bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of ebv‐carrying b‐cell populations in healthy seropositive individuals with regard to density, release of transforming virus and spontaneous outgrowth
Authors: Lewin Nongnit , Åman Pierre , Masucci Maria Grazia , Klein Eva , Klein George , Öberg Bo , Strander Hans , Henle Werner , Henle Gertrude 
Published: February 2007

AbstractPeripheral or tonsil lymphocyte populations of EBV‐ seropositive donors give rise to EBV‐ carrying LCLs upon In vitro explanation. Such lines can arise either by a 2‐step mechanism, namely release of virus from some of the explanted cells followed by infection of previously uninfected B cells, or by direct outgrowth of virus‐harboring B cells (Rickinson et al., 1974; Dalens et al., 1975; Hinuma and Katsuki 1978; Katsuki et al., 1979). We observed that cells responsible for both the 2‐step mechanism and for direct outgrowth are found in the purified B‐cell compartment. Virus release was more frequent than direct outgrowth. The majority of virus‐releasing cells were found in the low‐density fraction that contains large, activated B blasts. Cells that were capable of spontaneous outgrowth in the presence of the viral inhibitor PFA and of virus‐neutralizing antibody gave rise to cell lines that carried the sex chromosome marker of the original donor, rather than that of admixed cord blood lymphocyte of the opposite sex. Such cells were found in both the low‐ and the highdensity fractions. The majority of the EBV‐carrying B cells in vivo are thus low‐density blasts. Rare small B cells of high density harboring EBV were capable of spontaneous outgrowth. This may be indicative of a host control mechanism that is removed upon cultivation in vitro.
Serum ca 50 as a tumor marker in pancreatic cancer: A comparison with CA 19‐9
Authors: Haglund Caj , Kuusela Pentti , Jalanko Hannu , Roberts Peter J. 
Published: February 2007

AbstractCA 50 is a new tumor marker based on a monoclonal antibody (MAb) against a human colorectal carcinoma cell line. The CA 50 antigen is similar, but not identical, to the tumor marker CA 19‐9. The serum concentrations of CA 50 were measured by an immunoradiometric assay (CA 50 IRMA) in 95 patients with pancreatic cancer and in 94 patients with benign pancreatic, biliary and hepatocellular diseases. The CA 50 concentration was above the cut‐off limit of 17 U/ml in 71% of the patients with pancreatic cancer. Elevated CA 50 levels were also seen in 29% of the patients with benign diseases (up to 250 U/ml), especially in patients with extra‐hepatic cholestasis (34%) and hepatocellular jaundice (46%). The results of the immunoradiometric assay were compared to those of the commercially available CA 50 RIA inhibition test. The sensitivities of the two CA 50 assays for pancreatic cancer were similar, but the specificity of the IRMA assay was higher. The CA 50 and CA 19‐9 values showed a strong positive correlation and the assay parameters of the tests were almost similar. CA 50 seems a promising tumor marker in the detection and follow‐up of patients with pancreatic cancer.
Proteins phosphorylated on tyrosine as markers of human tumor cell lines
Authors: Giordano S. , Di Renzo M. F. , Cirillo D. , Naldini L. , Piat L. Chiado , Comoglio P. M. 
Published: February 2007

AbstractPrevious work has shown that proteins phosphorylated on tyrosine are selectively detectable by antibodies against phosphotyrosine (P‐Tyr) in cells transformed by retroviral class‐1 oncogene‐encoded kinases endowed with non‐regulated activity (Di Renzo et al., 1986). In this work P‐Tyr antibodies were used to investigate the existence of human tumors expressing abnormal levels of tyrosine phosphoproteins and tyrosine kinases. Among 18 cell lines examined, the antibodies identified a number of tumors with a detectable level of proteins phosphorylated on tyrosine. Among these were a major protein with an approximate Mr of 150,000 in a gastric carcinoma; 2 proteins, with Mr of 130,000 and 110,000 in a colon carcinoma; a major protein with Mr of 170,000, tyrosine phosphorylated in both a urinary bladder and an epidermoid carcinoma; a 100,000 Mr protein phosphorylated in lung and breast carcinomas. An 80,000 Mr tyrosine phosphorylated protein was found in a fibrosarcoma and in a rhabdomyosarcoma. Among the hemopoietic malignancies screened, in 2 Philadelphia‐positive chronic myelogenous leukemias P‐Tyr antibodies recognized the chimeric bcr‐abl 210,000 Mr protein and its substrates. Two tyrosine phosphorylated proteins, one of Mr 70,000 and one of Mr 60,000, were detected in a Burkitt lymphoma line. These phosphoproteins were not found in samples harvested from normal gastro‐intestinal or urinary bladder epithelium, nor in control fibroblasts and lymphocytes. Two of the above proteins have associated tyrosine kinase activity: the 170,000 Mr protein of bladder carcinoma cells was found to be a constitutively phosphorylated EGF receptor.
Expression of multiple growth factors in a human lung cancer cell line
Authors: Betsholtz Christer , Bergh Jonas , Bywater Margaret , Pettersson Monica , Johnsson Ann , Heldin Carl‐Henrik , Ohlsson Rolf , Knott Timothy J. , Scott James , Bell Graeme I. , Westermark Bengt 
Published: February 2007

