Evidence map›Paper›PMID 21983857›Full record

ArticleNature medicine2011

A crucial requirement for Hedgehog signaling in small cell lung cancer.

Kwon-Sik Park, Luciano G Martelotto, Martin Peifer, Martin L Sos, Anthony N Karnezis, Moe R Mahjoub, Katie Bernard, Jamie F Conklin, Anette Szczepny, Jing Yuan and 16 more

Abstract read
In one paragraph

Article in Nature medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

164 citing papers in PubMed, 246 citations in OpenAlex.

  1. Trial
  2. Vismodegib.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
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104 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

26 authors at 6 institutions in 3 countries.

Kwon-Sik ParkDepartment of Pediatrics, Stanford University, Stanford, California, USA.
Luciano G Martelotto
Martin Peifer
Martin L Sos
Anthony N Karnezis
Moe R Mahjoub
Katie Bernard
Jamie F Conklin
Anette Szczepny
Jing Yuan
Ribo Guo
Beatrice Ospina
Jeanette Falzon
Samara Bennett
Tracey J Brown
Ana Markovic
Wendy L Devereux
Cory A Ocasio
James K Chen
Tim Stearns
Roman K Thomas
Marion Dorsch
Silvia Buonamici
D Neil Watkins
Craig D Peacock
Julien Sage
Stanford University · USMonash University · AUNovartis (United States) · USJohns Hopkins University · USMax Planck Society · DEUniversity of California, San Francisco · US

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
GENETICS TRAINING PROGRAM FOR PHD CANDIDATEST32GM007790 · NIGMS · STANFORD UNIVERSITY · PI BRUNET, ANNE, KINGSLEY, DAVID M · 1985 to 2020
$12.8M
GAMMA TUBULIN AND CENTROSOME STRUCTURE AND FUNCTIONR01GM052022 · NIGMS · STANFORD UNIVERSITY · PI STEARNS, TIM · 1995 to 2017
$6.5M
Hedgehog Pathway Blockade by Small-Molecule Gli AntagonistsR01CA136574 · NCI · STANFORD UNIVERSITY · PI CHEN, JAMES K · 2009 to 2013
$1.6M
NCI NIH HHS 5T32 CA009302-33NCI NIH HHS R01 CA136574NCI NIH HHS T32 CA009302NIGMS NIH HHS R01 GM052022NIGMS NIH HHS T32 GM007790
6 · The paper itself

Abstract

Small-cell lung cancer (SCLC) is an aggressive neuroendocrine subtype of lung cancer for which there is no effective treatment. Using a mouse model in which deletion of Rb1 and Trp53 in the lung epithelium of adult mice induces SCLC, we found that the Hedgehog signaling pathway is activated in SCLC cells independently of the lung microenvironment. Constitutive activation of the Hedgehog signaling molecule Smoothened (Smo) promoted the clonogenicity of human SCLC in vitro and the initiation and progression of mouse SCLC in vivo. Reciprocally, deletion of Smo in Rb1 and Trp53-mutant lung epithelial cells strongly suppressed SCLC initiation and progression in mice. Furthermore, pharmacological blockade of Hedgehog signaling inhibited the growth of mouse and human SCLC, most notably following chemotherapy. These findings show a crucial cell-intrinsic role for Hedgehog signaling in the development and maintenance of SCLC and identify Hedgehog pathway inhibition as a therapeutic strategy to slow the progression of disease and delay cancer recurrence in individuals with SCLC.

Indexed as

AnimalsDisease Models, AnimalDrug Resistance, NeoplasmEpithelial CellsHedgehog ProteinsHumansLungLung NeoplasmsMiceMice, KnockoutMice, NudeNeoplasm TransplantationRecombinant Fusion ProteinsRetinoblastoma ProteinSignal TransductionSmall Cell Lung CarcinomaHedgehog ProteinsRecombinant Fusion ProteinsRetinoblastoma ProteinTumor Suppressor Protein p53

Identifiers

PMID21983857
PMCPMC3380617
OpenAlexW2023028445

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.