bluuebunny/crossref_metadata_2025_split huggingface dataset:
Remission of oral leukoplakias and micronuclei in tobacco/betel quid chewers treated with beta‐carotene and with beta‐carotene plus vitamin A
Authors: Stich Hans F. , Rosin Miriam P. , Hornby A. Paul , Mathew Babu , Sankaranarayanan R. , Nair M. Krishnan 
Published: February 2007

AbstractFishermen from Kerala (India) who chewed tobacco‐containing betel quids daily (17.2 ± 9.6 quids per day) and had well‐developed oral leukoplakias with elevated frequencies of micronucleated cells participated in a short‐term intervention trial. Beta‐carotene (180 mg/week) (Group I), beta‐carotene (180 mg/week) plus vitamin A (100,000 IU/week) (Group II), and placebo (Group III) capsules were given twice weekly for 6 months under strict supervision. The remission of oral leukoplakias, the inhibition of new leukoplakias, and the reduction of micronucleated oral mucosal cells were recorded at the 3rd and 6th months of the trial period. After 3 months, the frequency of micronucleated cells was significantly reduced in Group I (from 4.09% to 1.1% in areas of leukoplakia, and from 4.1% to 1.0% in the normal mucosa). At this time, remission of oral leukoplakias did not differ significantly from that observed in the placebo group. After 6 months of treatment, remission of leukoplakias in Group I (14.8%) and Group II (27.5%) differed significantly from that seen in Group III (3.0%). The development of new leukoplakias during the 6 months period was strongly inhibited in Group II (7.8%), and to a lesser degree in Group I (14.8%), as compared to Group III (21.2%). During the trial period, all participants continued to chew tobacco‐containing betel quids in their accustomed manner. Thus, remission and inhibition of new oral leukoplakias and reduction of micronucleated mucosal cells occurred in the groups receiving beta‐carotene and beta‐carotene plus vitamin A during the continuous presence of carcinogens derived from tobacco and areca nut.
The Danish case‐control study of cutaneous malignant melanoma. I. Importance of host factors
Authors: Østerlind A. , Tucker M. A. , Hou‐Jensen K. , Stone B. J. , Engholm G. , Jensen O. M. 
Published: February 2007

AbstractThe relationshop between cutaneous malignant melanoma and possible host factors was Investigated in a populationbased case‐control study from East Denmark over a 3‐year period. A total of 474 melanoma patlents and 926 population controls aged 20–79 years were interviewed. Patients with lentigo maligna melanoma were not included. The major constitutional risk factors were: number of raised naevi on the arms (RR = 5,1 for 5+ vs, none), degree of freckling (RR = 2.9 for many vs, none), and light hair colour (RR = 1.7 for blond/fair vs. dark brown/black), which were independent of one another. An apparent synergy between number of raised naevi on the arms and degree of freckling was found. Thus, persons at high risk of melanoma may be identified by a simple assessment of naevi and degree of freckling. No significent difference was found between superficial spreading melanoma and nodular melanoma with regard to the most important host factors.
Immunolocalization of an angiogenic factor (HAF) in normal, inflammatory and tumor tissues
Authors: Fröhbeis Bärbel , Zwadlo Gabriele , Broöcker Eva‐Bettina , Osthoff Klaus Schulze , Hagemeier Hana‐Hermann , Topoll Heinrich , Sorg Clemenns 
Published: February 2007

AbstractThe distribution of a novel human angiogenic factor (HAF) (Schulze Ostoff et al., 1987) has been investlgated on various human cell lines, isolated blood cells as well as in normal, inflammatory and tumor tissues. Localization was performed by using the monoclonal antibody (MAb) 5F4 directed against HAF. It was found that 30% of freshly isolated human monocytes expressed the 5F4 antigen. The number of postitive cells increased to 75–90% on day 4 to 7 upon culture and then decreased. Twenty percent of freshly isolated human lymphocytes also stained positively, whereras graunlocytes and platelets were negative. In cryostat sections of normal human tissue (skin, lung, liver, spleen, placenta) 5F4 is positive with capillary endothelial cells and few macrophages. In inflammatory tissue derived from gingivitis and rheumatoid arthrritis, more macrophages than in normal tissues and less endothelial cell were postitive, In tumor tissues some endothelia cells and a subset of tumor‐infiltrating macrophages expressed the antigen. Tumor cells were positive in advanced melanoms, but only occasionlally in stomach carcinomas. We conclude that the angiogenic factor is produced mainly by a subset of inflammatory macrophages which appear to be the principal source of HAF in regenerating or growing tissues.
Isolation of a normal B cell subset with a Burkitt‐like phenotype and transformation in vitro with Epstein‐Barr virus
Authors: Gregory C. D. , Edwads C. F. , Milner A. , Wiels J. , Lipinski M. , Rowe M. , Tursz T. , Rickinson A. B. 
Published: February 2007