AbstractU‐1810, a human large‐cell lung cancer line, was found to express a PDGF‐like growth factor. 35S‐cysteine labelling and immunoprecipitation revealed the synthesis and secretion of a 31‐kDa PDGF‐like protein. Serum‐free conditioned medium contained PDGF‐receptor‐competing and mitogenic activity when tested on human fibroblasts. Whereas the receptor‐competing activity was fully neutralized by anti‐PDGF antibodies, the mitogenic activity was only partially affected. We therefore probed U‐1810 mRNA with a panel of growth‐factor DNA clones. We found expression of the genes for PDGF A‐ and B‐chains, TGF‐α, TGF‐β and IGF‐11 but not EGF or IGF‐1. U‐1810 cells lacked specific binding sites for PDGF but showed specific binding of EGF and expressed EGF‐receptor transcripts. Thus, U‐1810 is an example of a human tumor cell line that expresses multiple growth factor genes; in the intact tumor the corresponding growth factors may operate in autocrine stimulation of the tumor cells as well as in paracrine growth reactions (i.e. stroma recruitment).
Structure and expression of mos sequences in spontaneous and moloney murine sarcoma virus‐induced yolk sac carcinomas in rats
Authors: Decock B. , Sobis H. , Van Hove L. , Vandeputte M. , Billiau A. 
Published: February 2007

AbstractFacilitation of yolk‐sac carcinoma (YSCa) development in fetectomized rats by the Moloney murine sarcoma virus/murine leukemia virus (Mo‐MSV/MLV) complex was found to be closely associated with the presence of Mo‐MSV sequences in the genomes of the YSCa cells. The virus‐induced YSCas consisted of cells of mono‐ or oligoclonal origin which always contained in their genomes at least 1 randomly integrated Mo‐MSV provirus. In YSCas which developed in the absence of virus, no rearrangement or amplification of c‐mos could be detected. In addition, blot hybridization analysis of cellular RNA failed to detect mos‐related RNA in cell lines derived from Mo‐MSV‐induced as well as from non‐virally induced YSCas. The methylation level of c‐mos DNA was low in all YSCa cell lines. In contrast, v‐mos DNA in cell lines derived from Mo‐MSV‐induced YSCas was heavily methylated.
Influence of the administration schedule on the therapeutic effect of interleukin‐2
Authors: Vaage Jan , Pauly John L. , Harlos James P. 
Published: February 2007

AbstractThe local and systemic therapeutic effects of multiple peritumoral injections of recombinant human interleukin‐2 (IL‐2) were tested against the syngeneic, immunogenic mammary carcinoma MC2 implanted subcutaneously into C3H/He mice. Multiple (12) low‐dose injections had a greater local therapeutic effect than the same total amount of IL‐2 given in 2 injections. Peri‐tumoral injections were equally effective in inhibiting the growth of the injected tumors in normal and in immunized mice. The systemic therapeutic effect was manifested by the inhibition of tumors implanted contra‐laterally to the injected tumors, and was only discernible in non‐immunized mice.
Benzo(a)pyrene metabolism by lymphocytes from normal individuals and individuals carrying the mediterranean variant of glucose‐6‐phosphate dehydrogenase
Authors: Feo F. , Ruggiu M. E. , Lenzerini L. , Garcea R. , Daino L. , Frassetto S. , Addis V. , Gaspa L. , Pascale R. 
Published: February 2007

