Τομέας ΧειρουργικήςLibrary of the School of Health Sciences
Σ. Στεργιόπουλος, Επίκουρος Καθηγητής, Ιατρική, ΕΚΠΑ
Δ. Περρέα, Καθηγήτρια, Ιατρική, ΕΚΠΑ
Δ. Δημητρούλης, Επίκουρος Καθηγητής, Ιατρική, ΕΚΠΑ
Μ. Τζιβράς, Καθηγητής, Ιατρική, ΕΚΠΑ
Ν. Νικητέας, Καθηγητής, Ιατρική, ΕΚΠΑ
Κ. Κοντζογλού, Αναπληρωτής Καθηγητής, Ιατρική, ΕΚΠΑ
Χ. Βερύκοκος, Επίκουρος Καθηγητής, Ιατρική, ΕΚΠΑ
Μελέτη της καλποπρωτεκτίνης και προαλβουμίνης του ορού, σε ασθενείς με καρκίνο του παχέος εντέρου.
The coloration of calpoprotectin and prealbumin serum levels in patients With
Under inflammatory conditions, calprotectin is released from neutrophils as a heterodimeric complex composed of S100A8 and S100A9 proteins, from the S100 protein family. The S100A8/A9 complex has the capacity to induce apoptosis, by direct binding to MM46 cells via zinc regulation. Simultaneously, the acute phase response (APR) is initiated, raising the number of cytokines which trigger the synthesis of the positive acute phase reactants, including CRP, and down-regulate plasma concentrations of albumin, transferrin, and prealbumin, a tetramer composed of four identical subunits that binds to triiodothyronine (T3)and holo-retinol-binding protein (RBP).
To examine the coloration between, calpoprotecin and prealbumin serum concentrations, and colorectal cancer, serum samples from 80 healthy subjects (control) and 80 colorectal cancer patients with 0.0 CRP levels were collected. The samples were analyzed using commercially available Enzyme-linked immunosorbent assay (ELISA) Kits.
In the healthy subjects the mean concentration was as follows: for preabumin 12.937 ± 7.24ng/mL and for calprotectin 7.199 ±6.71 ng/mL with p-values <0.001. Whereas, in patients with colorectal cancer, the median concentration of preabumin was 4.531 ± 3.866 ng/mL and calprotectin 17.938 ± 14.9.74 ng/mL with p-values <0.001.
The results of our study regarding pre-albumin are in accordance to the pertinent literature. Regarding calpoprotecin the increased number of false negative results (low concentration levels) could be a result of genetic mutation in the coding sequence of either calprotectin itself or a member of its pathway, via which apoptosis is normally induced. Such inactivation could be the cause for the low calprotectin levels in false negative results and the cell’s incapability to enter an apoptotic cycle. Further experimentation, such as sequencing would be needed to verify this hypothesis and indicate the cause for the abnormal low calpoprotecin levels in false negative results. However the results indicate that a combination of both protein reads could lead to a cheap and non-invasive diagnostic tool, which could also potentially reflect the mutated DNA location, aiding with the patient’s therapy.
Main subject category:
Calpoprotectin, Prealbumin, Colorectal Cancer
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