Evidence map›Paper›PMID 10651943›Full record

ArticleImmunology2000

CD95 ligand expression as a mechanism of immune escape in breast cancer.

M Müschen, C Moers, U Warskulat, J Even, D Niederacher, M W Beckmann

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. sFasL-The Key to a Riddle: Immune Responses in Aging Lung and Disease.International journal of molecular sciences · 2021
    Review
  6. miR-21 targets Fas ligand-mediated apoptosis in breast cancer cell line MCF-7.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2014
    Article
  7. Recent advances in the development of breast cancer vaccines.Breast cancer (Dove Medical Press) · 2014
    Review
  8. Article
  9. Article
  10. Article
  11. Tumor vaccines for breast cancer.Cancer investigation · 2009
    Review
  12. Review
  13. Article
  14. Tumour escape: antitumour effectors too much of a good thing?Cancer immunology, immunotherapy : CII · 2004
    Review
  15. Article
  16. Article
  17. Alleviating oxidative stress in cancer immunotherapy: a role for histamine?Medical oncology (Northwood, London, England) · 2000
    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 2 countries.

M MüschenInstitut Pasteur, Department of Immunology, Unité de Biologie Moléculaire du Gène, Paris, France.
C Moers
U Warskulat
J Even
D Niederacher
M W Beckmann
Heinrich Heine University Düsseldorf · DEHochschule Düsseldorf University of Applied Sciences · DEInstitut Pasteur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interaction of CD95 (Apo-1/Fas) and its ligand (CD95L) plays an important role in the regulation of the immune response, since CD95+ lymphocytes may be killed after engagement of the CD95 receptor. Studying the CD95/CD95L system in 40 cases of breast cancer, the malignant cells expressed CD95L, but lost CD95 expression, when compared with non-malignant mammary tissue. Jurkat T cells incubated on breast cancer sections underwent CD95L-specific apoptosis. The rate of apoptosis correlated with the CD95L mRNA levels of the tissue samples. In four breast cancer cell lines, CD95L expression was increased by interferon-gamma (IFN-gamma), which resulted in higher levels of CD95L-specific apoptosis in co-cultured Jurkat T cells. Since IFN-gamma is mainly secreted by activated T cells, up-regulation of CD95L in breast cancer cells in response to IFN-gamma may thus counterselect activated tumour-infiltrating T cells and favour the immune escape of breast cancer. As demonstrated by inhibition of matrix metalloproteinases, CD95L expressed on breast cancer cells can also be shed from the cell membrane into the culture supernatant. Supernatants derived from cultured breast cancer cells induced apoptosis in Jurkat T cells via CD95L. In breast cancer patients, depletion of CD4+ and CD8+ peripheral blood lymphocytes was significantly correlated with CD95L expression in the tumours. This might be suggestive for a relationship between CD95L expression by breast cancer and systemic immunosuppression.

Indexed as

ApoptosisBreast NeoplasmsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesEnzyme-Linked Immunosorbent AssayFas Ligand Proteinfas ReceptorFemaleFlow CytometryHumansImmunohistochemistryJurkat CellsLymphocyte CountMembrane GlycoproteinsProtein IsoformsReverse Transcriptase Polymerase Chain ReactionFASLG protein, humanFas Ligand Proteinfas ReceptorMembrane GlycoproteinsProtein IsoformsRNA, Messenger

Identifiers

PMID10651943
PMCPMC2327134
OpenAlexW1975033372

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.