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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↗
PubMed1976

Induction or suppression of B cell proliferation and differentiation by phytohemagglutinin or concanavalin A in mouse spleen cell cultures.

Cultures of mouse spleen cells or various mixtures of mouse T and B cells were stimulated with PHA or Con A, and the T, B, or plasmablast nature of the transformed cells, was determined by immunofluorescence 2 to 4 days later. The lectins enhanced B cell proliferation and plasmablast differentiation ("helper" effect) provided one of the following conditions was fultilled: a) suboptimal doses of lectin were used, b) cultures were performed at low cell concentration, c) cultures were made of spleen cells containing a small percentage of T cells, d) the cultures contained a mixture of T-depleted spleen cells and T cells rendered unable to proliferate by irradiation. In contrast, cultures performed with 1.5 10(6) or more spleen cells/ml and optimal doses of lectin contained almost exclusively T blasts, as did cultures stimulated in the same conditions with both PHA and LPS. This last observation idicates the existence of a lectin-induced "suppressor" effect, since LPS, a B cell mitogen, induces, in the absence of PHA, a marked B cell proliferation and differentiation into plasmablasts. These helper and suppressor effects were entirely mediated by T cells, since they were not observed in spleen cell cultures depleted in T cells by anti-thets + C. Analysis of the cultures by immunofluorescence and radioautography after pulses of 3H-thymidine showed that these antagonistic effects could be related to the number of T blasts present in the culture and to their proliferative behavior. Heoper effect is observed in cultures containing a relatively low number of T blasts (or none in cultures made with irradiated T cells), whereas suppressive effect is observed in cultures containing a high number of T blasts, a large proportion of them having left the proliferative cell cycle. It is proposed that when a critical concentration of T blasts is reached ("saturation density"), further proliferation and differentiation is prevented, resulting in a suppressive effect on the generation of plasmablasts. The helper effect of lectin-activated T cells seems to be exerted on a subpopulation of B cells which was, at least in part, already proliferating in vivo, and to result in a polyclonal IgM plasmablast differentiation.

Animals↗
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↗
PubMed1976

The effect of ischemic villus cell damage on crypt cell proliferation in the small intestine: evidence for a feedback control mechanism.

In recent years the hypothesis that the number of villus cells regulates crypt cell proliferation in the epithelium of the small intestine has been brought forward by a number of investigators. To test this hypothesis, the villus cell population was reduced by clamping the superior mesenteric artery and vein in rats for 1 hr and the effects on the intestinal epithelium were studied during the first 24 hr. It was shown that temporary interruption of the blood flow to the small intestine led to a marked decrease in the number of functional villus cells within 2 hr; preferentially, cells from the upper part of the villus were lost and the number of crypt cells was not affected. This reduction in the number of villus cells led to an increase in the percentage of labeled crypt cells after pulse labeling with [3H]thymidine, and an expansion of the proliferative cell compartment in the crypt. After a peak of proliferative activity at 16 hr, the investigated crypt cell kinetic parameters approached control values after 24 hr, as did the number of villus cells. The enzyme activities of nonspecific esterase and neutral alpha-glucosidase showed marked decreases in isolated crypt and villus cell compartments as crypt cell proliferation increased. These data support the view that the feedback control of crypt cell proliferation by the functional villus cells, and confirm earlier data on the influence of changing cell kinetics on crypt cell maturation. Additional data which were obtained after creating temporary ischemia in part of the small intestine support the hypothesis of a feedback control of crypt cell proliferation by the functional villus cells, and confirm earlier data on the influence of changing cell kinetics on crypt cell maturation. Additional data which were obtained after creating temporary ischemia in part of the small intestine support the view that the feedback control of proliferation by the villus cells is a local control mechanism.

Animals↗
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↗
PubMed1979

A comparison of cell proliferation at different sites within the large bowel of the mouse.

