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PubMed1977

Cell proliferation in human cutaneous squamous cell carcinoma.

Squamous cell carcinoma (SCC) of the skin, a fairly slow-growing locally invasive tumor that occasionally matastasizes, was studied in 12 patients in vivo with the use of intralesional tritiated thymidine as a marker for cell proliferation kinetics. Analysis of the cell cycle of the germinative population revealed that the duration of S-phase was 12.5 hours; G1-phase, 28.8 hours; mitotic period (M-phase), 2 hours; G-pahse, 6.9 hours; and the total germinative cell cycle, 50.2 hours. The application of cell kinetics to programming chemotherapy for skin cancer with phase-specific cytotoxins was discussed.

Antineoplastic Agents↗
PubMed1977

The effects of neuraminidase and galactose oxidase on murine lymphocytes. I. Evidence for the differential delivery of signal(s) leading to cell proliferation and the differentiation of cytotoxic T cells.

The sequential treatment of normal C57BL/6 mouse spleen cell populations with neuraminidase (NA) and galactose oxidase (GO) resulted in cell proliferation, but not in the differentiation of cytotoxic T cells. In contrast, C57BL/6 spleen cells derived from animals primed 5 to 8 months earlier with alloantigen (P815 mastocytoma cells of the DBA/2 strain) both proliferated and demonstrated T cell-mediated cytotoxicity after NAGO stimulation. T cells differentiating into cytotoxic cells after NAGO treatment demonstrated properties similar to alloantigen-specific 'memory' T cells. These were: 1) cytotoxicity developed only from 'primed' cell populations, 2) cytotoxicity developed within 24 hr after NAGO treatment, 3) DNA synthesis was not required for the differentiation of cytotoxic cells during the first 24 hr of culture but both DNA synthesis and cell proliferation were required for the cytotoxicity developing after 24 hr, and 4) all cytotoxicity induced by NAGO showed specificity for the priming alloantigen. It was found, furthermore, that cytotoxicity could be induced at much lower GO concentrations than needed for increased DNA synthesis. We interpret this finding as an indication that NAGO can differentially deliver two 'signals' to T lymphocytes: one leading to cell proliferation, the other causing the differentiation of memory T cells into cytotoxic effectors.

Animals↗
PubMed1979

A simple reliable system for studying antigen-specific murine T cell proliferation.

Antigen-specific T cell proliferation can be readily elicited from the popliteal lymph node cells of mice which have received immunizations of antigen in the hind footpads. The advantages of our system over other published methods are (i) simplicity in method and materials, (ii) much improved reproducibility, (iii) negligible concomitant B cell proliferation, (iv) large degrees of antigen specific proliferation with very low background, and (v) complete dependence of the response on accessory cells or macrophages. These results were brought about by proper immunization procedures for mice and judicious choice of culture conditions. Our data show that the system is very suitable for the study of macrophage-T cell interaction in the induction of T cell proliferation as well as the genetic basis of responsiveness or non-responsiveness to protein and polypeptide antigens.

Animals↗
PubMed1978

Inhibitor of hematopoietic cell proliferation derived from a human leukemic cell line.

A continuously growing human myeloid leukemia cell line (K562) produced a potent high-molecular-weight inhibitor of hematopoietic cell proliferation. It was most active against myeloid stem cells (CFU-C) and proliferating T lymphocytes; it was less active against erythroid precursors (CFU-E) and did not inhibit fibroblasts or established lines of epithelioid cells or B lymphocytes. Inhibition of CFU-C was by direct interaction rather than by modulation of production of colony-stimulating activity and probably occurred at restricted points in the cell cycle. Inhibition could, within limits, be reversed by washing the target cells. Production of inhibitors of hematopoiesis is not a general property of established cell lines, and only two have thus far been identified in screening of 30 such lines.

Bone Marrow Cells↗
PubMed1978

Factors influencing endothelial cell proliferation in vitro.

