Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Image analysis with a SAMBA 2005 (ALCATEL-TITN, Co) was used to quantify the Ki-67 stained area percentage in 46 T-cell malignant lymphomas (T-ML), classified according to the updated Kiel classification. This parameter demonstrated correlation with the number of Ki-67-positive cellular profiles (r = 0.88, P less than 0.001) and was more reproducible than cell counting. A significant difference was found between low and high grade T-ML (mean values +/- SEM respectively of 10.20 +/- 1.82 per cent and 25.63 +/- 3.15 per cent). The most interesting findings were that: (1) AILD-type T-ML showed an intermediate proliferation rate (15.55 +/- 2.72 per cent) between pleomorphic T-ML with medium and with large cells (respectively 12.53 +/- 3.64 per cent and 22.43 +/- 3.46 per cent), both of which belong to the high grade malignancy group. This finding is in accordance with the poor prognosis of this subtype despite its classification in the low grade malignancy group. (2) Subclassification of the pleomorphic MLs according to the predominance of small, medium or large cells, demonstrated significant differences between these three subtypes. However, the great overlap of values between pleomorphic T-ML with medium and with large cells, seems to indicate that the subclassification of these two subtypes is less valid. (3) A wide range of values with overlap was observed in AILD-type ML, in pleomorphic with medium or large cells and in lymphoblastic T-ML: for these T-ML with variable survival courses, the Ki-67 area percentage, one parameter of proliferative activity, appears worth studying as a prognostic factor.
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PMID:Quantitative study of KI-67 antibody staining in 46 T-cell malignant lymphomas using image analysis. 174 99

Plasma cells isolated from bone marrow (BM) aspirates of 15 patients with active multiple myeloma (MM) were cultured and analysed for in vitro proliferative response and Ig-synthesis upon stimulation with interleukin-3 (IL-3), interleukin-4 (IL-4) and interleukin-6 (IL-6). The proliferative response, determined as Ki-67 positivity in concentrated plasma cells, was increased by IL-6 (Stimulation Index, SI = 1.77 +/- 0.21 (M +/- SEM] but not by IL-3 or IL-4. This proliferation could be blocked by anti-IL-6. In vitro Ig-synthesis was stimulated by IL-4 (SI = 1.62 +/- 0.12 (M +/- SEM) P less than 0.05) but not by IL-6 or IL-3. This effect was not antagonized by anti-IL-6. An inverse correlation was found in this group of patients between the IL-6 induced stimulation of plasma cell proliferative activity and the IL-4 induced increase of Ig-synthesis (P = 0.027). These data indicate in MM that Ig-synthesis and the in vitro proliferative activity may be stimulated by different haematopoietic growth factors, which may reflect the involvement of different responding cells.
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PMID:In vitro Ig-synthesis and proliferative activity in multiple myeloma are stimulated by different growth factors. 177 80

HLA-DR expression, lymphocyte subsets, and the distribution of proliferating cells were studied in hyperplastic polyps from the colorectum. The density of T-cells (CD5+) (mean of cells/mm2 of tissue +/- SEM) was higher in the lamina propria of hyperplastic polyps (64.2 +/- 4.2) than in normal colonic mucosa (36.7 +/- 2.6, P less than .001). The CD4/CD8 ratio was higher in hyperplastic polyps (6.3 +/- 0.9, P less than .0001) and in colonic adenomas (5.9 +/- 0.9, P less than .001) compared with normal mucosa (2.3 +/- 0.2). Lymphocytes of the lamina propria were never Ki-67 positive either in normal mucosa or in hyperplastic polyps or adenomas. The epithelial layer of hyperplastic polyps and of normal mucosa did not express the HLA-DR antigen, whereas pericryptal fibroblasts and most of the leukocytes of the lamina propria were strongly positive for this antigen. In the epithelial layer proliferating cells were localized exclusively in the lower part of epithelial crypts, as was the case in normal mucosa, whereas in adenomas Ki-67-positive cells were present throughout the entire height of the mucosa. Thus, in hyperplastic polyps lymphocytes are increased in the lamina propria, with a predominance of the CD4 subset in close contact with HLA-DR positive pericryptal fibroblasts.
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PMID:Expression of histocompatibility antigens and characterization of the lymphocyte infiltrate in hyperplastic polyps of the large bowel. 231 8

