Evidence map›Paper›PMID 11042681›Full record

ArticleOncogene2000

A novel germ line juxtamembrane Met mutation in human gastric cancer.

J H Lee, S U Han, H Cho, B Jennings, B Gerrard, M Dean, L Schmidt, B Zbar, G F Vande Woude

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

139 citing papers in PubMed, 327 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Tumor biomarkers for diagnosis, prognosis and targeted therapy.Signal transduction and targeted therapy · 2024
    Review
  7. Review
  8. Review
  9. An Observatory for theCancers · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. NovelDiagnostics (Basel, Switzerland) · 2020
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. The Function of the HGF/c-Met Axis in Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2020
    Review
  19. Review
  20. Article

79 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

9 authors at 5 institutions in 2 countries.

J H LeeNCI-Frederick Research and Development Center, P.O. Box B, Frederick, Maryland, MD 21702, USA.
S U Han
H Cho
B Jennings
B Gerrard
M Dean
L Schmidt
B Zbar
G F Vande Woude
Ajou University · KRScience Applications International Corporation (United States) · USCancer Research Center · USFrederick National Laboratory for Cancer Research · USVan Andel Institute · US

Funding

OPERATIONS &TECHNICAL SUPPORTN01CO056000 · CO · SCIENCE APPLICATIONS INTERNATIONAL CORP · PI FISCHINGER, PETER J · 1995 to 2000
$95.0M
NCI NIH HHS N01-CO-56000
6 · The paper itself

Abstract

Activating mutations in the Met receptor tyrosine kinase, both germline and somatic, have been identified in human papillary renal cancer. Here we report a novel germline missense Met mutation, P1009S, in a patient with primary gastric cancer. The dosage of the mutant Met DNA was elevated in the tumor when compared to its matched normal DNA. Therefore, as with hereditary renal papillary cancer, the mutant Met allele may also be selectively duplicated in the tumor. Different from previously reported Met mutations, which occur in the tyrosine kinase domain, this missense mutation is located at the juxtamembrane domain, and is not constitutively activated. However, following treatment with HGF/SF, the P1009S mutant Met protein, expressed in NIH3T3 cells, displays increased and persistent tyrosine phosphorylation compared to the wild-type Met. Importantly, these cells also form colonies in soft agar, and are highly tumorigenic in athymic nude mice. A second nucleotide change in this region of Met, T1010I, was found in a breast cancer biopsy and a large cell lung cancer cell line. Although this previously reported 'polymorphism' did not stimulate NIH3T3 cell growth in soft agar, it was more active than the wild-type Met in the athymic nude mice tumorigenesis assay, suggesting that it may have effects on tumorigenesis. Met has been shown to be highly expressed in human gastric carcinoma cell lines, and our results raise the possibility that activating missense Met mutations could contribute to tumorigenesis of gastric cancer.

Indexed as

3T3 CellsAdenocarcinomaAmino Acid SequenceAnimalsCell MembraneDNA, NeoplasmExonsFemaleGene AmplificationGene Expression Regulation, NeoplasticGerm-Line MutationHepatocyte Growth FactorHumansMiceMice, NudeMolecular Sequence DataDNA, NeoplasmHepatocyte Growth FactorProto-Oncogene Proteins c-metTyrosine

Identifiers

PMID11042681
OpenAlexW2048097275

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.