AbstractIn vitro growing human lymphocytes (HL) and fibroblasts, isolated from glucose‐6‐phosphate dehydrogenase (G6PD)‐de‐ficient subjects (Mediterranean variant), show a sharp decrease in this enzymatic activity and in NADPH:NADP+ ratio. These cells are less able than controls to hydroxylate benzo(a)pyrene (BaP) when tested in the absence of an exogenous NADPH‐generating system. They exhibit great resistance to the toxic effect of BaP. G6PD‐deficient fibroblasts are less prone than controls to in vitro transformation by BaP. To investigate whether this depends on a decreased production of active BaP metabolites and BaP:DNA adducts by G6PD‐deficient cells, BaP metabolism was studied in G6PD‐deficient HL cultured in vitro in the presence of mitogens and treated with BaP for 24 hr. HPLC profiles of organo‐ and water‐soluble metabolites revealed that both types of benzo(a)anthracene (BaA)‐induced HL produced: 4,5‐, 7,8‐, 9,10‐diols, 1,3‐, 3,6‐quinones, 3‐, 9‐hydroxy and 2 peaks of more polar metabolites. There was a 25‐76% decrease of organo and water‐soluble metabolites in the G6PD‐deficient cells. When HL were incubated with 7,8‐diol, the formation of metabolites mutagenic for Salmonella typhimurium (His‐) was very low in G6PD‐deficient cells. BaP:deoxyadenosine (dAde) and BaP:deoxyaguanosine (dGua) adducts were identified after incubation of both types of HL with BaP. There was a 31‐79% fall in adduct formation by G6PD‐deficient cells. Our results indicate that G6PD‐deficient human lymphocytes are less able to metabolize BaP than normal lymphocytes. We suggest that the NADPH pool is inadequate, in deficient cells, for active BaP metabolism.
Aryl hydrocarbon hydroxylase in lymphocytes and lung tissue from lung cancer patients and controls
Authors: Kärki Niilo T. , Pokela Risto , Nuutinen Lauri , Pelkonen Olavi 
Published: February 2007

AbstractThe inducibility of aryl hydrocarbon hydroxylase (AHH) activity in peripheral mitogen‐treated lymphocytes, and of AHH and other monoxygenase activities in lung samples, was studied in 41 patients–34 with pulmonary carcinoma, 4 with a benign lung tumour and 3 with chronic obstructive pulmonary disease. Lymphocyte AHH induction alone was studied in 43 non‐smoking and 37 smoking surgical patients. Absolute induced and non‐induced AHH activities were at about the same level in the lymphocytes from the lung cancer patients as in those from the non‐smoking controls, whereas the activities in smoking controls were about 100% higher. The mean inducibility ratios were very similar in all groups, ranging from 4.4 in the benign tumour patients to 5.4 in both control groups. Thymidine incorporation was on average about 40% lower in the lymphocytes from the lung cancer patients. AHH activity was detectable in all the peripheral lung samples, both normal or tumorous tissue, and its inter‐individual variation was more than 67‐fold. ECDE activity was also detectable in all the samples studied and its correlation with AHH activity was statistically significant (r = 0.888), suggesting that the same enzyme metabolizes both substrates. ERDE was detectable only in the samples with the highest AHH and ECDE activities. There was no correlation between basal or induced lymphocyte AHH activities and lung tissue AHH activity, but there were statistically significant correlations between lung AHH activity and the inducibility ratio with (r = 0.618) or without correction by thymidine incorporation (r = 0.442). These correlations suggest that there are common regulatory factors for AHH inducibility in different tissues. No significant difference in any drug metabolism parameter measured was observed between the lung cancer patients and the controls.
Human papillomavirus type 17 transcripts expressed in skin carcinoma tissue of a patient with epidermodysplasia verruciformis
Authors: Yutsudo Masuo , Hakura Akira 
Published: February 2007

AbstractCertain types of human papillomavirus (HPV) are involved in skin carcinogenesis in epidermodysplasia verruciformis. However, no gene or gene product of HPV associated with skin carcinogenesis has yet been identified. Here, we report HPV‐17 transcripts expressed in skin carcinoma tissue of an epidermodysplasia verruciformis patient infected with HPV‐17. Further, we show that one of these transcripts was localized to a portion of the genome which contains the 3′ open reading frames of the early region (E2, E3, E4 and E5). The analogous region in bovine papillomavirus type I has been shown to contain a transforming gene (Nakabayashi et al., 1983; Sarver et al., 1984; Yang et al., 1985a).
Ultrastructural evidence of collagenolytic activity in ductal infiltrating carcinoma of the human breast
Authors: Pucci‐Minafra Ida , Luparello Claudio , Schillaci Rosario , Sciarrino Serafina 
Published: February 2007

AbstractThe stroma of ductal infiltrating carcinoma of the human breast shows characteristic and localized areas of collagen rarefaction and fragmentation. This finding has been correlated with a peculiar type of fibrillar damage, observed in a small percentage of collagen fibrils isolated in the native state from the tumour stroma. The same pattern of lesion has been reproduced in vitro by human collagenase digestion on reconstituted fibrils. No effect has been detected by other nonspecific proteases in the same system.
Karyotypic analyses of metastatic and non‐metastatic mouse tumor cells by g‐and c‐banding
Authors: Verschaeve L. , De Baetslier P. , Kirsch‐Volders M. 
Published: February 2007