AbstractEpstein‐Barr virus (EBV) is causally linked with endemic Burkitt's lymphoma (BL), a tumour whose homogeneous cell surface phenotype suggests derivation from a particular subset of activated germinal centre B cells in vivo. Endemic BL also shows an unusual form of EBV in fection with downregulation of certain of the virus latent proteins which are constitutively expressed when EBV infects and transforms normal resting B cells in vitro. Here we question whether this virus:cell interaction is unique to malignant BL cells or whether it might be reproduced by in vitro infection of those particular germinal centre cells displaying the BL‐like phenotype. Firstly, we show by biochemical meanns that a subset of normal tonsillar B cells does indeed express the globotriaosylceramide glycolipid BLA and the common acute lymphoblastic leukaemia antigen CALLA, 2 important markers of the BL phenotype. Secondly, using 2‐colour immunofluorescence labelling with anti‐BLA and anti‐CALLA monoclonal antibodies (MAbs), 4 subsets of low buoyant density tonsillar B cells (BLA+ CALLA+, BLA+ CALLA−, BLA− CALLA+, BLA− CALLA−) have been separated by means of a FACS and tested for their susceptibility to EBV‐induced growth transfromation in a limiting dilution assay. The BLA+ CALLA+ (i. e., BL‐like) subset contained the highest proportion of cells already actively in cycle in vivo and gave the lowest yield of transformants, perhaps reflecting the greater efficiency with which EBV transforms resting target cells. Of the cell lines established from the BLA+ CALLA+ population, a significant number retained BLA expression but CALLA was always lost. In 2 further respects, these lines resembled conventional in vitro transformants rather than lines of BL type; thus the cells expressed cellular “activation” antigens (CD23, CD39, CD30, Ki‐24) characteristic of the lymphoblastoid phenotype and contained the full spectrum of EBV latent proteins.
Recombinant IL‐2‐activated NK cells mediate LAK activity against ovarian cancer
Authors: Lotzová Eva , Savary Cherylyn A. , Freedman Ralph S. , Edwards Creighton L. , Wharton J. Taylor 
Published: February 2007

AbstractWe investigated the ability of endogenous and recombinant interleukin‐2 (IL‐2)‐stimulated NK cells from normal donors and ovarian cancer patients to mediate lysis of ovarian tumors, and found that peripheral blood (PB) mononuclear cells of normal donors or cancer patients did not display tumoricidal activity against ovarian cell line or fresh ovarian tumors. In addition, ovarian cancer patients displayed a defect in NK‐cell activity against the highly NK‐sensitive target, K‐562. However, lytic activity against ovarian tumors (including cultured and primary tumors) was induced and that against K‐562 was potentiated in PB of normal donors and PB and peritoneal cavity of ovarian cancer patients after enrichment of LGL on Percoll density gradient or after stimulation of effector cells with recombinant IL‐2 in vitro. The IL‐2‐generated cytotoxic cells in PB were characterized as NK cells displaying CD16+, NKHI (Leu‐19)+, CD3− and CD5− phenotype, while those in the peritoneal cavity were predominantly CD16−, NKHI+, CD3− and CD5−. Studies on the mechanism of IL‐2‐dependent generation of cytotoxicity showed that such an effect was mediated via recruitment of tumor‐binding cells as well as by an increase in the frequency of cytotoxic cells.
Proliferative and/or cytotoxic activity of lymphocyte clones to autologous human melanoma
Authors: Fossati Giuseppe , Anichini Andrea , Squarcina Paola , Mazzocchi Arabella , Parmiani Giorgio 
Published: February 2007

