title: [PHENOTYPE OF PERIPHERAL BLOOD NEUTROPHILS IN THE INITIAL STAGE OF ENDOMETRIAL CANCER].
abstract: We have examined peripheral blood neutrophils from 123 patients with primary endometrial cancer at stage Ia. Receptor system and the ability of neutrophils to form extracellular traps were assessed by fluorescence microscopy, the spontaneous production of cytokines IL-2, IFN-γ, g-CSF, matrix metalloproteinases-1,9,13 by the method of enzyme-linked immunosorbent assay, phagocytic activity, myeloperoxidase activity, the level of cationic proteis activity in NBT-test were evaluated by cytochemical methods, activity of neutrophils in the spontaneous NBT-test was used to evaluate the oxygen-dependent bactericidal action of neutrophils. The topology and the rigidity of the membrane of neutrophils were assessed by scanning probe microscopy. We have shown that the increase in the relative number of neutrophils lead to a change in their receptor system, aerobic and anaerobic cytotoxicity and ability to phagocytosis are enchanced while reducing NET-activity. We have observed a change in the secretory activity of neutrophils, which is characterized by increased level of MMP-1, possibly initiated by enhanced production of reactive oxygen species, by a reduction in the IL-2 level (inductor of cytotoxic activity) and a sharp increase in the level of the G-CSF. Architectonics of neutrophils in the case of endonetrial cancer at stage Ia is characterized by changing the shape and loss of grit. The rigidity of the cell membrane decreased. Changes in the morphology of neutrophils on the background of the continuing hyperactivity suggests that a state of balance between the immune system and the tumor is already in stage Ia endometrial cancer.
authors.forename: T V
authors.initials: TV
authors.lastname: Abakumova
authors.forename: I I
authors.initials: II
authors.lastname: Antoneeva
authors.forename: T P
authors.initials: TP
authors.lastname: Gening
authors.forename: D R
authors.initials: DR
authors.lastname: Dolgova
authors.forename: S O
authors.initials: SO
authors.lastname: Gening
mesh_terms: D002462:Cell Membrane / Q000737:chemistry / Q000648:ultrastructure*; D016889:Endometrial Neoplasms / Q000473:pathology*; D065206:Extracellular Traps / Q000737:chemistry* / Q000378:metabolism; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D016179:Granulocyte Colony-Stimulating Factor / Q000235:genetics / Q000276:immunology; D006801:Humans; D016130:Immunophenotyping; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology; D007376:Interleukin-2 / Q000235:genetics / Q000276:immunology; D020781:Matrix Metalloproteinase 1 / Q000235:genetics / Q000276:immunology; D053509:Matrix Metalloproteinase 13 / Q000235:genetics / Q000276:immunology; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000276:immunology; D008560:Membrane Fluidity; D018625:Microscopy, Atomic Force; D009367:Neoplasm Staging; D009504:Neutrophils / Q000378:metabolism / Q000648:ultrastructure*; D009195:Peroxidase / Q000235:genetics / Q000276:immunology; D010587:Phagocytosis; D010641:Phenotype; D061251:Primary Cell Culture; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D007376:Interleukin-2; D017382:Reactive Oxygen Species; D016179:Granulocyte Colony-Stimulating Factor; D007371:Interferon-gamma; D009195:Peroxidase; D053509:Matrix Metalloproteinase 13; D020780:Matrix Metalloproteinase 9; D020781:Matrix Metalloproteinase 1