AbstractCytogenetic studies using G‐ and C‐banding were performed in order to compare non‐metastasizing BWO mouse thymoma cells with their metastatic BW‐IS‐Li and BW‐O‐Lil variants. BW‐IS‐Li and BW‐O‐Lil cells were obtained from liver metastases generated respectively after intra‐splenic or intravenous inoculation of mice with BWO cells. BW‐O‐Lil cells contained normal chromosomes 4 and 18 which were never found in BWO or BW‐IS‐Li cells. As they also contained several markers common to the BWO parental cell line, our data provide definite evidence that the BW‐O‐Lil cell line results from spontaneous in vivo cell fusion between a BWO cell and a normal host cell. Chromosome 3 was also shown to be “rearrangement‐prone” and was less represented among metastatic cell variants. These variants also lack a C‐band‐deficient marker chromosome which was found in most of the BWO cells. However, as many complex chromosome rearrangements were found in all 3 cell lines, at least some chromosomal material may be present in a hidden form. We were not able in this particular cell system to link the presence or absence of a single chromosome, chromosome fragment or rearrangement to the acquisition or expression of metastatic properties.
Evidence for a warfarin‐sensitive serum factor that participates in factor x activation by lewis lung tumor cells
Authors: Fasco Michael J. , Wilson Adrian C. , Lincoln David , Gierthy John 
Published: February 2007

AbstractMouse Lewis lung (LL) carcinoma cells possess a factor X activator (procoagulant) that is inhibited in vivo by warfarin treatment or diet‐induced vitamin K deficiency. This inhibition suggests that vitamin‐K‐dependent proteins are involved in LL cell activation of factor X. A LL primary tumor clone (LL13) was isolated which contained a warfarin‐sensitive vitamin‐K cycle of metabolism and expressed factor X procoagulant activity. LL13 cells exposed to media containing warfarin or deficient in vitamin K grew as well as cells in normal media, and activated factor X to similar extents. In contrast, administration of warfarin to mice bearing LL13 cells inhibited factor X procoagulant activity as well as the vitamin K cycle of metabolism in the primary tumors. In relation to LL13 cells grown in media containing fetal bovine serum, those incubated for 20 hr in media containing mouse serum or the sera from LL13‐bearing mice exhibited 9‐ to 10‐times higher levels of factor X procoagulant activity. However, LL13 cells exposed to media containing the sera of warfarin‐treated LL‐13‐bearing mice or to barium‐sulfate‐adsorbed normal mouse serum activated factor X much less efficiently. Collectively, these data suggest that inhibition of vitamin K function in LL cells does not affect the extent of factor X activation and thus the intrinsic factor X procoagulant is not a vitamin‐K‐dependent protein. They further suggest that both a warfarin‐sensitive (vitamin‐K‐dependent) protein present in normal mouse serum and a LL13 cell component participate in factor X procoagulant activity.
Lifespan extension of basal cell nevus syndrome fibroblasts by transfection with mouse pro or v‐myc genes
Authors: Shimada T. , Dowjat W. K. , Gindhart T. D. , Lerman M. I. , Colburn N. H. 
Published: February 2007

AbstractDermal fibroblasts from patients with the autosomal dominant cancer‐prone disease Basal Cell Nevus Syndrome (BCNS) exhibit a serum dependence, anchorage dependence and in vitro lifespan (about 20 population doublings or less) similar to those of fibroblasts from normal age‐, race‐ and sexmatched controls. Transfection with v‐myc or with an activated mouse pro‐1 gene (which specifies sensitivity to promotion of neoplastic transformation in JB6 mouse epidermal cells) specifically conferred partial immortality on the BCNS fibroblasts by substantially extending their population doubling levels by more than 19 population doublings. This suggests that either v‐myc or pro‐1 gene can cooperate with BCNS gene(s) to produce an extension of lifespan or partial immortality. However, the transfected BCNS fibroblasts that escaped senescence were anchorage‐dependent even after exposure to the tumor promoters 12‐O‐tetradecanoyl‐phorbol‐13‐acetate (TPA), epidermal growth factor (EGF) or plateletderived growth factor (PDGF). These observations indicate that BCNS fibroblasts differ from their normal counterparts in susceptibility to extended growth and may therefore be pre‐neoplastic. It is clear that they require more than an activated pro or myc gene for progression to the tumor cell phenotype.
Monoclonal antibody DLC‐48: An effective reagent for use in the depletion of malignant lymphoma from human bone marrow
Authors: Winter Jane N. , Marder Robert J. , Radosevich James A. , Epstein Alan L. 
Published: February 2007