This study was undertaken in order to compare cell proliferation at different sites along the length of the large bowel of the mouse. Simple morphometry has been used along with 3HTdR labelling studies and metaphase arrest with vincristine. Differences have been described in the shape and size of crypts, the distribution of proliferating cells, the duration of the cell cycle, as well as in the rate of cell production by the crypts. The findings explain some of the apparent inconsistencies in the literature.

Animals↗
PubMed1979

Effects of glucocorticosteroids on cultured human skin fibroblasts. V. Influence of anabolic steroids on the inhibitory effects of clobetasol-17-propionate on cell proliferation and collagen synthesis.

As previously found, the glucocorticosteroid clobetasol-17-propionate inhibits cell proliferation during the early growth stage of normal baby foreskin fibroblasts and collagen synthesis in confluent cultures of these cells. The degree of inhibition of cell proliferation decreases with increasing cell density and, moreover, is transient. The anabolic steroids nandrolone and nandrolone-phenyl-propionate have similar effects on these cells. Likewise the magnitude of the inhibition is dose-dependent. When present together the two types of drug do not act in an additive manner. Even at low concentrations the anabolic steroids abolish the inhibitory effect of the glucocorticosteroid on cell proliferation. Furthermore, in this case only the inhibitory effect of the glucocorticosteroid on collagen synthesis is found and there is no further increase in this effect due to the presence of the anabolic steroids. Our results imply that the use of low concentrations of anabolic steroids combined with glucocorticosteroids in topical application to the skin may abolish some of the undesirable side effects of the glucocorticosteroids.

Betamethasone↗
PubMed1976

A comparison of cell proliferation in normal and neoplastic intestinal epithelia following either biogenic amine depletion or monoamine oxidase inhibition.

Epithelial cell proliferation was studied in the jejunum and in the colon of normal rats, in the colon of dimethylhydrazine-treated rats and in dimethylhydrazine-induced adenocarcinoma of the colon using a stathmokinetic technique. Estimates of cell proliferation rates in these four tissues were then repeated in animals which had been depleted of biogenic animes by treatment with reserpine and in animals whose monoamine oxidase was inhibited by treatment with nialamide. In amine-depleted animals cell proliferation essentially ceased in all four tissues examined. Inhibition of monoamine oxidase did not significantly influence cell proliferation in nonmalignant tissues but accelerated cell division in colonic tumours.

Adenocarcinoma↗
PubMed2026

Mechanistic insights into CAR-mediated repression of the HNF4α-FABP1 axis and inhibition of HepG2 cell proliferation.

The constitutive androstane receptor (CAR) modulates the transcription of numerous genes involving drug metabolism, energy homeostasis, and cell proliferation. While rodent studies suggest an oncogenic role for murine CAR in liver cancer development, emerging evidence indicates that human CAR (hCAR) may exhibit a tumor-suppressive role in hepatocellular carcinoma; notably, overexpressing hCAR suppresses human hepatoma cell proliferation. Yet, the molecular mechanisms whereby hCAR suppresses hepatoma cell proliferation are poorly understood. Our recent RNA-seq analysis of human hepatoma cells revealed that fatty acid binding protein 1 (FABP1), a pleiotropic modulator of lipid metabolism and cancer progression, was a top gene downregulated by hCAR. Here, we report a molecular mechanism whereby hCAR downregulates FABP1 expression by modulating HNF4α signaling. Knocking down hCAR expression in a HepG2-hCAR stable cell line restores the suppressed expression of FABP1 and HNF4α, while knocking down HNF4α alone is sufficient to suppress FABP1 expression. Luciferase reporter assays revealed concentration-dependent hCAR suppression of HNF4α-mediated FABP1 transactivation. This inhibitory crosstalk between hCAR and HNF4α was further confirmed by chromatin immunoprecipitation assays, where hCAR decreased HNF4α occupancy of the FABP1 promoter. Mechanistically, hCAR inhibits HNF4α expression by prompting deacetylation of histone H3 in the HNF4α P1 enhancer region, resulting in a repressive chromatin configuration and reduced HNF4α transcription. Furthermore, overexpressing FABP1 partially rescued hCAR-suppressed cell growth. Collectively, these results uncover the hCAR-HNF4α-FABP1 axis as a novel mechanism underlying hCAR-mediated gene repression.

