Evidence map›Paper›PMID 22369969›Full record

ReviewDiscovery medicine2012

Hedgehog pathway and GLI1 isoforms in human cancer.

Richard L Carpenter, Hui-Wen Lo

Open access · greenAbstract readReview
In one paragraph

Review in Discovery medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Cells · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Antitumor activity and mechanism of cucurbitacin B in A549/DDP cells.Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Statins: a repurposed drug to fight cancer.Journal of experimental & clinical cancer research : CR · 2021
    Review
  15. Review
  16. Review
  17. Hedgehog Signaling: Implications in Cancers and Viral Infections.International journal of molecular sciences · 2021
    Review
  18. Review
  19. When Viruses Cross Developmental Pathways.Frontiers in cell and developmental biology · 2021
    Review
  20. GLI1: A Therapeutic Target for Cancer.Frontiers in oncology · 2021
    Review

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

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

2 authors at 1 institution in 1 country.

Richard L CarpenterDepartment of Division of Surgical Sciences, Department of Surgery, Duke University School of Medicine, Durham, North Carolina 27710, USA.
Hui-Wen Lo
Duke University · US

Funding

Nuclear EGFR Signaling Network in Human CancerK01CA118423 · NCI · DUKE UNIVERSITY · PI LO, HUI-WEN · 2006 to 2010
$713k
NCI NIH HHS K01 CA118423NCI NIH HHS K01-CA118423
6 · The paper itself

Abstract

The Hedgehog signaling pathway regulates normal cell growth and differentiation. When deregulated, the Hedgehog pathway leads to tumorigenesis and supports more aggressive phenotypes of human cancers, such as progression, metastasis, and therapeutic resistance. The glioma-associated oncogene homolog 1 (GLI1) family of zinc finger transcription factors is the nuclear mediator of the Hedgehog pathway that regulates genes essential for various stages of tumor development and progression. Consequently, several components of the Hedgehog pathway are major targets of cancer therapy, including GLI1 and smoothened. Although the GLI1 gene was initially identified as an amplified gene in glioblastoma, its amplification was found to be relatively rare. No somatic mutations have been reported in the GLI1 gene. Notably, two decades after the discovery of the GLI1 gene, the GLI1 transcript was recently found to undergo alternative splicing forming two shorter isoforms, an N-terminal deletion variant (GLI1ΔN) and a truncated GLI1 (tGLI1). These variants appear to have different patterns of tissue expression and functions. Most notably, the tGLI1 isoform behaves as a gain-of-function GLI1 that can induce expression of genes not regulated by GLI1 and promotes more aggressive cancer phenotypes. Therefore, this review will focus on the structural and functional differences between these isoforms, and also on their contributions to important cancer cell characteristics, including proliferation, motility, invasion, and angiogenesis.

Indexed as

Hedgehog ProteinsHumansNeoplasmsProtein IsoformsTranscription FactorsZinc Finger Protein GLI1GLI1 protein, humanHedgehog ProteinsProtein IsoformsTranscription FactorsZinc Finger Protein GLI1

Identifiers

PMID22369969
PMCPMC3632644
OpenAlexW28353582

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.