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PubMed1995

Assessment of cellular proliferation of sebaceous neoplasms by AgNOR counts and immunohistochemical demonstrations of PCNA and Ki-67.

We assessed cellular proliferation of sebaceous neoplasms by AgNOR counts and the immunohistochemical demonstration of proliferating cell nuclear antigen (PCNA) and Ki-67, using formalin-fixed and paraffin-embedded tissue specimens. We used three categories of sebaceous neoplasms: four cases of sebaceoma, three cases of basal cell carcinoma with sebaceous differentiation (BCSD), and seven cases of sebaceous carcinoma (SC). Significant differences were noted between SC and non-SC tumors (sebaceoma and BCSD) in AgNOR counts and semi-quantitative grading of PCNA and Ki-67 labelling indices (P < 0.01). When a cut-off value of 6 was chosen, the AgNOR value discriminated SC from non-SC tumors with high specificity and sensitivity. When a cut-off value of 25% was chosen, PCNA and Ki-67 labelling indices also discriminated between these tumors. Significant differences were not observed between sebaceoma and BCSD with PCNA and Ki-67 labelling indices. AgNOR counts of BCSD were a little higher than those of sebaceoma, but the number of cases was too small to perform statistical assessment. We consider AgNOR counts and semi-quantitative grading of PCNA and Ki-67 labelling indices to be useful in differentiating SC from BCSD and sebaceoma.

Cell Division↗

PubMed2001

Purine nucleoside-dependent inhibition of cellular proliferation in 1321N1 human astrocytoma cells.

We examined the effects of purines and the pyrimidine UTP on cellular proliferation in the human astrocytoma cell line 1321N1. Treatment of cultured cells with 100 microM ATP or 2-chloroadenosine (2-CA) resulted in significant reductions in cell numbers after 2 days, whereas adenosine (ADO) exhibited a slower time course of inhibition of cell growth. Treatment with 100 microM UTP had no effect on cell numbers. 2-Chloroadenosine but neither ATP nor ADO resulted in an increase in cell death rates. A significant portion of the inhibitory response to ATP, ADO, or 2-CA was sensitive to the purine nucleoside transport inhibitor S-(p-nitrobenzyl)-6-thioguanosine, suggesting that uptake into cells was required for the inhibitory response. At least the majority of the observed responses to purines was not mediated by P1 (adenosine) receptors, because effects of ATP, ADO, or 2-CA were not affected by treatment of cells with the P1 receptor antagonist 8-(p-sulfophenyl)-theophylline. The absence of any known P2 (nucleotide) receptors in 1321N1 cells, coupled with the failure of the relatively stable ATP analog adenosine 5'-O-(3-thiotriphosphate) to alter cell growth rates, suggests that ATP acts indirectly to inhibit proliferation via one or more metabolic products. Although intracellular effects of purine nucleosides should be taken into account in future studies using 1321N1 cells, our findings also suggest 1321N1 cells as an excellent model for intracellular actions of nucleosides.

2-Chloroadenosine↗

PubMed1982

[Influence of histological type on the kinetics of tumor growth and cellular proliferation in autochtonous tumors of mice].

The influence of the tumoral histological characters upon growth kinetics and cellular proliferation parameters was studied for autochtonous chemo-induced tumors in mice. In our experimental conditions, the initial minimum volume from which epithelial tumors on one hand and connective tumors on the other hand are observed and then follow a Gompertzian law, was defined. The change of the histological characters of malignancy was observed during the tumoral growth. Intermitotic delays, durations of the cell cycle phases, growth fraction and degree of cell loss were calculated for epithelial and connective tumors.

Animals↗

PubMed1997

Evaluation of cellular proliferation on collagenous membranes.

Collagenous membranes are used in guided tissue regeneration designed to repair damage done to the periodontium by disease. The cells primarily responsible for the process are desmodontal fibroblasts. We have studied the behavior and proliferation of fibroblasts grown on collagenous membrane. Fibroblasts grown on plastic served as control. Cellular proliferation was evaluated using a colorimetric test for cytotoxicity and by flow cytometry. Scanning electron microscopy was used to observe cellular morphology. Results showed a reduction in cell number, together with a modification in cell cycle, but good preservation of cellular morphology for cultures grown on collagenous membrane. These results support the in vivo use of collagenous membrane in guided tissue regeneration.

3T3 Cells↗

PubMed2005

Hereditary gingival fibromatosis: report of a five-generation family using cellular proliferation analysis.