The relative roles of blood cell products and plasma factors on endothelial cell proliferation were evaluated by studying the proliferative response of human umbilical vein endothelial cells to cell free plasma derived serum (CFPDS), whole blood serum (WBS), platelet released factors, fibroblast growth factor and macrophage conditioned medium in vitro. Human adult arterial smooth muscle cells were treated in a similar manner for comparison. The rate of endothelial cell proliferation was directly related to the concentrations of both WBS and CFPDS. Grwoth rate in WBS was marginally greater than that observed in CFPDS during early culture, however, similar confluent densities were achieved. The addition of platelet released factors to CFPDS did not further stimulate endothelial cell proliferation. In contrast smooth muscle cells were quiescent in CFPDS despite increasing serum concentrations, but proliferated actively in response to platelet released factors. Both human macrophage conditioned medium and fibroblast growth factor increased endothelial cell proliferation significantly when compared with CFPDS alone. It is concluded that endothelial cell proliferation in preconfluent cultures is dependent on plasma factors while human vascular smooth muscle cells also require cell derived mitogens such as platelet growth factor to proliferate. The release of a substance by human macrophages mitogenic for endothelial cells may be involved in endothelial cell proliferation in vivo.

Blood↗
PubMed1979

Modulation of cell proliferation and senescence of WI-38 cells by hydrocortisone.

The specific binding of glucocorticoid hormones has been studied in the normal diploid human cell line WI-38. These cells were found to contain high affinity glucocorticoid binding sites whose molecular specificity showed a high correlation to that required for the stimulation of cell growth. When hydrocortisone (HC) was selectively added to or removed from parasynchronously dividing cultures, we observed that HC -enhanced stimulation of cell growth was associated with the hormone's presence in the pre-DNA synthetic period of the cell cycle. Similarly, the specific binding of [3H]dexamethasone in stimulated quiescent cells was found to increase significantly in the pre-DNA synthetic period. The concentration of specific binding sites per cell achieved in stimulated cell cultures was found to decrease with increasing in vitro age. These results suggest that the stimulation of WI-38 cell proliferation by HC involves specific glucocorticoid receptors whose concentration per cell is under cell cycle control. The age-associated decrease in specific glucocorticoid binding sites may explain, in part, our previously observed loss of responsiveness to HC in aging cell cultures.

Cell Cycle↗
PubMed1977

Cell proliferation and histologic classification of bronchogenic carcinoma.

The rate of cell proliferation of 99 bronchogenic carcinomas (94 primary tumors and 5 metastases) was evaluated from the labeling index after in vitro incorporation of [3H]thymidine; the rate was then correlated with the histologic tumor type according to the classification of the World Health Organization (WHO). Cell proliferation was significantly slower in adenocarcinoma (WHO type III) than in squamous cell carcinoma (WHO type I), small cell anaplastic carcinoma (WHO type II), and large cell carcinoma (WHO type IV). Cells proliferated at a significantly higher rate in large cell carcinoma than in the squamous cell type, whereas no significant difference was observed between the other cell types. Dedifferentiated forms of squamous cell carcinomas had a higher rate of cell proliferation than did differentiated forms of the same cell type. Metastases of small cell anaplastic carcinoma did not differ in cell proliferation from primary tumors of the same cell type.

Adenocarcinoma↗
PubMed1978

Ageing of chick embryo fibroblasts in vitro. II. Relationship between cell proliferation and increased multinuclear cells.

The cell lines of chick embryo fibroblasts obtained from different embryos were sequentially cultivated and relationship between growth potential and increased multinuclear cells was examined. During ageing in vitro multinuclear cells increased with decreasing growth rate. Their percentage in the senescent cell populations reached 11--15% when the cells stopped growing, and 20--25% just before the cultures died out. This phenomenon may be useful as a parameter for cellular ageing. Most of the multinuclear cells were binucleates. The mean cell volume of the cells also increased through their lifespan with a sharp rise at the latest passages.

Aging↗
PubMed1977

The influence of adrenoceptor activity on cell proliferation in colonic crypt ipithelium and in colonic adenocarcinomata.

