Evidence map›Paper›PMID 18340114›Full record

ArticleCancer biology & therapy2008

C. elegans as a model organism for in vivo screening in cancer: effects of human c-Met in lung cancer affect C. elegans vulva phenotypes.

Shahid S Siddiqui, Sivakumar Loganathan, Soundararajan Krishnaswamy, Leonardo Faoro, Ramasamy Jagadeeswaran, Ravi Salgia

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-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

12 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. TheBiochemistry and biophysics reports · 2017
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. The MET axis as a therapeutic target.Update on cancer therapeutics · 2009
    Article
  10. Article
  11. Review
  12. Review
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

6 authors at 1 institution in 1 country.

Shahid S SiddiquiSection of Pulmonary and Critical Care, Department of Medicine, University of Chicago Medical Center, Pritzker School of Medicine, Chicago, Illinois 60637, USA.
Sivakumar Loganathan
Soundararajan Krishnaswamy
Leonardo Faoro
Ramasamy Jagadeeswaran
Ravi Salgia
University of Chicago · US

Funding

Role of c-Met in SCLC and Potential for Novel TherapyR01CA100750 · NCI · UNIVERSITY OF CHICAGO · PI SALGIA, RAVI · 2004 to 2012
$2.2M
Studies of a Novel Therapeutic Target in Non-Small Cell Lung Cancer (NSCLC)R01CA125541 · NCI · UNIVERSITY OF CHICAGO · PI SALGIA, RAVI · 2007 to 2011
$1.4M
NCI NIH HHS R01 CA100750NCI NIH HHS R01 CA100750-04NCI NIH HHS R01 CA125541
6 · The paper itself

Abstract

Cancers typically harbour several mutant forms of key cellular genes that contribute to its complex phenotype. Our lab has previously identified gain-of-function mutations in some of the receptor tyrosine kinases such as c-Met in lung cancer. In order to investigate the mutant gene in the context of a whole organism, the current choice of in vivo model is limited to the mouse. To rapidly screen the functional aspects of mutant forms of c-Met detected in lung cancer, we used the nematode C. elegans as the model organism. Transgenic worms were generated that harbour wild type or the frequently seen mutant forms of c-Met in lung cancer (c-MetR988C and c-MetT1010I). Expression of the mutant human c-Met forms in C. elegans consistently resulted in significantly low fecundity and abnormal vulval development characterized by hyperplasia. Interestingly, exposure of c-Met mutant transgenic worms to nicotine resulted in enhanced abnormal vulval development, fecundity and locomotion. Our studies provide first evidence that human c-Met mutations can be studied in C. elegans, and that carcinogens can enhance mutant c-Met function expressed in C. elegans transgenic animals. We therefore propose the use of C. elegans as a model to rapidly assess the role of cancer specific gene mutations in the context of a whole organism.

Indexed as

Drug Screening Assays, AntitumorAnimalsAnimals, Genetically ModifiedAntineoplastic AgentsCaenorhabditis elegansFemaleHumansLung NeoplasmsMutationNicotinePhenotypeProtein Structure, TertiaryProto-Oncogene Proteins c-metRNA InterferenceVulvaAntineoplastic AgentsNicotineProto-Oncogene Proteins c-met

Identifiers

PMID18340114
PMCPMC2580824
OpenAlexW2053205173

What OpenQuestion holds

Textmetadata
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.