bluuebunny/crossref_metadata_2025_split huggingface dataset:
Elevation of serum placental alkaline phosphatase levels in cigarette smokers
Authors: Tonik Susan E. , Ortmeyer Ann E. , Shindelman Jeffrey E. , Sussman Howard H. 
Published: February 2007

AbstractIn an ongoing longitudinal study for tumor markers in breast cancer patients, levels of placental alkaline phos‐phatase (PAP) measured by RIA were found to be elevated in 34% of patients who smoked cigarettes as opposed to 5 % of non‐smoking subjects. A normal range was established (0‐2.14 ng/ml) using healthy non‐smoking females. In an expanded analysis by disease state, PAP levels were found to be elevated significantly (p<0.02) in the smoking groups of each category. This isoenzyme, when detected at elevated serum levels by RIA, was enzymatically active in 48% of the patients as analyzed by immunoenzymatic assay. One smoker with high PAP levels discontinued smoking following a myocardial infarction. Her PAP levels returned to normal within 2 months.
Chemotactic activity for mononuclear phagocytes of culture supernatants from murine and human tumor cells: Evidence for a role in the regulation of the macrophage content of neoplastic tissues
Authors: Bottazzi Barbara , Polentarutti Nadia , Balsari Andrea , Boraschi Diana , Ghezzi Pietro , Salmona Mario , Mantovani Alberto 
Published: February 2007

AbstractCulture supernatants from 14 mouse solid tumors, 2 mouse lymphomas, 8 human solid tumor lines and 3 human leukemia‐lymphomas were examined for chemotactic activity in blind‐well chemotaxis chambers using murine peritoneal macrophages and human blood monocytes as indicator cells. Culture supernatants from various murine and human solid tumors had appreciable chemotactic activity for mononuclear phagocytes. Chemotactic activity was found in murine tumors of different histology and transplantation history, including autochthonous mammary carcinomas and chemically‐induced sarcomas. Chemotactic activity was not unique to neoplastic cells because is was detected also in supernatants of two preparations of mouse embryo fibroblasts and two human lung embryo fibroblast lines. Production of tumor‐derived chemo‐attractants did not require serum in the culture medium, was inhibited by the protein synthesis inhibitor Cycloheximide, but was unaffected by the DNA synthesis inhibitor Mitomycin C. Murine supernatants were active on human monocytes and vice‐versa. A first preliminary characterization of the chemotactic activity of the human sarcoma line 8387 revealed that it was not dialyzable, that most of the activity was retained at 56deg;C for 30 min, but not at 100deg;C, and that it was susceptible to proteolytic enzymes (trypsin and proteinase K) but unaffected by DNase and RNase. Upon fractionation on a Sephadex G‐75 column, the activity eluted in a single, relatively broad peak in the cytocrome C region, corresponding to an apparent molecular weight of about 12,000. In the heterogeneous series of murine solid tumors studied, a significant, though far from absolute, correlation (r=0.71, p=0.013) was found between chemotactic activity in culture supernatants (expressed as area under the chemotaxis titration curve) and the percentage of tumor‐associated macrophages. It is suggested that tumor‐derived chemotactic factor(s) play a role in the regulation of the macrophage content of neoplastic tissues.
Splenic variations affecting sarcomagenesis among mice of an inbred strain
Authors: Prehn Richmond T. , Karcher Christine A. 
Published: February 2007

AbstractAmong overtly identical mice of an inbred strain, some are relatively susceptible and some relatively resistant to sarcomagenesis by large concentrations of 3‐methyl‐cholanthrene (MCA) (Prehn, 1975a). Spleen cells from mice, subsequently shown to be relatively susceptible, conveyed a relative resistance to oncogenesis when transferred to irradiated recipients; spleen cells from mice, subsequently shown to be relatively resistant, conveyed to secondary hosts a relative susceptibility.
Natural host defence during oncogenesis. NK activity and dimethylbenzanthracene carcinogenesis
Authors: Ehrlich Rachel , Efrati Margalit , Malatzky Elinor , Shochat Lea , Eyal Aviva Bar , Witz Isaac P. 
Published: February 2007