BACKGROUND: Hereditary gingival fibromatosis (HGF) is an uncommon condition characterized by an accumulation of extracellular matrix resulting in a fibrotic enlargement of the gingiva. The goal of this article is to describe one kindred affected with HGF and discuss the diagnosis, treatment, and control of the disease. The pattern of inheritance, histopathologic characteristics, and proliferative potential of epithelial and mesenchymal cells of HGF are also emphasized. METHODS: To characterize the pattern of inheritance and the clinical appearance of gingival overgrowth, 117 family members were examined. The recurrence risk was estimated by the use of a genetic analysis program. Immunohistochemistry against the proliferating cell nuclear antigen (PCNA) and pKi-67 was performed to assess cellular proliferation of normal gingiva (NG) and HGF cells. RESULTS: Examination of the family pedigree demonstrated an autosomal dominant trait of inheritance, and a sibling recurrence risk of 0.085 and an offspring recurrence risk of 0.078, indicating that HGF was a consequence of genetic alteration with low penetrance. Unaffected and affected members transmitted the disease to their offspring. The affected patients showed a generalized but mild gingival overgrowth. Surgical treatment consisted of a combination of gingivectomy and gingivoplasty. Histologic examination showed that the gingival lesions of all patients were quite similar, with increased amounts of collagen fiber bundles in the connective tissue. Immunohistochemistry revealed that the proliferative potential of epithelial cells was significantly higher in the HGF group compared to the NG group, whereas mesenchymal cells from both groups were negative for the proliferative markers. CONCLUSION: Our data demonstrated that, in the studied family, HGF is transmitted by an autosomal dominant pattern with incomplete disease penetrance, and although the gingival enlargement resulted from an excessive accumulation of collagen fibers, HGF is characterized by an increase in the proliferation rate of epithelial cells.

Cell Proliferation↗

PubMed1996

Dysregulation of cellular proliferation and apoptosis mediates human autosomal dominant polycystic kidney disease (ADPKD).

The proto-oncogene c-myc has been implicated in both cellular proliferation and apoptosis, and we have shown that overexpression of c-myc can induce polycystic kidney disease in transgenic mice. To elucidate the molecular and cellular defects underlying cystogenesis, we have investigated the potential roles of cell proliferation and apoptosis as they relate to c-myc and modulators of c-myc function in human autosomal dominant polycystic kidney disease (ADPKD). Renal c-myc expression was consistently elevated, up to 15-fold, in ADPKD. High levels of c-myc expression correlated with 10- to 100-fold increased proliferation index in cystic epithelium. Interestingly, steady-state levels of bcl-2 mRNA were also increased up to 20-fold and Bcl-2 protein was markedly elevated. In contrast, the expression of bax and p53 was virtually unchanged. However, apoptosis was consistently and significantly increased in ADPKD kidneys, unchecked by high levels of Bcl-2. Together with proliferation, apoptosis may thus represent a general mechanism for cyst growth and tissue remodeling. We conclude that both epithelial cell proliferation and apoptosis required for normal kidney homeostasis are deregulated in ADPKD, recapitulating the renal developmental program. Furthermore, abnormal expression of proto-oncogenes regulating these processes is an important mediator of cystogenesis in human ADPKD.

Adult↗

PubMed1998

Cellular proliferation in the rat pineal gland during postnatal development.

To establish a possible correlation between the rate of cellular proliferation and already documented functional and morphological characteristics of the rat pineal gland during postnatal development, the bromodeoxyuridine labelling method was used to evaluate the fraction of cells at the S phase of the cell cycle in paraffin sections from 1-, 7-, 14- and 28-day-old rats. Numerical density, taken as an indirect measure of cell hypertrophy, was also evaluated. During the first week after birth the percentage of S phase-cells in the rat pineal gland sharply decreased from around 9% to 1.3%. A smaller but also significant decrease was found from the 7th to the 14th postnatal day where S phase cells were less than 0.5% of all pineal cells. A very low percentage was also seen in samples from 28-day-old rats. Numerical density, namely, the total number of cells per surface unit of pineal section, decreased from birth to the end of the first month. This decrease was also steeper from birth to the 7th postnatal day than at any other period of the study. These results support the idea that a strong expansion of the cellular population of the rat pineal gland precedes morphological and functional maturation and opens the way to further exploration of the relationship between functional and proliferative responses of the pineal gland.

Animals↗

PubMed2005

Cellular proliferation in the urorectal septation complex of the human embryo at Carnegie stages 13-18: a nuclear area-based morphometric analysis.