The effects of chemical sympathectomy and of the injection of amines or amine-receptor blocking drugs on cell proliferation in colonic crypts and in dimethylhydrazine-induced colonic carcinomata is examined in rats using a stathmokinetic technique. In animals which had been chemically sympathectomized by injection of 6-hydroxydopamine cell proliferation essentially ceased in the colonic crypts but continued at a normal rate in the tumours. Stimulation of alpha-adrenoceptors by metaraminol, a drug with properties similar to noradrenaline, caused acceleration of cell proliferation in colonic crypts but not in tumours. Conversely, blockade of alpha-adrenoceptors by phentolamine inhibited cell proliferation in crypts but not in tumours. Injection of adrenaline, predominantly a beta-adrenergic agonist, inhibited cell proliferation in the tumours but not in colonic crypts whereas blockade of beta-adrenoceptors by propranolol accelerated cell proliferation in tumours but not in colonic crypts. It is postulated that cell proliferation in the crypts of Lieberkühn in rat colon resembles that in rat jejunum in being controlled by the autonomic nervous system. However, tumour cell proliferation does not appear to be subject to such regulation.

Adenocarcinoma↗
PubMed1979

A study of glial cell proliferation in the molecular layer of the dentate gyrus of the rat following interruption of the ventral hippocampal commissure.

The proliferation of glial cells in the molecular layer of the dentate gyrus in response to lesions of the ventral hippocampal commissure, has been studied autoradiographically following intraventricular injections of 3H-thymidine. Within 24 h of commissurotomy there is an appreciable increase in the number of labeled cells throughout the molecular layer which reaches its peak at approximately 36 h. This generalized glial hyperplasia persists for at least 5--6 weeks and there does not appear to be a secondary re-distribution of the newly-generated glial cells as has been reported after entorhinal lesions (Gall et al., 1979). In semi-thin plastic sections most of the proliferating cells more closely resemble the "medium-shade oligodendrocytes" of Ling et al. (1973) than typical microglia; the reactive astrocytes do not appear to participate in the glial proliferation.

Animals↗
PubMed1977

Effects of fibroblast and epidermal growth factors on ovarian cell proliferation in vitro. II. Proliferative response of luteal cells to FGF but not EGF.

The effect of fibroblast growth factor (FGF) and epidermal growth factor (EGF) on luteal cell proliferation in vitro has been examined. Luteal cells maintained in the presence of low serum (1%) go through a doubling after 7 days. Addition of EGF induced one more doubling of the cells, after which the cells became resting. In contrast, FGF induced the cells to divide logarithmically with a cell cycle of 48 h. The effect of FGF was dependent on the serum and FGF concentrations. It has been obtained with serum concentrations ranging from 0.1% to 10% and with FGF concentrations ranging from 0.1 ng to 10 ng/ml. The half-maximal FGF response was observed at 1.5 x 10(-11)M. In contrast, EGF has no effect besides causing an initial cell doubline within the same range of serum or FGF concentrations. Since granulosa cells have been shown to be highly sensitive to EGF as well as FGF, it can be concluded that during the luteinization process that sensitivity of the cells to EGF is lost, while the sensitivity of FGF is retained. This demonstrates that although luteal cells and granulosa cells are interrelated cell types their sensitivity to growth factors such as EGF is quite different.

Blood↗
PubMed1979

Chronic myelogenous leukemia with reticulum-cell-sarcoma-like cell proliferation--significance of eosinophilic granules in sarcomatous cells.

A case of chronic myelogenous leukemia (CML) associated with proliferation of atypical cells resembling those of reticulum cell sarcoma (RCS-like cells) is presented. A number of immature eosinophils were present mingled with ordinary leukemic cells, which infiltrated in the bone marrow, lymph nodes, spleen, liver, lungs and testes. RCS-like cells either formed solitary nodular foci or randomly mingled with infiltrating leukemic cells. Charcot-Leyden crystals were seen in some areas where RCS-like cells proliferated. As a peculiar feature the presence of eosinophilic granules in some of the RCS-like cells was noted. They were proved to be immature form of specific granules of eosinophils by their staining properties and ultrastructural aspects. Based on these findings the myelogenous origin of RCS-like cells is suggested. The patient died of cerebral complication of aspergillosis.

Adult↗
PubMed1975

Inhibiton of tumor cell proliferation: second role for suppressor cells?