Occlusion of saphenous vein grafts is a major problem after coronary artery bypass grafting. Segments of occluded and suboccluded implanted aortocoronary grafts were obtained during re-intervention bypass grafting in 47 patients yielding a total of 80 vein grafts. The grafts were studied by immunohistochemistry for smooth muscle cells (alpha-SMC actin), macrophages (HAM56), cell replication (PCNA, Ki-67) and transmission and scanning electronmicroscopy (TEM, SEM). In 81% of the examined grafts the (sub)occlusion was due to a myo-intimal thickening and an associated luminal accumulation of foam cells and mural thrombi. The foam cells were constantly found at the luminal site of the myo-intimal thickening and within the luminal part of adherent thrombi. Transmission electronmicroscopy demonstrated phagocytosis of platelets and platelet fragments by the foam cells. A significant fraction of the foam cells demonstrated nuclear immunoreactivity for Ki-67 and PCNA. The myo-intimal thickening of the vein grafts was composed of smooth muscle cells lying in a fibrous tissue matrix. The smooth muscle cells were surrounded by prominent basal lamina and showed ultrastructural features of apoptosis. Our results support the hypothesis that phagocytosis of lipid rich platelets by monocytes set up a mechanism for foam cell formation and replication in human saphenous vein grafts. The transformation of a smooth muscle cell rich myointimal thickening towards a fibrous, cell poor intimal thickening could be induced by progressive smooth muscle cell loss through apoptosis.
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PMID:Foam cell replication and smooth muscle cell apoptosis in human saphenous vein grafts. 783 42

An immunohistochemical study of snuff-induced lesions with a monoclonal antibody (DO-7) specific to p53 mutant and wildtype antioncogene product demonstrated nuclear overexpression of the mutant protein in 45.9 nuclear profiles/mm2 epithelium (SEM 10.8; n = 15) compared with only 0.18 positively stained nuclear profiles/mm2 in the control group (SEM 0.18; n = 4). Furthermore, the biopsy material was also stained with the antibody Ki-67, which has been shown to be excellent for the estimation of the growth fraction in both normal and malignant human tissues. Ki-67 stained positive in 566.1 nuclear profiles/mm2 epithelium (SEM 85.0; n = 15) in the snuff-group compared with 20.2 nuclear profiles/mm2 (SEM 4.9; n = 4) in the control group. To the best of our knowledge, this is the first study showing overexpression of p53 protein and Ki-67 in snuff-induced lesions. The results may indicate that the p53 gene is involved in the initial events leading to subsequent malignant transformation of oral mucosa exposed to snuff. Furthermore, mutations of the p53 gene have been associated with increased cellular proliferation with greater risk of perpetuation of mutations and malignant transformation.
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PMID:Assessment of p53 and Ki-67 expression in snuff-induced lesions. 890 32