In order to analyse the patterns of cellular proliferation both in the mesenchyme of the urorectal septum (URS) and in the adjacent territories (posterior urogenital mesenchyme, anterior intestinal mesenchyme and cloacal folds mesenchyme), as well as their contribution to the process of cloacal division, a computer-assisted method was used to obtain the nuclear area of 3874 mesenchymal cells from camera lucida drawings of nuclear contours of selected sections of human embryos [Carnegie stages (CSs) 13-18]. Based on changes in the size of the nucleus during the cellular cycle, we considered proliferating cells in each territory to be those with a nuclear area over the 75th percentile. The URS showed increasing cell proliferation, with proliferation patterns that coincided closely with cloacal folds mesenchyme, and with less overall proliferation than urogenital and intestinal mesenchymes. Furthermore, at CS 18, we observed the beginning of the rupture in the cloacal membrane; however, no fusion has been demonstrated either between the URS and the cloacal membrane or between the cloacal folds. The results suggest that cloacal division depends on a morphogenetic complex where the URS adjacent territories could determine septal displacement at the time that their mesenchymes could be partially incorporated within the proliferating URS.

Cell Cycle↗

PubMed2001

The E2F1-3 transcription factors are essential for cellular proliferation.

The retinoblastoma tumour suppressor (Rb) pathway is believed to have a critical role in the control of cellular proliferation by regulating E2F activities. E2F1, E2F2 and E2F3 belong to a subclass of E2F factors thought to act as transcriptional activators important for progression through the G1/S transition. Here we show, by taking a conditional gene targeting approach, that the combined loss of these three E2F factors severely affects E2F target expression and completely abolishes the ability of mouse embryonic fibroblasts to enter S phase, progress through mitosis and proliferate. Loss of E2F function results in an elevation of p21Cip1 protein, leading to a decrease in cyclin-dependent kinase activity and Rb phosphorylation. These findings suggest a function for this subclass of E2F transcriptional activators in a positive feedback loop, through down-modulation of p21Cip1, that leads to the inactivation of Rb-dependent repression and S phase entry. By targeting the entire subclass of E2F transcriptional activators we provide direct genetic evidence for their essential role in cell cycle progression, proliferation and development.

Animals↗

PubMed2002

Interleukin 1beta (IL-1beta), IL-10, tumor necrosis factor-alpha, and cellular proliferation index in peripheral blood mononuclear cells in patients with ankylosing spondylitis.

OBJECTIVE: To evaluate cytokine production and cellular proliferation index (CPI) in peripheral blood mononuclear cells (PBMC) of patients with ankylosing spondylitis (AS), and their association with clinical variables. METHODS: In a cross sectional study we compared the production of tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta), and IL-10 and CPI in response to phytohemagglutinin (PHA) in PBMC of 27 patients with AS and 24 healthy controls. We also assessed clinical characteristics including disease activity index (BASDAI) and functional index (BASFI). RESULTS: Levels of IL-1beta were higher in patients with AS (median 242 pg/ml) than in controls (median 65 pg/ml); p = 0.002. No differences were observed in median levels of TNF-alpha or IL-10 between AS and controls. Patients had a reduction in CPI (1.2 in AS vs 1.8 in controls; p < 0.001). A positive correlation was observed between IL-10 production and age (rho = 0.34, p = 0.01). A borderline negative correlation was observed between CPI and age (rho = -0.26, p = 0.07). CONCLUSION: Patients with AS had high production of IL-1beta compared with controls and a poor response in CPI. These findings may explain the lack of response for microbial antigens mediated by the innate immune response.

Adolescent↗

PubMed1984

C3d-K, a kallikrein cleavage fragment of iC3b is a potent inhibitor of cellular proliferation.

The C3d-K fragment generated from human iC3b by plasma kallikrein is a potent suppressant of cellular proliferation. Originally characterized as inhibiting human and murine T lymphocyte function, C3d-K is shown in these studies to suppress mitogen-induced B cell growth, the spontaneous proliferation of several tumor cell lines, as well as all forms of T cell proliferation, including that induced by interleukin 2 (IL 2). In addition, synthesis of IL 2 in mixed lymphocyte cultures is blocked by C3d-K, but not IL 2 synthesis induced by Con A. The C3d-K fragment has no effect on resting cells; however, sensitivity to the inhibitory effect of C3d-K is acquired during the activation process. Because the proliferation of mitogen-activated spleen cells is not inhibited by exposure to C3d-K for the initial 24 hr of culture, only late steps in the cell activation process are C3d-K sensitive. When C3d-K is present throughout the course of the 72-hr culture, suppression was observed. Data obtained with the tumor cell lines suggest that once suppression is achieved, it is long-lasting even in the absence of C3d-K.