AbstractIn this study we determined the effect of administering the chemical carcinogen dimethylbenzanthracene (DMBA) on NK activity mediated by murine splenocytes. The intragastric administration of six weekly l‐mg doses of DMBA to 2‐ to 3‐month‐old mice either following a pituitary graft or not, resulted in a tumor incidence which was higher than 60 %. The cellularity of the spleens decreased significantly after the third DMBA feeding and the NK activity of these spleens was selectively suppressed. There was no spontaneous reconstitution of the NK activity following cessation of DMBA treatment and during the entire tumor‐free period. The adoptive transfer of normal bone marrow, thymus or spleen cells did not restore NK activity in DMBA‐treated mice. The NK activity of DMBA‐fed mice could be augmented by interferon and by interferon inducers such as poly I:C and dsRNA from Us‐tilago virus. The effect of these biological response modifiers on NK activity was short‐lived but it was possible to restimulate this activity every 24h. Consecutive treatments of DMBA‐fed mice with poly I:C maintained a high level of NK activity for at least 3 weeks.
Liposome induction or enhancement of macrophage‐mediated cancer cell lysis
Authors: Jeannin Jean‐Fraņcois , Olsson Nils‐O. , Martin Françcois 
Published: February 2007

AbstractLiposomes of different composition have been used to modify macrophage‐mediated destruction of syngeneic cancer cells through a modulation of membrane lipid content of macrophages and/or tumor cells. Dipalmitoylphos‐phatidylcholine (DPPC)1 liposomes induce cancer cell lysis by normal, non‐tumoricidal, peritoneal macrophages and enhance tumor cell destruction by BCG‐activated macrophages. This effect was produced by large and small unilamellar liposomes, which are in the 25,000 g supernatant of sonicated preparations. Addition of cholesterol or negative charges carried by dicetylphosphate supressed the effect of DPPC liposomes on macrophage‐mediated cytolysis. Enhancement of macrophage‐mediated tumor cell lysis was observed when both cancer cells and macrophages were incubated with DPPC liposomes, but not when macrophages and/or tumor cells were preincubated with liposomes prior to their coincubation. Liposomes did not promote the binding of the cancer cells to the macrophages. Liposomes could promote formation of phospholipid domains within the plasma membrane of both tumor cells and macrophages leading to the destruction of cancer cells through a temporary fusion with the macrophages.
In vivo generation and selection of variants with altered sensitivity to natural resistance (NR): A model of tumor progression
Authors: Chow Donna A. , Ray Manoranjan , Greenberg Arnold H. 
Published: February 2007

AbstractThe stability of a cloned murine tumor for sensitivity to NR was examined following growth in vivo in order to test the hypothesis that tumor progression proceeds through the generation and selection of variants. Clonal sensitivity to the [131l]‐dUrd elimination assay of NR was assessed for the L5178Y‐F9 tumor grown in syngeneic DBA/2 mice or maintained solely in tissue culture. Sub‐clones derived from a tumor obtained from the injection site 31/2 weeks after the s.c. inoculation of 25 cells were less sensitive to NR in comparison with subclones derived from cells grown only in vitro. Subclones from the cells grown in vivo exhibited increased heterogeneity in sensitivity to NR in addition to their expanded range of susceptibility to complement‐mediated lysis by CBA serum natural antibodies. The extent of the heterogeneity argues against tumor “adaptation” forming the basis for the phenotypic alteration while chromosomal studies eliminate the possibility that a new tumor was induced. These data support the hypothesis that tumor progression proceeds through the random generation of variants and host‐mediated selection for the proliferation of clones with an increased ability to survive.
Clonal development of lymphomas induced by rauscher leukemia virus
Authors: Reddy A. Lakshma , Fialkow Philip J. 
Published: February 2007

AbstractThe number of cells from which tumors induced by neonatal injection of Rauscher Leukemia virus (RLV) develop was investigated using F1 (C57BL/6 X Feral) female mice heterozygous at the X‐linked phosphoglycerate kinase (PGK) locus. Because of inactivation of one of the two X chromosomes in each somatic cell which occurs during embryogenesis in female mice, only one of the two PGK genes is active in each somatic cell. Thus, tumors that develop clonally in these mice exhibit one enzyme type, B or A, whereas those with a multicellular origin may exhibit both enzymes. Seventeen of 22 PGK heterozygous mice injected with RLV developed lymphosarcomas after an average latency of 38 weeks. Twelve of these lymphomas exhibit a single‐enzyme type, A or B. In three of five tumors with double‐enzyme phenotypes, the minor enzyme component comprised 20% or less of the total PGK activity, and histological examination revealed that these tumors contained a mixture of malignant and normal‐appearing cells, suggesting that the minor PGK component was not contributed by the malignant cells. In the two remaining lymphomas, the ratio of A:B PGK activity was close to l:l. However, lymphomas which developed in recipients after transplantation of cells from these two tumors into newborn mice showed only single‐enzyme PGK phenotypes, suggesting that the neoplastic cells in the primary tumors had single‐enzyme phenotypes. Thus, these results indicate that lymphosarcomas induced by RLV in mice develop clonally.
Relationship between the amounts of EBV‐DNA and ebna per cell, clonability and tumorigenicity in two EBV‐negative lymphoma lines and their EBV‐converted sublines
Authors: Ernberg I. , Klein G. , Giovanella B. C. , Stehlin J. , McCormick K. J. , Andersson‐Anvret M. , Åman P. , Killander D. 
Published: February 2007