AbstractPeripheral blood lymphocytes (PBL) of a patient with metastatic melanoma were cultured with autologous melanoma cells (Auto‐Me) and recombinant interleukin 2 (IL‐2) (MLTC‐PBL). Thirty‐five days later, when no cytotoxicity against Auto‐Me or K562 was detectable, MLTC‐PBL were cloned in the presence of Auto‐Me, IL‐2 (25 U/ml) and Daudi cells as feeder. Eighty‐one growing clones were simultaneously screened for proliferative and cytotoxic activity to Auto‐Me. Twenty‐two clones proliferated in the presence of Auto‐Me only, 29 in the presence of IL‐2 only and 41 in the presence of Auto‐Me. Six clones expressed both cytotoxic and proliferative activity to Auto‐Me. The phenotype of 6 proliferative clones tested was CD3+, CD4+, WT31+, CD8−, CD16−, Leu19−, whereas that of 2 cytotoxic‐proliferative clones tested was CD3+, CD8+, Leu19+, WT31+, CD4−, CD16−. Specificity analysis of proliferative response of 6 clones and of cytotoxicity of 7 clones, tested on a panel of 14 different target cells, revealed a complex pattern of reactivity, each clone expressing a peculiar specificity. Our results suggest the possibility of isolating, from melanoma patients' PBL, T‐cell clones with proliferative activity to Auto‐Me and Auto‐Me plus IL‐2, and T‐cell clones which apparently express both proliferative and cytotoxic activity to Auto‐Me.
Subsequent development of acute non‐lymphocytic leukemia in patients treated for Hodgkin's disease
Authors: van der Velden J. W. , van Putten W. L. J. , Guinee V. F. , Pfeiffer R. , van Leeuwen F. E. , van der Linden E. A. M. , Vardomskaya I. , Lane W. , Durand M. , Lagarde C. , Hagemeister F. B. , Hagenbeek A. , Eghbali H. 
Published: February 2007

AbstractA nested case control study was carried out to investigate the association between treatment of patients with Hodgkin's disease (HD) and the risk of developing acute non‐lymphocytic leukemia (ANLL). Seven Cancer Centers of the International Cancer Patient Data Exchange System of the UlCC participated. A study cohort was selected consisting of 1,681 nonpretreated patients with HD, diagnosed from 1972 through 1978, and followed up through 1984. The median follow‐up time was 66 months. Eighteen cases of leukemia were observed in the cohort. The risk of development of ANLL was significantly greater for male than for female patients. The treatment characteristics associated with an increased risk of developing ANLL were extensive radiotherapy, splenectomy and the chemotherapy combination of vincristine, procarbazine and mechlorethamine.
Differential immunoreactivity and ca2+ ‐dependent degradation of vimentin in human fibroblasts and fibrosarcoma cells
Authors: Virtanen Ismo , Närvänen Outi , Lehto Veli‐Pekka 
Published: February 2007

AbstractImmunostaining of normal human fibroblasts with a monoclonal antibody (MAb) (V22AC 12) revealed typical cytoplasmic arrays of vimentin filaments in both mitotic and interphase cells. In human A8387 fibrosarcoma cells and SV40‐virus‐transformed human fibroblasts, the same antibody showed positivity only in mitotic cells and in interphase cells only after treatment of the fixed cells with alkaline phosphatase. Upon immunoblotting with the MAb, an Mr 57,000 vimentin polypeptide was seen in normal fibroblasts. In fibrosarcoma cells the same polypeptide was revealed by this antibody only after treatment with alkaline phosphatase. The Mr 57,000 vimentin polypeptide was a major cytoskeletal protein in both fibroblasts and fibrosarcoma cells. Inclusion of Ca2+ into the cytoskeleton extraction medium brought about a somewhat increased degradation of vimentin in fibroblasts. In fibrosarcoma cells, such treatment caused a quantitative disappearance of the Mr 57,000 protein with a concomitant appearance of 3 distinct, low‐molecular‐weight degradation products in the detergent‐soluble fraction. Another Ca2+‐induced change in the polypeptide profile of fibrosarcoma cells was the disappearance of the Mr 240,000 non‐erythroid α‐spectrin and the concomitant appearance of a prominent Mr 140,000 degradation product. Inclusion of proteolysis inhibitors in the Ca2+‐supplemented extraction medium inhibited degradation of both vimentin and α‐spectrin polypeptides. The results suggest differences in the composition of the cytoskeletons of normal fibroblasts and fibrosarcoma cells, manifested in the differential Ca2+‐susceptibility of vimentin and non‐erythroid α‐spectrin. Results with MAb V22AC12 suggest that differential phosphorylation of vimentin could account for at least part of this difference.
Skin papillomas and other neoplasms induced by murine sarcoma viruses in mid‐gestation‐infected mice
Authors: Rossi Lorenzo , Barbieri Ottavia , Capurro Gloria , Aiello Cinzia , Ruzzon Tiziana , Muratore Olimpio 
Published: February 2007