Humans↗
PubMed1978

[Kinetics of cell proliferation and cancer: introduction (author's transl)].

Research in the kinetics of cell proliferation directly interests oncologists for fundamental and pragmatic reasons. Since cancer is a perturbation of the control of cell proliferation and differentiation, such research may help to understand, the regulation mechanisms, in particular the role of microenvironment, of long range humoral factors, and of membrane site receptors. Furthermore the kinetics of cell proliferation in a normal tissue, or a tumour, influences its response to radiation or drugs. From this evolves the practical interest in research on hemopoietic tissues and on human and experimental tumors. Finally, the growth kinetics of human tumors explain their natural history and opens prospects for the treatment of intraclinical neoplastic disease and metastasis.

Animals↗
PubMed1976

Alteration by malignant transformation of the calcium requirements for cell proliferation in vitro.

Cells from the thigh muscles of normal fetal rats proliferated rapidly and indefinitely in a medium containing adult rat "plasma" and a normal free-calcium concentration, but they could not proliferate in calcium-deficient plasma medium. As the animals grew older, the cells became increasingly less able to proliferate even in normal (high-calcium) plasma medium, though they retained the potential to proliferate in a more conventional medium containing fetal bovine serum. By contrast, neoplastic adult cells from malignant rhabdomyosarcomas (induced by Ni3S2) proliferated rapidly and indefinitely in both normal and low-calcium plasma medium

Animals↗
PubMed1978

Age-related and carcinogen-induced alterations of the extracellular growth factor requirements for cell proliferation in vitro.

Cells from thigh muscles of fetal rats proliferate readily in vitro in medium containing homologous adult rat "plasma". As the donor animals mature, these cells become unable to make DNA and proliferate in "plasma" medium, but retain an ability to proliferate in medium containing fetal bovine serum (FBS). This age-related loss of the ability to proliferate in "plasma"-medium is due to an increasing need by the cells for an exogenous prereplicative promoter which is found in FBS and a crude preparation of bovine luteinizing hormone. Adult cells (and possibly fetal cells) also require a "cycle-completion" factor which is found in FBS and adult rat "plasma". The requirements for such external proliferative promoters is completely eliminated by neoplastic transformation in vivo, and neoplastic adult cells isolated from a nickel sulfide-induced mixed rhabdomyo-fibro-sarcoma can make DNA and proliferate in vitro in the complete absence of exogenous growth factors.

Blood↗
PubMed1977

A stimulator of stem cell proliferation in regenerating bone marrow.

A factor, capable of stimulating resting haemopoietic stem cells into DNA-synthesis has been extracted from regenerating bone marrow. It has a molecular weight in the range of 30.000-50.000 daltons and is not detectable in normal bone marrow. Used in combination with a stem cell proliferation inhibitor, previously described, it will restimulate proliferation in stem cells initially stopped by the inhibitor. Conversely, stimulation produced by this factor can be reversed by the addition of inhibitor. It is concluded that stem cell proliferation is controlled by an appropriate balance of endogenously produced stimulatory and inhibitory factors.

Animals↗
PubMed1978

Dexamethasone inhibition of experimental endothelial cell proliferation in retinal venules.

The observation that endothelial cell proliferation in retinal blood vessels is induced by ocular trauma in rats has been extended to mice. Indomethacin, 10 mg/kg/day, failed to block incorporation of tritiated thymidine into nuclei of venular endothelial cells in rat retinas observed 40 hr after puncturing the lens, but dexamethasone effectively suppressed tritiated thymidine incorporation, with 50% inhibition obtained with 0.2 mg/kg/day. The prostaglandin pathway does not appear essential to the activation of endothelial cell proliferation in this system.

