Evidence map›Paper›PMID 10327054›Full record

ArticleOncogene1999

Novel mutations of the MET proto-oncogene in papillary renal carcinomas.

L Schmidt, K Junker, N Nakaigawa, T Kinjerski, G Weirich, M Miller, I Lubensky, H P Neumann, H Brauch, J Decker and 9 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
165citing papers in PubMed, 4 pooled it
8.6field-weighted citation impact, top 1% 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

165 citing papers in PubMed, 4 syntheses or guidelines pooled it, 504 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Phase II and biomarker study of the dual MET/VEGFR2 inhibitor foretinib in patients with papillary renal cell carcinoma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2013
    Trial
  9. Trial
  10. Trial
  11. Review
  12. Article
  13. Article
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  15. Article
  16. Article
  17. Review
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  19. An Observatory for theCancers · 2023
    Review
  20. Review

105 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

19 authors at 11 institutions in 4 countries.

L SchmidtIntramural Research Support Program, SAIC Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702, USA.
K Junker
N Nakaigawa
T Kinjerski
G Weirich
M Miller
I Lubensky
H P Neumann
H Brauch
J Decker
C Vocke
J A Brown
R Jenkins
S Richard
U Bergerheim
B Gerrard
M Dean
W M Linehan
B Zbar
National Cancer Institute · USNational Institutes of Health · USFrederick National Laboratory for Cancer Research · USBicêtre Hospital · FRGrant Medical Center · USJohannes Gutenberg University Mainz · DEKarolinska Institutet · SEMayo Clinic · USSchiller International University · FRUniversität Hamburg · DEUniversity of Freiburg · DE

Funding

OPERATIONS &TECHNICAL SUPPORTN01CO056000 · CO · SCIENCE APPLICATIONS INTERNATIONAL CORP · PI FISCHINGER, PETER J · 1995 to 2000
$95.0M
Single Nucleotide Polymorphisms in Cancer Related GenesZ01BC005652 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DEAN, MICHAEL · 1996 to 2008
$1.9M
Functional Analysis of Cancer Genes from Human Chromosome 3pZ01BC008579 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LERMAN, MICHAEL · 1996 to 2008
$804k
NCI NIH HHS N01-CO-56000
6 · The paper itself

Abstract

Hereditary papillary renal carcinoma (HPRC) is characterized by multiple, bilateral papillary renal carcinomas. Previously, we demonstrated missense mutations in the tyrosine kinase domain of the MET proto-oncogene in HPRC and a subset of sporadic papillary renal carcinomas. In this study, we screened a large panel of sporadic papillary renal carcinomas and various solid tumors for mutations in the MET proto-oncogene. Summarizing these and previous results, mutations of the MET proto-oncogene were detected in 17/129 sporadic papillary renal carcinomas but not in other solid tumors. We detected five novel missense mutations; three of five mutations were located in the ATP-binding region of the tyrosine kinase domain of MET. One novel mutation in MET, V1110I, was located at a codon homologous to an activating mutation in the c-erbB proto-oncogene. These mutations caused constitutive phosphorylation of MET when transfected into NIH3T3 cells. Molecular modeling studies suggest that these activating mutations interfere with the intrasteric mechanism of tyrosine kinase autoinhibition and facilitate transition to the active form of the MET kinase. The low frequency of MET mutations in noninherited papillary renal carcinomas (PRC) suggests that noninherited PRC may develop by a different mechanism than hereditary papillary renal carcinoma.

Indexed as

Point MutationProto-Oncogenes3T3 CellsAdenomaAdenosine TriphosphateAmino Acid SequenceAnimalsBinding SitesCarcinoma, PapillaryCell Transformation, NeoplasticCodonDNA Mutational AnalysisDNA, NeoplasmHumansKidney NeoplasmsMiceAdenosine TriphosphateCodonDNA, NeoplasmMAS1 protein, humanNeoplasm ProteinsProto-Oncogene MasProto-Oncogene Proteins c-met

Identifiers

PMID10327054
OpenAlexW2106582614

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.