AbstractThe effect of EBV‐conversion of two EBV‐negative lymphoma lines (Ramos and BJAB) on agarose clonability and tumorigenicity in nude mice was explored. The cloning frequency was increased in all 9 sublines investigated, between I.I and 4.9 times compared to the original “parental” lines. Tumorigenicity was increased in one out of 2 BJAB‐derived, EBV‐positive lines and in 3 of 6 Ramosderived lines, while it was decreased in 3 others. A strong positive correlation between the number of genomes/cell and the amount of EBNA/cell was detected, and in 7 of 9 converted lines the cloning frequency also correlated to the number of EBV genomes. On the other hand, no relation was established between the number of EBV‐genomes/cell, the amount of EBNA/cell and tumorigenicity.
Precision in the first stage of the gastric carcinoma mass survey
Authors: Yoshida Yuji , Yamaguchi Yumiko , Tebayashi Akio , Arisue Taro , Tamura Koichi , Ichikawa Heizaburo 
Published: February 2007

AbstractA new method of estimating false‐negative rate (FNR) in gastric carcinoma mass surveys is reported. It is called the “ADC method”, since estimation of FNR is based on “Accidentally Detected Carcinoma”. ADC is a carcinoma detected by chance upon close examination because of abnormalities falsely pointed out in the first stage of the mass survey (mass screening) in a region other than the one in which carcinoma is located. This method was tested in the gastric carcinoma mass survey program conducted by the Hokkaido Anti‐cancer Association. Overall FNR was estimated at 28.3%. The FNRs estimated by the ADC method appear more reasonable and reliable indicators of precision of the mass survey program. The ADC method is discussed in comparison with the previously used “follow‐up study” and several advantages of this new method are presented.
Effect of hormones on the expression of proviral genes Mtv‐2 and Mtv‐3 in mouse mammary gland
Authors: Sluyser Mels , Verstraeten Rob A. , Van Hie Roberta 
Published: February 2007

AbstractWe have investigated the expression of the Mtv‐2 and Mtv‐3 proviral genes in mouse mammary glands by examining the effect of hormones on levels of mammary tumor virus (MTV)3 proteins p27 (gag) and gp52 (env) in mouse mammary explants. We also investigated the effect of the hormones on DNA synthesis in the explants. The mammary glands were derived from inbred GR and 020 mice, and from the respective congenic mouse strains GR/Mtv‐2− and 020/Mtv‐2+. The addition of insulin to the culture medium caused increases in p27 and gp52 levels in GR and 020/Mtv‐2+ glands; a further increase in the viral proteins was obtained by also adding dexamethasone. Prolactin in combination with progesterone enhanced p27 and gp52 levels, but to a lesser extent than did dexamethasone. Dexamethasone caused a slight but significant increase in p27 protein in mammary explants from GR/Mtv‐2− mice. Our data indicate that the Mtv‐2 locus and the Mtv‐3 locus in mouse mammary gland are under separate glucocorticoid control, and that Mtv‐2 expression is also stimulated by the prolactin and progesterone combination. Whereas dexamethasone enhances MTV protein levels in mouse mammary explants, it inhibits DNA synthesis in the explants.
Effect of treatment with interferon and cyclophosphamide on the growth of a spontaneous liposarcoma in rats
Authors: Marquet R. L. , Schellekens H. , Westbroek D. L. , Jeekel J. 
Published: February 2007

AbstractA spontaneous non‐immunogenic transplantable liposarcoma in BN rats was found to be sensitive to the antitumor effects of rat fibroblast interferon (RIF) when it was administered from the day of tumor implantation onwards. Treatment with RIF starting at 7 days after implantation was not effective. Tumor growth was markedly inhibited by cyclophosphamide (Cyclo). At the time and dose schedules used, Cyclo was more effective than RIF. When the growth of the tumor was inhibited by Cyclo, subsequent treatment with RIF did not lead to an additional retardation of tumor growth. Administration of RIF interfered with the beneficial effect of Cyclo when both agents were given concomitantly. RIF and Cyclo gave similar results to those obtained with RIF alone and these were inferior to those obtained with Cyclo alone.
Metabolic properties of isolated rat liver cell preparations enriched in epithelial cells other than hepatocytes
Authors: Ledda G. M. , Sells M. A. , Yokoyama S. , Lombardi B. 
Published: February 2007