Animals↗
PubMed1977

Feline panleukopenia. II. The relationship of intestinal mucosal cell proliferation rates to viral infection and development of lesions.

Proliferation rates of small intestinal mucosal cells of noninfected germfree and specific pathogen-free kittens were compared to the incidence of infected cells and microscopic lesions in kittens experimentally infected with panleukopenia virus. Mucosal crypt length, cells per crypt, mitotic index and villous length were greater in specific pathogen-free kittens than in germfree kittens. Crypt cells per unit length and villous length per crypt length ratio were greater in germfree kittens. The cryptal cell proliferation rate of specific pathogen-free kittens was 2.24 times that of germfree kittens. Mucosal crypt length, cell per crypt and villous length were greater in the proximal jejunum than in the midjejunum of kittens within groups. Cell proliferation rates per crypt did not differ between areas of the intestine in kittens within groups. There were more virus-infected cells and lesions in specific pathogen-free kittens than in germfree kittens. The incidence of virus-infected cells and lesions was greater in the proximal jejumum and decreased along the small intestine.

Animals↗
PubMed2026

PDZ-binding kinase promotes ovarian cancer cell proliferation and invasion via CCNB1 regulation.

BACKGROUND: Ovarian cancer is one of the most lethal gynecological malignancies, characterized by late diagnosis, frequent recurrence, and high mortality. PDZ-binding kinase (PBK), a serine/threonine kinase of the mitogen-activated protein kinase kinase (MAPKK) family, has been implicated in the tumorigenesis of multiple cancers, yet its role in ovarian cancer remains incompletely characterized. This study aimed to investigate the effect of PBK on the proliferation and invasion of ovarian cancer cells. METHODS: The expression of PBK and cyclin B1 (CCNB1) in normal ovarian tissues and ovarian cancer tissues was analyzed using online databases including Gene Expression Profiling Interactive Analysis 2 (GEPIA2), Clinical Proteomic Tumor Analysis Consortium (CPTAC), and Kaplan-Meier Plotter. Clinical tissue specimens were collected to detect the expression of PBK and CCNB1 by immunohistochemistry. Quantitative real-time polymerase chain reaction (PCR) was performed to detect PBK messenger RNA (mRNA) expression levels in clinical specimens and cell lines. Western blot was used to detect PBK protein expression in ovarian cancer cell lines. ES2 and A2780 cells with higher PBK expression were selected to construct PBK knockdown cell lines using lentiviral interference vectors. Cell Counting Kit-8 (CCK-8) assay, colony formation assay, and 5-ethynyl-2'-deoxyuridine (EdU) assay were performed to explore the effect of PBK knockdown on cell proliferation. Transwell assay was used to investigate the effect on cell invasion. The Cancer Genome Atlas (TCGA) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases were utilized to analyze PBK-related pathways and predict CCNB1 as the gene most closely related to PBK. RESULTS: PBK was significantly overexpressed in ovarian cancer tissues and cell lines compared with normal controls, and high PBK expression was associated with poor overall survival (OS) and progression-free survival (PFS). Knockdown of PBK expression inhibited the proliferation, colony formation, and invasion of ovarian cancer cells. Bioinformatics analysis revealed that CCNB1 was significantly overexpressed in ovarian cancer and high CCNB1 expression was associated with poor OS. CCNB1 was also significantly highly expressed in ovarian cancer tissues as validated by immunohistochemistry and was associated with lymph node metastasis. PBK and CCNB1 expression showed a significant positive correlation in TCGA ovarian cancer datasets. Knockdown of PBK inhibited CCNB1 expression in ovarian cancer cells. CONCLUSIONS: PBK promotes ovarian cancer cell proliferation and invasion. PBK knockdown leads to CCNB1 downregulation. These findings suggest that CCNB1 contributes to PBK-mediated oncogenic effects and identify the PBK-CCNB1 axis as a potential therapeutic target for ovarian cancer treatment.

PDZ-binding kinase (PBK)↗