In order to improve our ability to predict the regrowth of nonfunctioning pituitary adenomas, we tried to assess the correlation between growth fractions with Ki-67 and PCNA (proliferating cell nuclear antigen) and tumour doubling times in regrowing tumours, and also to find out any difference of growth fractions between the regrowing and the cured cases. In 33 patients with non-functioning pituitary adenomas, 14 cases including 11 with cavernous sinus invasion showed residual tumour on MRI after the operation (regrowing group) and 19 cases had no tumour regrowth on MRI within 5 years after the operation (cured group). Immunocytochemical studies were done with monoclonal antibodies (anti-PCNA, anti-Ki-67: MIB-1). The growth fraction of each tumour was estimated by calculating the ratio of the positive nuclei to the total number of tumour cells with the aid of an image analyser (Mac SCOPE). The tumour doubling times were estimated from serial CT or MRI with the aid of the image analyser (NIH image). Ki-67 staining indices ranged from 0.2% to 1.5% (n = 14, 0.86 +/- 0.10%; mean +/- SEM) in the regrowing group, and from 0.1% to 0.5% (n = 19, 0.23 +/- 0.03%) in the cured group. PCNA staining indices of the regrowing group ranged from 0.6% to 24% (n = 14, 3.7 +/- 1.6%). In the regrowing group, the tumour doubling times ranged from 200 to 2550 days (930 +/- 180 days), and showed a significant inverse correlation with Ki-67 staining indices, but no correlation with PCNA staining indices. The regrowing group showed a significantly higher Ki-67 staining index (n = 14, 0.86 +/- 0.10%) than the cured group (n = 19, 0.23 +/- 0.03%) (p < 0.01). These results indicate that immunocytochemical studies using MIB-1 may be better than those with PCNA for the prediction of regrowth in non-functioning pituitary adenomas. Immunocytochemical study with MIB-1 could lead to the accurate prediction of the rapid regrowing lesions in non-functioning adenomas.
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PMID:The correlation of Ki-67 staining indices with tumour doubling times in regrowing non-functioning pituitary adenomas. 903 Mar 53

The aim of this study was to determine the proliferation rates within the lining layer of the rheumatoid arthritis (RA) synovial membrane (SM) as opposed to the SM of other degenerative and neoplastic joint diseases and to characterize the proliferating cells. 13 RA, 23 osteoarthritis (OA), 21 joint trauma (JT), and 9 synovial sarcoma (SS) specimens were immunostained for Ki-67 and PCNA, silver-stained for nucleolar organizer regions (AgNORs), and double stained with either T-cell- (CD3), macrophage- (CD68), or polymorphonuclear neutrophilic leucocytes (PMN)-markers (CD15). The frequency of PCNA positive synovial lining cells (SLCs) varied from 15.7 +/- 8.7% in RA (mean +/- SEM), 30.97 +/- 4.13% in JT, and 48.55 +/- 3.66% in OA to more than half of all cells in SS (67.2 +/- 3.1%). MIB-1 labeling was observed in 20.0 +/- 8.4% of SS cells., but only in 0.6 +/- 0.2% RA or < or = 1.1% in JT and OA SLCs. Mean AgNOR number per cell ranged from 2.9 +/- 0.1 in JT, 3.6 +/- 0.05 in OA and 4.3 +/- 0.3 in RA to 7.3 +/- 0.3 in SS. Significant differences were observed for Ki-67 and AgNORs, between SS and all other diseases and also between RA and OA (p < 0.01, U-test). In RA, Ki-67 was solely expressed in lymphocytes of germinal centres, but not in macrophages or PMN; in the lining layer expression of Ki-67 was only found in fibroblast-like cells. Our study confirms that T-cell or macrophage proliferation is rare in the RA SM. Also, the proliferation rates of fibroblast-like cells in the RA lining layer are rather low, in particular when compared to a sarcoma in the same anatomical location.
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PMID:[Proliferation of T-cells, macrophages, neutrophilic granulocytes and fibroblast-like cells in the synovial membrane of patients with rheumatoid arthritis]. 906 26

Prolactinomas in women commonly present as small intrasellar tumors, but are usually much larger in men. This discrepancy has generally been attributed to differences in the delay before diagnosis. However, studies comparing clinical and pathological correlates of growth of these tumors in both sexes are lacking. We conducted a retrospective study comparing 45 men and 51 women bearing prolactinoma to determine whether the predominance of large tumors in men was due to a delay in diagnosis or, rather, to a fundamental sex-related difference in tumor growth. Basal PRL levels (mean +/- SEM, 2789 +/- 573 ng/mL) and mean tumor diameter (26 +/- 2 mm) were significantly higher in men than in women (292 +/- 74 ng/mL and 10 +/- 1 mm, respectively; P < 0.001), but were not correlated to the age at diagnosis or the duration of symptoms. Giant tumors (n = 8) occurred in males only. The frequencies of bromocriptine-resistant tumors (30 vs.5%; P < 0.01) and invasive macroadenomas (52 vs.27%; P < 0.001) were significantly greater in men than those in women. Lastly, macroprolactinomas in males exhibited higher indexes of proliferating cells by Ki-67 immunoreactivity (2.6 +/- 1.1% of positive nuclei) than did similar tumors in female patients (0.4 +/- 0.2%; P = 0.08). We conclude that the predominance of large prolactinomas in men is due to a high frequency of rapidly growing tumors, which are often invasive and frequently bromocriptine resistant.
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PMID:Sex-related difference in the growth of prolactinomas: a clinical and proliferation marker study. 1129 30

