Evidence map›Paper›PMID 23536000›Full record

ArticleMedical oncology (Northwood, London, England)2013

Study of critical role of c-Met and its inhibitor SU11274 in colorectal carcinoma.

Wei Gao, Xue Bing, MingYan Li, Zhanhua Yang, Ying Li, Hua Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. HGF/c-Met Axis: The Advanced Development in Digestive System Cancer.Frontiers in cell and developmental biology · 2020
    Review
  12. HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers.International journal of molecular sciences · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. [Dysregulation of HGF/c-Met signal pathway and their targeting drugs in lung cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2014
    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 3 institutions in 1 country.

Wei GaoDepartment of Oncology, Central Hospital of Jinan, Jiefang Road 105, Jinan 250013, People's Republic of China. gjygw-1994@163.com
Xue Bing
MingYan Li
Zhanhua Yang
Ying Li
Hua Chen
Taishan Medical University · CNJinan Central Hospital · CNWeifang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

c-Met plays an important role in colorectal tumorigenesis and disease progression and thus is believed to be an attractive inhibitory target for receptor molecular therapeutic. SU11274 was identified as a small molecule, ATP competitive inhibitor of the catalytic activity of the c-Met kinase. Our study had investigated the relationship between the high expression of c-Met and colorectal carcinoma and the effect of c-Met inhibitor SU11274 in colorectal carcinoma in vitro and vivo. Immunohistochemistry was used to detect the expression of c-Met in 60 patients with colorectal cancer and 20 patients with benign adenoma and surrounding normal colon tissues. The effect of SU11274 on human colorectal carcinoma LoVo cells was detected by Western blot and MTT. And the influence of SU11274 on cell cycle was determined by flow cytometry. In addition, LoVo cell-transplanted tumor growth and expression of c-Met in nude mice was examined for inhibition of SU11274 in vivo. We found c-Met had high expression and was closely related to lymph node metastasis and TNM stage in colorectal carcinoma tissues. SU11274 significantly suppressed the phosphorylation of c-Met as well as the survival and proliferation of LoVo cell lines. G1-phase arrest was also induced by SU11274. SU11274 apparently restrained the growth of the xenograft tumor in nude mice. Our data suggest developing therapies that specifically inhibit the activation of c-Met may represent a novel therapeutic modality for patients with colorectal carcinoma expressing high levels of c-Met.

Indexed as

AdenomaAdultAgedAged, 80 and overAnimalsCell Line, TumorColorectal NeoplasmsFemaleHumansIndolesMaleMiceMice, NudeMiddle AgedPiperazinesProtein Kinase Inhibitors((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)IndolesPiperazinesProtein Kinase InhibitorsReceptor Protein-Tyrosine KinasesRON proteinSulfonamides

Identifiers

PMID23536000
OpenAlexW1995402931

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.