 protein, mouseSox4 protein, mouseSOXC Transcription FactorsZinc Finger Protein GLI1Zinc Finger Protein Gli2Zinc Finger Protein Gli3

Identifiers

PMID24276242
PMCPMC4309268
OpenAlexW2002418081

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.