Evidence map›Paper›PMID 10075923›Full record

ArticleThe EMBO journal1999

Dual roles of sialyl Lewis X oligosaccharides in tumor metastasis and rejection by natural killer cells.

C Ohyama, S Tsuboi, M Fukuda

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 186 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
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  6. Review
  7. A roadmap for translational cancer glycoimmunology at single cell resolution.Journal of experimental & clinical cancer research : CR · 2022
    Review
  8. Aberrant Protein Glycosylation in Brain Cancers, with Emphasis on Glioblastoma.Advances in experimental medicine and biology · 2022
    Article
  9. A Water Soluble PdChemistry (Weinheim an der Bergstrasse, Germany) · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Elevated serum levels of sialyl Lewis X (sLeBreast cancer research and treatment · 2019
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

2 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

3 authors at 1 institution in 1 country.

C OhyamaCancer Research Center, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
S Tsuboi
M Fukuda
Cancer Research Center · US

Funding

Polylactosamines in Development and CancerR01CA048737 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI FUKUDA, MINORU · 1989 to 2007
$3.1M
GLYCOPROTEINS IN DIFFERENTIATION AND ONCOGENESISR37CA033000 · NCI · BURNHAM INSTITUTE FOR MEDICAL RESEARCH · PI FUKUDA, MINORU · 1995 to 2004
$2.1M
NCI NIH HHS R01 CA48737NCI NIH HHS R37 CA33000
6 · The paper itself

Abstract

Aberrant expression of cell surface carbohydrates such as sialyl Lewis X is associated with tumor formation and metastasis. In order to determine the roles of sialyl Lewis X in tumor metastasis, mouse melanoma B16-F1 cells were stably transfected with alpha1, 3-fucosyltransferase III to express sialyl Lewis X structures. The transfected B16-F1 cells, B16-FTIII, were separated by cell sorting into three different groups based on the expression levels of sialyl Lewis X. When these transfected cells were injected into tail veins of C57BL/6 mice, B16-FTIII.M cells expressing moderate amounts of sialyl Lewis X in poly-N-acetyllactosamines produced large numbers of lung tumor nodules. Surprisingly, B16-FTIII.H cells expressing the highest amount of sialyl Lewis X in shorter N-glycans died in lung blood vessels, producing as few lung nodules as B16-FTIII.N cells which lack sialyl Lewis X. In contrast, B16-FIII.H cells formed more tumors in beige mice and NK cell-depleted C57BL/6 mice than did B16-FTIII.M cells. B16-FTIII.H cells bound to E-selectin better than did B16-FTIII.M cells, but both cells grew at the same rate. These results indicate that excessive expression of sialyl Lewis X in tumor cells leads to rejection by NK cells rather than tumor formation facilitated by attachment to endothelial cells.

Indexed as

Cytotoxicity, ImmunologicAnimalsCell DivisionE-SelectinFlow CytometryFucosyltransferasesGraft RejectionKiller Cells, NaturalLewis X AntigenLung NeoplasmsMelanoma, ExperimentalMiceMice, Inbred C57BLNeoplasm MetastasisNeoplasm TransplantationOligosaccharidesE-SelectinFucosyltransferasesgalactoside 3-fucosyltransferaseLewis X AntigenOligosaccharidesRecombinant ProteinsSialyl Lewis X Antigen

Identifiers

PMID10075923
PMCPMC1171240
OpenAlexW2001475156

What OpenQuestion holds

Texttitle and abstract
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.