An antimitotic factor for mouse tumor cells was isolated from the supernatant fluids of antigen-stimulated ovalbumin-immune mouse spleen cells. A similar antimitotic factor was obtained from the supernatant fluids of phytohemagglutinin-stimulated non-immune spleen cells. The inhibitor prevented the multiplication of mouse L929 fibroblast cells in vitro and the in vivo proliferation of Ehrlich ascites tumor cells. Inhibition was not due to cytotoxic effects and the antimitotic effects were reversible. The antimitotic activity may be species-specific since the purified factor obtained from mouse spleen cells had no effect on human or monkey cell lines. This factor appears to be the same as the T lymphocyte-dependent suppressor for antibody production that we described previously. Several implications for the production of the suppressor in response to tumor cells that may be beneficial or harmful to the host are discussed.

Animals↗
PubMedDate not supplied

[The mechanism of cell proliferation in acute (immature-cell) leukemia].

In 40 patients with acute leukaemias the 3H-thymidine and mitosis indices were determined in the population of blast cells in bone marrow and the cellularity of bone marrow was determined. The studies were carried out in the first episode of the disease before treatment and in some patients (13) they were repeated during relapse after remission or improvement. The results showed that proliferative activity of blast cells was reduced in relation to precursors of normal granulopoiesis in all forms of acute leukaemia. Myeloblastic leukaemias showed a greater scater of values of both proliferation parameters in relation to lymphoblastic leukaemias. It was found, moreover, that in highly cellular bone marrow the proliferative activity of blast cell population was significantly lower than in patients with low bone marrow cellularity. On the ground of this observation the authors put forward the view that in acute leukaemias the intrinsic mechanism controlling the proliferation of cells is disturbed.

Acute Disease↗
PubMed1977

Quantitative studies of immunoglobulin deposition in the kidney, glomerular cell proliferation and glomerulosclerosis in NZB/NZW F1 hybrid mice.

Using the NZB and NZB/NZW F1 (B/W) hybrid mouse as a model for systemic lupus erythematosus, an effort has been made to quantitate: (1) immune complex deposition in the glomeruli by immunofluorescent staining of immunoglobulin, (2) glomerular cellular proliferation by radioautographic measurement of [3H]Tdr incorporation into the glomerular cells in vivo, and (3) glomerular scarring by PAS staining. The relationship between these changes and increasing age has been examined. By radioautography it was observed that dividing glomerular cells were labelled in vivo after injection of [3H]Tdr. This provided a reproducible measure of the proliferative process in the nephritis of B/W mice. In C57B1/6J and CBA/J mice, which have a low incidence of glomerular disease, little change in the amount of glomerular cell proliferation was observed with increasing age. The NZB strain of animals showed a somewhat increased level of proliferation but this did not increase with age. In striking contrast, glomerular cell proliferation in the B/W mice increased rapidly with age. The earliest change observed in the kidney was the deposition of immunofluorescent material in the mesangium and glomerular capillary basement membrane beginning between 3 and 5 months of age and reaching a peak at 9 months. Increase in glomerular cell proliferation began about 2 months after the onset of immune complex deposition but also reached a maximum at 7 months. Glomerular sclerosis was the last change to appear and continued after the other two parameters measured has begun to decline. These data suggest that the deposition of immune complexes in the glomerulus may be an important triggering mechanism for renal cell proliferation and glomerulosclerosis in the B/W mouse. The techniques described would provide a sensitive and reproducible quantitative method for analysing the differential effects of various types of treatment of immune complex nephritis in animals.

Age Factors↗
PubMed1977

Glomerular cell proliferation in human and experimental glomerulonephritis. Light- and electron-microscopical, and autoradiographic observations.

Three mitoses of endothelial glomerular cells have been observed by electron microscopy in 3 different nephropathies (a mixed membranous and proliferative glomerulonephritis, an intracapillary glomerulonephritis, and a mixed IgG-IgM cryoglobulinemia). Further light- and electron-microscopical and autoradiographic investigations on the occurrence and nature of the dividing cells responsible for glomerular hypercellularity in glomerulonephritis have been carried out in rats with an immunocomplex-induced glomerulonephritis. A statistically significant difference between treated and control animals have been found in the number of mitoses and DNA-synthesizing nuclei. All dividing glomerular cells observed by electron microscopy were endothelial. It is therefore proved that in glomerulonephritis an actual glomerular cell proliferation does occur; proliferating cells are suggested to be endothelial in nature.

Animals↗