Animals↗

PubMed1998

Effect of the mannose-binding Artocarpus integer lectin on the cellular proliferation of murine lymphocytes.

The effect of the mannose-binding champedak (Artocarpus integer) lectin-M on the cellular proliferation of murine lymphocytes was investigated in this study. Our data demonstrated that the lectin was the main mitogenic component in the crude extract of the champedak seeds. It stimulated the proliferation of murine T cells at an optimal concentration of 2.5 microg/ml in a 3 day culture. Lectin-M appeared to be a T-cell mitogen as it does not induce significant DNA synthesis when cultured with spleen cells from the nude mouse. In the absence of T cells, the lectin was incapable of inducing resting B cells to differentiate into immunoglobulin secreting plasma cells.

Animals↗

PubMed1997

Cellular proliferation and fibroblast growth factors in the corpus luteum during early pregnancy in ewes.

To determine the relationship between cellular proliferation and the presence of FGF-1 and FGF-2 in the ovine corpus luteum (CL) during early pregnancy, ewes received an intravenous injection of bromodeoxyuridine (BrdU) 1 h before slaughter (n = 3/day) on day 12 after estrus (nonpregnant) or on days 12, 18, 24 or 30 after mating (pregnant). The labeling index (LI; number of BrdU-labeled nuclei expressed as a percentage of total nuclei) of each CL was determined by immunohistochemistry and subsequent image analysis. FGF-1 and FGF-2 were immunolocalized by using specific antibodies, and indirect immunoperoxidase detection. Moreover, FGF-2 was immunolocalized by using a primary antibody and fluorescein isothiocyanate (FITC)-labeled secondary antibody, and immunofluorescence was quantified by using an interactive laser cytometer and image analysis. Results demonstrated that the LI was similar for CL of nonpregnant and pregnant ewes on day 12 (4.27 +/- 0.23 vs 5.10 +/- 0.14%) and decreased (P < 0.05) from days 12-30 of pregnancy (2.73 +/- 0.08, 2.02 +/- 0.09 and 1.70 +/- 0.04% on days 18, 24 and 30, respectively). FGF-1 was present in the cytoplasm of large and a few small parenchymal luteal cells, and the distribution and intensity of staining was similar for nonpregnant and pregnant ewes on day 12 as well as across days of pregnancy. In contrast, FGF-2 immunoreactivity was present only in luteal nonparenchymal cells and interstitial areas and was greater (P < 0.05) for pregnant than nonpregnant CL on day 12 (2.34 +/- 0.12 vs 0.14 +/- 0.01%). Although FGF-2 immunoreactivity decreased (P < 0.01) from days 12-30 of pregnancy (0.70 +/- 0.04, 0.22 +/- 0.01 and 0.06 +/- 0.02% on days 18, 24, and 30, respectively), it was highly correlated (r = 0.99, P < 0.01) with luteal LI. We therefore suggest that FGF, and especially FGF-2, play a role in luteal cell proliferation or turnover during early pregnancy, and may thereby contribute to the maintenance of luteal function, which is critical for the successful establishment of pregnancy.

Animals↗

PubMed2000

Clinical significance of MUC1 and E-cadherin expression, cellular proliferation, and angiogenesis at the deepest invasive portion of colorectal cancer.

We examined MUC1 and E-cadherin expression, cellular proliferation, and tumor vascularization at the deepest invasive portion of colorectal cancer in relation to prognosis. One hundred and ten surgically resected specimens of advanced colorectal carcinoma were studied. E-cadherin and MUC1 expression and Ki-67 labeling index (Ki-67 LI) were examined immunohistochemically at the site of deepest tumor invasion. Tumor vascularization was also examined immunohistochemically using anti-CD34 antibody to determine the microvessel count (MVC). In curative resection, patients with a high Ki-67 LI, reduced E-cadherin expression, MUC1-positive and high MVC lesion showed a significantly poorer prognosis than those with a low Ki-67 LI, E-cadherin normal, MUC1-negative and low MVC lesion, respectively. Furthermore, patients with both a high Ki-67 LI and MVC lesion showed a significantly poorer prognosis than those with other Ki-67 LI and MVC relations. Patients with both a MUC1-positive and E-cadherin reduced lesion showed a significantly poorer prognosis than those with both a MUC1-negative and E-cadherin normal lesion. The significant risk factors in order of poorer prognosis by the multivariate analysis among these factors including routinely used clinicopathologic factors were the high MVC, E-cadherin reduced expression, and lymph node metastasis. These findings indicate a high MVC at the site of deepest tumor invasion to be the most important predictor of colorectal cancer prognosis among the factors studied here.