AbstractDuring extensive investigations on the effects of oncogenic retroviruses in developing rodents, the ability of MSV to mount a neoplastic response in CD‐I Swiss mouse embryos was determined. By infecting the animals directly in utero at selected stages of post‐implantation development, we detected a peculiar reaction of the embryonal tissues to certain MSVs: when mice were exposed to KiMSV at mid‐gestation, the newborn developed characteristic tumors, in addition to mesenchymal cell sarcomas, not induced in fetuses and neonates. These included pulmonary alveologenic tumors and skin papillomas and were seen in mice infected on days 8 and 10 of pregnancy, roughly corresponding to 15 and 35 somites, respectively. To determine the specificity of these events, other 8‐ and 10day‐old embryos were infected with retroviruses of the same or different families. HaMSV and MoMSV also induced mesenchymomas and a low incidence of skin papillomas (10% and 15% compared to 40% in the KiMSV group) but not pulmonary tumors. In contrast, FBRMSV was inactive in this respect and only osteogenlc sarcomas were detected in the offspring. Infecting the embryos on day 7 of pregnancy produced no tumors. Later infections (in 15‐day‐old fetuses and neonates) mainly induced mesenchymal sarcomas. No congenital malformations were detected in the embryos exposed to MSV during organogenesis, although some abortions and resorptions were seen.
Phorbol‐ester‐induced stable changes in the regulation of DNA synthesis and intracellular pH are accompanied by altered expression of protein kinase C in the monoblastoid cell line U‐937
Authors: Forsbeck Klas , Nilsson Kenneth , Nygren Peter , Larsson Rolf , Gylfe Erik , Skoglund Göran , Ingelman‐Sundberg Magnus 
Published: February 2007

Abstract12‐O‐tetradecanoylphorbol‐13‐acetate (TPA)‐induced changes in cytoplasmic PH, cytoplasmic Ca2+‐concentration, rate of DNA synthesis, and concentration and activity of protein kinase C (PKC) were studied in human monoblastoid cell lines. The cell line U‐937 GTB was compared to the subline U937 RES (adapted to growth in the presence of 10−9M TPA) and another subline U‐937 RESREV (U‐937 RES grown in TPA‐free medium) established in order to analyze the stability of the TPA‐induced differences. TPA induced half maximal inhibition of DNA synthesis in the wild‐type U‐937 GTB cell line at 10−9M, whereas 10 times higher concentrations of phorbol ester were needed for a corresponding inhibition of the U‐937 RES and U‐937 RESREV lines. Furthermore, the U‐937 RES cells exhibited a decreased sensitivity to TPA, and the U‐937 RESREV cells did not respond at all to this agent with regard to cytoplasmic alkalinization by an intracellular mechanism independent of Na+/H+ exchange. A Na+‐dependent system for extrusion of protons, which was activated by the Ca2+ ionophore ionomycin, was also severely depressed as a result of TPA‐adaptation. The concentration of PKC, measured by immunoblotting, was reduced by 34 and 24% in U‐937 RES and U‐937 RESREV cells, respectively, as compared to the wild‐type U‐937 GTB line. The corresponding reductions in PKC activity were 32 and 54% when histone III‐S was used as substrate. The data suggest that adaptation to growth in the presence of TPA results in stable modifications of several parameters, which are assumed to be involved in the regulation of proliferation and differentiation. Furthermore, the data from the U‐937 RESREV cells question a causal relationship between cytoplasmic alkalinization and control of proliferation.
Effects of the thiazolidinedione derivative CGP 19984 on growth and endocrine function of the Mtt‐W10 transplantable mammosmatotoropic pituitary tumor in female rats
Authors: Sylvester Paul W. , Utz Paul J. , Ip Margot M. 
Published: February 2007

AbstractThe thiazolidinedione derivative CGP 19984 has previously been shown to suppress the growth of hormone‐dependent mammary and prostatic tumors, primarily by reducing gonadotropin and subsequently gonadal steroid secretion. The present study examines the effects of CGP 19984 on the growth and hormone secretion of the autonomous, but estrogen‐responsive, MtT‐W10 mammosomatotropic transplantable rat pituitary tumor. Intact tumor‐bearing Wistar/Furth female rats were administered vehicle or 25, 100, or 250 mg/ kg CGP 19984 p. o. 5 × week for 4 weeks. CGP 19984 was found to significantly reduce MtT‐W 10 tumor growth and weight and reduce prolactin and growth hormone (GH) secretion in a dose‐responsive manner. A similar study in ovariectomized rats also showed that CGP 19984 treatment suppressed MtT‐W 10 pituitary tumor growth, weight and hormone secretion in a dose‐responsive manner, suggesting a direct inhibitory action of this drug on the tumor. In a third study, bromocryptine (CB‐154; 5 mg/kg) and CGP 19984 (50 mg/kg) were both found to be effective in suppressing growth of the MtT‐W 10 tumor in intact female rats. However, rats treated with CGP 19984 alone had reduced serum and tumor GH and prolactin concentrations, while rats treated with CB‐ 154 alone had reduced serum and tumor prolactin, but no change in GH concentrations. These results suggest that CGP 19984 effectively inhibits growth and hormone secretion of the autonomous MtT‐W 10 pituitary tumor by apparently suppressing both somatotropic and lactotropic cell populations within the tumor. Furthermore, these findings indicate that CGP 19984 may be an effective alternative to CB‐154 in the clinical treatment of prolactin‐producing adenomas, as well as other types of pituitary adenomas.
Effects of sodium cyclamate and sodium saccharin on focus induction in explant cultures of rat bladder
Authors: Nicholson Linda J. , Jani Harsha 
Published: February 2007