AbstractA selected fraction of non‐parenchymal cells was prepared from the liver of untreated rats, of rats 11‐13 days after ligation of the common bile duct, and of rats fed for 4‐5 weeks a choline devoid diet containing DL‐ethionine. The cell fraction isolated from these livers consisted of one type of mesenchymal cells (Kupffer cells), and of increasing proportions of γ‐glutamyltranspeptidase‐positive non‐parenchymal epithelial cells (bile ductule/oval cells). The activities of aminopyrine N‐demethylase and of aniline hydroxylase were determined in the three cell fractions, and were found to be less than 10% of the same enzyme activities of purified hepatocytes isolated from untreated rats. Primary cultures of untreated rat hepatocytes, and of the non‐parenchymal cell fraction prepared from the liver of untreated and treated rats, were exposed to aflatoxin B1. Less than 0.5% of the hepatocytes from untreated rats survived a 48 h exposure to a concentration of 10−6 m aflatoxin B1. On the other hand, 75% or more of the non‐parenchymal cells survived a 48 h exposure to a concentration of aflatoxin B1/cell two and a half times as great. It is concluded that non‐parenchymal epithelial cells of rat liver have low activities of aminopyrine N‐demethylase and of aniline hydroxylase in comparison to hepatocytes, and, in contrast to hepatocytes, are highly resistant to the cytotoxic action of aflatoxin B1. Preneoplastic and neoplastic hepatocytes are known to possess similar properties. Thus, the findings reported herein are consonant with the views that non‐parenchymal epithelial cells of rat liver may be alternate target cells, initiated by chemical carcinogens inducing hepatocellular carcinomas, and that the initiated cells may be progenitors of neoplastic hepatocytes.
Lectin‐resistant variants of mouse melanoma cells. II. In vitro characteristics
Authors: Tao Tien‐Wen , Jenkins Jennifer M. , Vosbeck Klaus , Matter Alex , Miller Marcia , Jockusch Brigitte M. , Shen Zhong‐Hou , Burger Max M. 
Published: February 2007

AbstractLectin‐resistant variants of B‐16 melanoma cells were selected with wheat‐germ agglutinin, ricin and concanavalin A. They exhibited altered metastasizing capacity and tumorigenicity in C57BL mice. Several in vitro properties were defined and compared including homotypic adhesiveness, microfilament organization, melanin release, activity of tyrosine hydroxylase, DNA content, and karyotypes. The possible relevance of these properties in vitro for the malignant behavior displayed in vivo is discussed. The usefulness of this approach of selecting surface variants to study the problem of metastasis is also discussed.
Comparison of fibrin clot retraction with other transformation parameters after hydridization of normal and established cell lines
Authors: Curatolo L. , Azzarone B. , Fally‐Crëpin C. , Morasca L. , MacIeira‐Coelho A. 
Published: February 2007

AbstractThe expression of transformation parameters (inhibition of cell division during cell crowding, anchorage dependence, loss of fibrin clot retractile activity and secretion of plasminogen activator) was studied in a hetero‐specific cellular hybrid, made between established L (TK−) cells and the normal human MRC‐5 cells. The hybrid nature of the cross was confirmed by the ability to incorporate [3H]‐thymidine, by growth in selective HAT medium, by the identification of human chromosomes and by the expression on the surface of 100% of hybrid cells of a human glycoprotein, which is recognized by the 4F2 monoclonal antibody. The hybrid cultures showed cell cycle inhibition which became less stringent with increasing population doublings and the loss of human chromosomes. Fibrin clot retraction and anchorage dependence were absent in spite of the presence of many human chromosomes. The two properties were present or lost simultaneously in the normal parent cells and in the transformed parent or hybrid cells respectively. The human type of plasminogen activator was secreted even with very little human genetic material left, and a complete dissociation between fibrin clot retraction and production of plasminogen activator was observed. The data strengthen the hypothesis that transformation is a multi‐step process that involves complex genetic control and where cells progressively express different phenotypes and escape growth control.
Lectins as probes for identification of tumor‐associated antigens on urothelial and colonic carcinoma cell lines
Authors: Paulie Staffan , Hansson Yngve , Lundblad Marie‐Louise , Perlmann Peter 
Published: February 2007