AbstractA combination of large‐cell lymphoma cell lines was used as immunogen in the production of DLC‐48, a mouse monoclonal antibody (MAb) to a B‐cell‐associated antigen. This reagent identifies a protein found on a majority of peripheral blood B‐cells, B‐cell derived tumor cell lines, and lymphoma biopsy specimens. In reactive lymph‐node sections, DLC‐48 stains both germinal center and mantle zone B‐lymphocytes when the immunoperoxidase technique is used. DLC‐48 is an IgM, and is highly cytotoxic in the presence of human serum complement. The conditions for complement‐mediated cytotoxicity were first optimized by utilizing the chromium‐release assay with 2 large‐cell lymphoma cell lines, and were then applied to the treatment of the cell lines prior to cloning in agar. A single treatment with antibody and human serum eliminated 4 orders of magnitude of target cells. The cytolytic activity of this antibody was not inhibited by the presence of a 20‐fold excess of normal human bone marrow. Treatment with antibody and autologous serum did not affect the growth of human hematopoietic progenitor cells (CFU‐GEMM and CFU‐GM). These results suggest that DLC‐48, either alone or in combination with other MAb reagents, should be effective in eliminating malignant cells of B‐lineage from human bone marrow for purposes of autologous bone‐marrow transplantation.
A comparison of fresh and cultured T lymphocytes from patients with ataxia telangiectasia using T‐cell subset markers and chromosome translocations
Authors: Butterworth S. V. , Taylor A. M. R. 
Published: February 2007

AbstractAtaxia telangiectasia (A‐T) is an autosomal recessive disorder in which patients show an unusual predisposition to lymphoid malignancies including T‐cell leukaemia. We compare here the surface phenotypes of fresh and cultured A‐T T cells. A total of 17 T‐cell cultures from 8 A‐T patients are compared with each other and with 5 T‐cell cultures from normal individuals. The large, cytogenetically abnormal t(14;14) and t(X;14) clones in 2 of the patients both occurred only in the CD8 + population of T lymphocytes. There was no difference in the rate of growth of A‐T T cells in vitro compared with those from normal individuals, although many of the original characteristics of the T cells were lost, including the cytogenetically abnormal clones seen in fresh A‐T lymphocytes.
Distribution pattern of human papilloma virus 16 genome in cervical neoplasia by molecular in situ hybridization of tissue sections
Authors: Schneider Achim , Oltersdorf Tilman , Schneider Volker , Gissmann Lutz 
Published: February 2007

AbstractUsing a highly sensitive method with single‐stranded RNA probes, we analyzed the distribution pattern of HPV 16 DNA by in situ hybridization in CIN 11 (10 cases), CIN III (11 cases) and in invasive cervical carcinoma (17 cases). The technique used detected as little as 20–50 viral genomes per cell. This sensitive technique unmasked HPV 16 genomes in the basal cells of all forms of CIN. In CIN III viral genomes were present throughout the entire thickness of the epithelium. There was a striking difference in the distribution of viral DNA in CIN II compared with CIN III and invasive cancer. Variable viral genome distribution was observed in CIN II with the highest copy number in the area of epithelial differentiation. In contrast, CIN III showed a uniform distribution pattern of HPV genomes reflecting the lack of epithelial maturation. The majority of invasive carcinomas showed the same uniform distribution of the HPV 16 genomes as CIN III.
Comparison between the effects of dietary fat level and of calorie intake on methylnitrosourea‐induced mammary carcinogenesis in female sd rats
Authors: Beth Maren , Berger Martin R. , Aksoy Meral , Schmähl Dietrich 
Published: February 2007

AbstractThe aim of this study was to separate the effects of calorie intake on tumorigenesis from those of fat content and fat composition in an animal model. Our principal observations were the following. (1) Decreasing the calorie level by 30% significantly inhibited tumor development in any observed parameter of tumorigenesis, independently of the level of fat. (2) The fat content of semi‐synthetic diets, although varying by 44.4%, did not significantly influence mammary tumorigenesis; in fact, carcinogenic expression was discontinuously related to the fat level. A plateau of tumor incidence was observed at the level of 35 energy percentage of fat. (3) Fat composition did not influence tumorigenesis or body weight gain. The role of caloric restriction is thus stressed in relation to possible dietary prevention of cancer.