AbstractThe tumour‐promoting activities of sodium cyclamate and sodium saccharin were investigated in an assay based on the induction of epithelial foci exhibiting enhanced growth potential in a rat bladder explant culture system. An initiating, nonfocus‐inducing dose was defined for the carcinogen N‐methyl‐N‐nitrosourea (MNU) to make promotion studies possible, Saccharin induced epithelial foci when added to cultures pretreated with an initiating dose of MNU, and also increased the incidence of foci in cultures treated with transforming doses of MNU. Cyclamate was found to induce a high incidence of foci when added to cultures by itself. When MNU and cyclamate treatments were combined, an additive effect could be detected. These results indicate that both cyclamate and saccharin can contribute to epithelial transformation in this system.
Association of adriamycin‐induced resistance to NK‐mediated lysis with sialic acid level and immunological reactivity of transferrin receptors and glycophorin A
Authors: Benoist Hervé , Madoulet Claudie , Trentesaux Chantal , Carpentier Yves , Joly Philippe , Jardillier Jean Claude , Desplaces Andrée 
Published: February 2007

AbstractAdriamycin (ADM) can increase sialic acid content in K 562 cells and reduce their susceptibility to NK‐mediated lysis. In this report, hypothetical relationship between this resistance and augmentation in sialylation has been investigated. Variations in the time of exposure to ADM showed that 12 hours were sufficient to cause maximal recruitment of benzidinepositive cells, growth inhibition and resistance to NK‐mediated lysis. On the contrary, the membrane sialic acid density seemed stable and 24 hours of drug exposure were necessary to observe a clear rise in sialic acid. Neuraminidase treatment of control and ADM‐treated K 562 cells was associated with an obvious enhancement in their susceptibility to NK‐mediated lysis which can be explained by an increase in the target‐effector binding ability as assessed by a direct conjugate‐forming cell assay. However, the neuraminidase treatment did not modify the sensitivity difference to lysis between untreated and ADM‐treated cells. As compared to control the reactivity of ADM‐treated cells was higher with an antiglycophorin A (GPA) MAb and lower with an antitransferrin receptor (TFR) MAb. Kinetic studies suggested that GPA expression is a better index of ADM‐induced resistance to NK‐mediated lysis than TFR expression. In addition, neuraminidase treatment showed that TFR and GPA modulations induced by ADM can be correlated with sialylation alterations.
The Danish case‐control study of cutaneous malignant melanoma. II. Importance of UV‐light exposure
Authors: Østerlind A. , Tucker M. A. , Stone B. J. , Jensen O. M. 
Published: February 2007

AbstractA population‐based case‐control study of 474 patients with cutaneous malignant melanoma and 926 population controls, conducted in East Denmark over a 3‐year period, included an evaluation of the relationship of UV‐light exposure to cutaneous melanoma risk. Patients with lentigo maligna melanoma were not included. Significantly increased risk was associated with severe sunburn before age 15 (RR = 2. 7 for 5 + vs. never), sunbathing (RR = 1. 6), boating (RR = 1. 4) and vacations spent in the sun (RR = 1. 4 for very sunny vs. never). A significant decrease in risk was associated with occupational exposure during the summer in males (RR = 0. 7), and no association with cutaneous microtopography was seen. These findings were independent of the effects of constitutional risk factors (naevi, freckles and light hair colour). No association was found between the risk of cutaneous melanoma and exposure to artificial UV‐light (fluorescent light, sun lamps, or sun beds). No significant difference was found between superficial spreading melanoma and nodular melanoma with regard to any of the sun exposure variables. Our data indicate that exposure to intermittent intense sunlight is an important risk factor for cutaneous malignant melanoma, while long‐term continuous exposure does not appear to be a risk factor for cutaneous malignant melanoma, while long‐term continuous exposure does not appear to be a risk factor.