Evidence map›Paper›PMID 19633846›Full record

ArticleCancer immunology, immunotherapy : CII2010

Systemic dysregulation of CEACAM1 in melanoma patients.

Gal Markel, Rona Ortenberg, Rachel Seidman, Sivan Sapoznik, Nira Koren-Morag, Michal J Besser, Jair Bar, Ronnie Shapira, Adva Kubi, Gil Nardini and 5 more

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Structural aspects of CEACAM1 interactions.European journal of clinical investigation · 2024
    Review
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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

15 authors at 2 institutions in 1 country.

Gal MarkelThe Ella Institute for Melanoma Research and Treatment, Sheba Cancer Research Center, Sheba Medical Center, 52621 Tel Hashomer, Israel. markel@post.tau.ac.il
Rona Ortenberg
Rachel Seidman
Sivan Sapoznik
Nira Koren-Morag
Michal J Besser
Jair Bar
Ronnie Shapira
Adva Kubi
Gil Nardini
Ariel Tessone
Avraham J Treves
Eyal Winkler
Arie Orenstein
Jacob Schachter
Sheba Medical Center · ILTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It was previously shown that CEACAM1 on melanoma cells strongly predicts poor outcome. Here, we show a statistically significant increase of serum CEACAM1 in 64 active melanoma patients, as compared to 48 patients with no evidence of disease and 37 healthy donors. Among active patients, higher serum CEACAM1 correlated with LDH values and with decreased survival. Multivariate analysis with neutralization of LDH showed that increased serum CEACAM1 carries a hazard ratio of 2.40. In vitro, soluble CEACAM1 was derived from CEACAM1(+), but neither from CEACAM1(-) melanoma cells nor from CEACAM1(+) lymphocytes, and directly correlated with the number of CEACAM1(+) melanoma cells. Production of soluble CEACAM1 depended on intact de novo protein synthesis and secretion machineries, but not on metalloproteinase function. An unusually high percentage of CEACAM1(+) circulating NK and T lymphocytes was demonstrated in melanoma patients. CEACAM1 inhibited killing activity in functional assays. CEACAM1 expression could not be induced on lymphocytes by serum from patients with high CEACAM1 expression. Further, expression of other NK receptors was impaired, which collectively indicate on a general abnormality. In conclusion, the systemic dysregulation of CEACAM1 in melanoma patients further denotes the role of CEACAM1 in melanoma and may provide a basis for new tumor monitoring and prognostic platforms.

Indexed as

AdultAgedAntigens, CDCell Adhesion MoleculesFemaleHumansKiller Cells, NaturalMaleMelanomaMiddle AgedNatural Cytotoxicity Triggering Receptor 1Natural Cytotoxicity Triggering Receptor 3NK Cell Lectin-Like Receptor Subfamily CReceptors, IgGSkin NeoplasmsT-LymphocytesAntigens, CDCD66 antigensCell Adhesion MoleculesNatural Cytotoxicity Triggering Receptor 1Natural Cytotoxicity Triggering Receptor 3NCR1 protein, humanNCR3 protein, humanNK Cell Lectin-Like Receptor Subfamily CReceptors, IgG

Identifiers

PMID19633846
PMCPMC11030926
OpenAlexW2169653713

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.