ArticleAnnals of surgical oncology1995
Augmentation of carcinoembryonic antigen release from intact, viable tumor cells by a factor in human serum.
Article in Annals of surgical oncology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- BTG1 Overexpression Might Promote Invasion and Metastasis of Colorectal CancerFrontiers in oncology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMeasurement of carcinoembryonic antigen (CEA) levels in human serum is frequently used to detect tumor recurrence in patients with resected primary colorectal cancers. These levels are highly variable from patient to patient, and the mechanism that determines these levels is still poorly understood.
methodsUsing a 6-h in vitro CEA-release assay, we determined that a factor in human and fetal bovine sera significantly augments the release of CEA from the tumor cell surface into cell culture supernatants.
resultsAs little as 1% serum admixed with tumor cells results in CEA release up to 200% greater than that of serum-free controls. It is not inhibited by 1,10-phenanthroline or heat inactivation (of serum) but is calcium dependent. The electrophoretic mobility and membrane linkage of CEA released by serum appear to be identical to those of CEA released by bacterial phospholipase C. Because bacterial phospholipase C is known specifically to cleave the phosphoinositol (PI) glycan moiety that anchors CEA to the tumor cell surface, a mechanism of action for serum cleaving this anchor is suggested.
conclusionsThe large range of CEA levels observed in patients with colorectal cancers may be related to differential sensitivity of the CEA membrane anchor to the CEA-releasing factor in serum.
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Registered trials
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.