Biomarkers, Tumor↗

PubMed1996

[Regulation of uterine cellular proliferation with estrogens and growth factors].

In this paper the role of estrogen and growth factors in the uterine cellular proliferation is analyzed. The evidences indicate that the estradiol-stimulate cell division is associated with the induction of expression of a variety of growth factors from the all major uterine cell types (epithelia, stroma and myometrium). These growth factors amplify the estrogen proliferation signal in autocrine and/or paracrin fashion. The best-studied growth factors in the uterine response to estradiol are epidermal growth factor (EGF) and insulin-like growth factor (IGF-1). Uterine cell proliferation is a complex process that involves interactions of several growth factors, ovarian steroids hormones action and cell to cell signaling.

Adult↗

PubMed1984

[Multiparametric cytofluorometry of the process of cellular proliferation, differentiation and maturation of the chondrocytes in the growing rat].

The present study was undertaken to analyze quantitatively the process of cellular proliferation, differentiation and maturation of the chondrocytes in both the epiphyseal cartilage plates and the articular cartilages of the growing rats, using the multiparametric cytofluorometry (NIKON SPM-RFl-D). The analyses involve the simultaneous determinations by cytofluorometry of nuclear DNA vs. cellular RNA contents, nuclear DNA vs. cellular protein contents, and nuclear DNA vs. silver grain amount of the 3H-leucine, 3H-glycine, 3H-thymidine and the 35SO4 autoradiography. In addition, for the detailed analysis of cell kinetics, DNA-RNA cytofluorometry was carried out in combination with 3H-thymidine autoradiography. According to the results obtained, the chondrocytes were quantitatively divided into subpopulations of G0-G1, S and G2 in the cell cycle by their nuclear DNA and cellular RNA contents, and the maturative chondrocytes had higher cellular RNA content than the proliferative ones. It was suggested that there were, among the chondrocytes in the epiphyseal cartilage plate, two other subpopulations of binuclear cells and mononuclear tetraploid cells, both having higher cellular RNA content than the mononuclear G2 cells. It is reasonable to assume that these two subpopulations are the polyploid cell groups accompanying highly active cell proliferation.

Animals↗

PubMed1977

Relationship of cellular proliferation and the generation of cytotoxic cells in an in vitro secondary immune response to syngeneic rat lymphoma cells.

The role of cellular proliferation for the generation of cytotoxic activity in an in vitro secondary immune response to syngeneic lymphoma cells was investigated. Spleen cells from W/Fu rats immunized with the syngeneic (C58NT)D tumor proliferate and generate cytotoxic potential for tumor targets after exposure to mitomycin C-treated (C58NT)D cells in vitro. Elimination of proliferating cells by exposure to high specific activity 3H thymidine at approximate intervals impaired the generation of cytotoxic activity. Elimination of cells proliferating to either syngeneic lymphoma or BN rat alloantigens allowed the remaining cells to generate cytotoxic potential to the second set of antigens. Elimination of proliferating cells also abrogated the ability of the in vitro generated cells to adoptively confer anti-tumor protection on nonimmune recipients. These results demonstrate that cellular division is required for the generation of cells which are cytotoxic in vitro and can adoptively confer anti-tumor protection in vivo.

Animals↗

PubMed1992

Cellular proliferation and genetic events involved in the genesis of Burkitt lymphoma (BL) in immune compromised patients.

A mathematical model simulating lymphomagenesis based on the two-hit theory of carcinogenesis is presented by contrasting the biologic variables responsible for a high risk of developing Burkitt lymphoma (BL) in three immunosuppressed groups with that of nonendemic BL. In this model, the pro-B lymphocyte is considered to be the target for BL-specific translocations such as t(8;14). With repeated mitosis, the target cell pool expands in the high-risk individual, and, thereby, the opportunities for a spontaneous translocation to arise are increased. The chromosomal translocation endows the target cell with survival advantages, and, hence, lymphoma develops. Modeling results demonstrate that this increased cell proliferation is sufficient in accounting entirely for the increase in tumor prevalence. Preventing enhanced cellular proliferation by obviating immune deficiency and treating patients with agents that restore immunity or have antiviral and antiproliferative properties prior to conversion from polyclonal B-cell proliferation to monoclonal malignancy could obviate the development of BL.

B-Lymphocytes↗