AbstractIn the search for tumor‐associated antigens, seven lec‐tins were used to investigate the cellular distribution of membrane‐associated glycoproteins on a panel of human cells derived from tumor or normal tissues. Surface labelled lysates of the different cells were precipitated with the lectins and the precipitates were separated on SDS‐PAGE. Comparison of the autoradiographic patterns revealed that a La‐reactive 115K glycopeptide (gp 115) was present on transitional‐cell carcinoma cells of the urinary bladder, on two spontaneously transformed urothelial cell lines and on a melanoma cell line. Gp 115 was absent from a non‐transformed urothelial cell line, a squamous bladder carcinoma line and five unrelated cell lines of miscellaneous tissue origin. When precipitation was performed with a rabbit antiserum raised against the La‐reactive components of a TCC cell line the same distribution of gp 115 was observed. From Helix pomatia hemagglutinin (HP) precipitates a 150K glycopolypeptide co‐migrating with a previously described HP‐reactive differentiation antigen associated with human T cells was present on one of the urothelial cell lines and on a colon carcinoma cell line. When different extracts depleted of ConA binding glycopeptides were compared, a group of three antigens (32K, 35K and 40K) were identified in the extracts of the colon carcinoma cell line, HT29. These antigens were shared by two other colon carcinoma cell lines but were absent from the unrelated cells of our panel. Furthermore, an extensively absorbed rabbit anti‐HT29 serum specifically precipitated one of these antigens (35K) from the three colon cell lines.
Quantitating the synergistic effect of smoking and alcohol consumption with the micronucleus test on human buccal mucosa cells
Authors: Stick Hans F. , Rosin Miriam P. 
Published: February 2007

AbstractThe micronucleus test was applied to exfoliated cells of the buccal mucosa of four population groups: (A) non‐smokers and non‐drinkers of alcoholic beverages, (B) non‐smokers but alcohol drinkers, (C) smokers but non‐drinkers, and (D) smokers and drinkers. An elevated frequency of micronucleated buccal mucosa cells was observed only in group D (smokers and alcohol drinkers). When group D was subdivided according to the number of cigarettes smoked, the frequency of micronucleated buccal cells and the average number of micronuclei per cell appeared to depend upon cigarette consumption. An approximately eight‐fold increase of micronucleated mucosa cells was seen among alcohol drinkers who smoked three or more packs of cigarettes per day, and an approximately 4.2‐fold elevation was observed when one to two packs were consumed. Neither smoking alone of up to and over 60 cigarettes per day nor ethanol drinking alone of up to 1.21 per day led to a detectable elevation of micronucleated buccal mucosa cells. Whether the strong synergistic effect between smoking and alcohol consumption, as seen by the frequency of micronucleated buccal mucosa cells, is related to their synergistic effect in the induction of oral cancers is an intriguing but open question.
Detection of H‐2Dd and H‐2Kd molecules in purified rauscher leukemia virus
Authors: Schaffar‐Deshayes L. , Choppin J. , Levy J. P. 
Published: February 2007

AbstractEvidence is presented that an H‐2 antigenic activity is associated with Rauscher murine leukemia virions grown in vitro. Purified Rauscher MuLV grown in fibroblasts of BALB/c (H‐2d), C57BL6 (H‐2d) or (BALB/c × C57BL/6)F1 (H‐2d/b) were used to absorb the activity of anti‐Dd, anti‐Kd, anti‐Dd, or anti‐Db anti‐Kb antisera tested against H‐2‐related targets by cellular radioimmunoassay. The results show that Dd and Kd activities were associated with the virions grown in H‐2d or H‐2d/b fibroblasts. No H‐2b antigenic activity was detected in the virions grown in C57BL/6 or F1 fibroblasts. Immunoprecipitation of surface‐labelled spleen cells revealed that Rauscher MuLV grown in BALB/c or F1, fibroblasts inhibited the precipitation of the 48 000 dalton peaks characteristic of the Dd and Kd molecules whereas the precipitation of H‐2b molecules was not modified by Rauscher MuLV grown in the different cell lines. Class II molecules (la) were not detected in Rauscher virions. Comparison of the absorbing activities of intact and disrupted viruses suggests that the H‐2 activity was localized at the viral surface. Taken together, these results confirm the possible non‐random association of H‐2 molecules to type‐C viral particles whatever the nature of this association and its possible cellular or extracellular origin. However, the H‐2 antigens found in the virions being a non‐restricting element of anti‐viral cytolytic T lymphocytes in the same system, these results give no particular support to the “altered self” hypothesis.