After balloon angioplasty, retarded endothelial cell recoverage of the injured segment may lead to enhanced intimal hyperplasia. We tested the hypothesis that long lesions result in more intimal hyperplasia than short lesions due to a prolonged time to complete endothelial cell recoverage. A 2-french Fogarty balloon was used to create 2.5- and 5-cm-long lesions in the rabbit carotid artery. After termination, the injured arteries (n = 9 for all groups) were serially processed for histochemistry. Endothelial cell coverage was assessed with an antibody to CD31 and cell proliferation with a monoclonal antibody to Ki-67 nuclear antigen. The intimal hyperplasia cross-sectional area was measured morphometrically. All data are mean +/- SEM. At 21 days, endothelial cell recoverage was almost complete in the 2.5-cm lesions. In the 5-cm lesions, endothelial cell recoverage was 66 +/- 6% in the middle segments (p = 0.04, 2.5 vs. 5 cm) and 100% at the cranial and caudal ends of the lesion. At 42 days, endothelial cell coverage had increased to 81 +/- 7% in the middle segments of the 5-cm lesions. The intimal hyperplasia area was similar in the 2.5- and the 5-cm lesions both at 21 days (0.19 +/- 0.02 and 0.20 +/- 0.01 mm2, respectively) and 42 days (0.27 +/- 0.02 and 0.26 +/- 0.03 mm2, respectively). The increase in intimal hyperplasia from 21 to 42 days was significant for both lesion lengths (p = 0.004). At 21 days, intimal proliferation was similar for the 2.5- and 5-cm lesions. After 42 days postinjury, intimal proliferation had decreased (p < 0.001) equally for both lesion lengths. Earlier recoverage by endothelium in the 2.5-cm lesions did not inhibit intimal hyperplasia compared to the 5-cm lesions which were still incompletely reendothelialized. We conclude that in the rabbit, rapid endothelial cell recoverage of Fogarty balloon-injured arteries may not limit intimal hyperplasia in the center of the lesion. It is conceivable that the inability of regenerated endothelium to inhibit intimal hyperplasia is due to its initially dedifferentiated and possibly dysfunctional phenotype.
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PMID:The influence of lesion length on intimal hyperplasia after Fogarty balloon injury in the rabbit carotid artery: role of endothelium. 925 85

The aim of this study was to assess the cell proliferation in ameloblastomas and to correlate this with clinical features and histology. Immunohistochemistry with Ki-67 monoclonal antibody was performed on fresh tissue from 54 ameloblastomas. A labelling index (LI) was calculated by expressing the percentage of Ki-67 positive cells. There was no significant correlation between LI and clinical features: age, sex or tumour size. Follicular ameloblastomas had significantly higher LI (5.0 +/- 0.5; mean +/- SEM) than plexiform tumours (3.2 +/- 0.6; P < 0.05). Plexiform ameloblastomas from the anterior mandible had a significantly lower LI (1.8 +/- 0.5) than those from the posterior (3.9 +/- 0.8; P < 0.05). LI was higher in squamous arcades (6.4 +/- 3.1%) than in epithelial cords and cysts (1.4 +/- 1.3%; P < 0.001). These results suggest that LI correlates most closely with the histological pattern of the epithelium of ameloblastoma, both within and between different tumours.
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PMID:Ki-67 antigen in ameloblastomas: correlation with clinical and histological parameters in 54 cases from Kenya. 932 91


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