bluuebunny/crossref_metadata_2025_split huggingface dataset:
Incidence of bovine leukemia virus‐specific antibodies in west african cattle
Authors: Walrand Francoise , Fumoux Francis , Roelants Georges , Parodi André‐Laurent , Levy Daniel 
Published: February 2007

AbstractA sero‐epidemiological survey of bovine leukemia virus (BLV) infection in indigenous West African cattle was undertaken using a radioimmunoassay and enzyme‐linked immunosorbent assay. A high incidence of anti‐BLV antibodies was found in the breeds tested and their crosses, whatever the test used. More extensive studies are needed to establish the prevalence of BLV infection in other parts of Africa; these may provide additional data on the similarities found between human and bovine leukemia viruses.
Protein phosphorylation at tyrosine residues IN v‐abl transformed mouse lymphocytes and fibroblasts
Authors: Saggioro D. , Ferracini R. , Di Renzo M. F. , Naldini L. , Chieco‐Bianchi L. , Comoglio P. M. 
Published: February 2007

AbstractPhosphotyrosine antibodies were employed to immunodecorate and immunoprecipitate proteins phosphorylated at tyrosine residues in cells transformed by Abelson murine leukemia virus (A‐MuLV). In pre‐B and pre‐T lymphoma cells transformed by A‐MuLV, the major phosphotyrosine‐containing protein has an MW of 160 kDa and shares immunologically detectable sequences with the v‐abl oncogene product. Moreover, two different proteins of approximately 100 and 68 kDa, heavily phosphorylated at tyrosine, were identified. Lack of immunological cross‐reactivity with viral products and phosphopeptide mapping showed that the 100 and 68 kDa proteins are coded by cellular genes. Phosphoproteins were undetectable in control resting lymphocytes. The 68 and the 100 kDa proteins were phosphorylated to different extents in proliferating lymphocytes, either stimulated by the growth factor IL‐2, or transformed by M‐MuLV (lacking the oncogene coded kinase). In fibroblasts transformed by A‐MuLV, phosphotyrosine antibodies identified 2 proteins of 120 and 70 kDa. By immunological cross‐reaction and by phosphopeptide mapping, the first was identified as a 120 kDa form of the v‐abl coded kinase. The 70 kDa protein is coded by a cellular gene, is not structurally related to the 120 kDa v‐abl kinase, and is different from any phosphotyrosine‐containing protein detected in A‐MuLV‐transformed lymphocytes. These data show that, upon v‐ablinduced transformation, phosphorylation at tyrosine takes place also on proteins other than the 160 or 120‐kDa oncogene products. In lymphocytes and fibroblasts these proteins are different, suggesting that the cascade of events triggered by the v‐abl gene in different cell types involves tyrosine phosphorylation of different specific proteins.
Natural killer‐cell immunodeficiency in patients with chronic myelogenous leukemia. I. Analysis of the defect using the monoclonal antibodies HNK‐1 (LEU‐7) and B73.1
Authors: Fujimiya Yoshiaki , Bakke Anthony , Chang Weng Cheng , Linker‐Israeli Marianna , Udis Barry , Horwitz David , Pattengale Paul K. 
Published: February 2007

AbstractQuantitative evaluation of natural killer (NK) cells using the HNK‐I (Leu‐7) and B73.1 monoclonal antibodies (MAbs) was correlated with NK activity in 13 patients with chronic myelogenous leukemia (CML) and compared to normal donor controls. A consistent observation was the presence of normal absolute numbers of B73.1 + lymphocytes as well as normal to increased absolute numbers of HNK‐I + lymphoid cells in the peripheral blood of chronic‐phase CML patients. Despite normal to increased numbers of B73.1 + and HNK‐I + lymphoid cells, these patients consistently demonstrated a significant impairment of lymphocyte‐mediated NK activity in their peripheral blood. Further experiments demonstrated that chronic‐phase CML patients, in contrast to normal controls, had significantly increased percentages of HNK‐I +, E+ and B73.1 +, E+ lymphoid cells and significantly decreased percentages of HNK‐I +, E− and B73.1, E− lymphoid cells, which resulted in significant reversals of the HNK‐I +, E+ to HNK‐I+, E− and B73.1+, E+ to B73.1 +, E− lymphoid cell ratios. (HNK‐I + [E+/E−] > B73.1+ E + [E+ /E−]). Furthermore, as compared to normals, both FACS‐sorted HNK‐I+ and B73.1 + lymphoid cells from the E+ fraction of CML patients were consistently defective in NK activity, and could not be substantially augmented with α‐interferon preparations. Although markedly defective in their ability to lyse K‐562, HNK‐I + lymphoid cells from the E+ fraction of CML patients were not defective in their ability to bind to the NK‐sensitive target, K‐562. In contrast, NK‐defective B73.1 + lymphoid cells were partially defective in their ability to bind to K‐562.
The copenhagen case‐control study of bladder cancer. II. Effect of coffee and other beverages
Authors: Jensen O. M. , Wahrendorf J. , Knudsen J. B. , Sørensen B. L. 
Published: February 2007

AbstractDuring the years 1979–1981 a population‐based case‐control study of bladder cancer including papilloma was performed in greater Copenhagen. A total of 371 patients (280 males; 91 females), and a comparable age‐and sex‐stratified group of 771 controls (577 males; 194 females) remained for logistic regression analysis. Controls were selected at random from the general population of the study area. All persons were questioned about their drinking habits with respect to coffee, tea and other beverages, as well as their exposure to a number of known or suspected risk factors for bladder cancer. After adjustment for tobacco smoking, the relative risk of bladder cancer in relation to coffee drinking was not statistically significant among either men or women. A significant association was found between bladder cancer and tea drinking among men, but with no regular trend for increasing consumption. An association was found between risk of bladder cancer and both total daily liquid intake and non‐cola soft drinks. This population‐based case‐control study provides no evidence of an isolated influence of coffee drinking or caffeine intake on bladder cancer risk.
Detection of IgG and IgA antibodies to epstein‐barr virus membrane antigen in sera from patients with nasopharyngeal carcinoma and from normal individuals
Authors: Zhu X. X. , Zeng Y. , Wolf H. 
Published: February 2007

AbstractIgG and IgA antibodies to Epstein‐Barr virus (EBV) membrane antigen (MA) were detected in sera from 96 NPC patients and normal individuals by the indirect immunofluorescence test. For MA/IgG antibody, 100% of NPC patients were positive with a GMT of 1:439.7 and 97.9% of normal individuals were positive with a GMT of 1:94.7. In contrast, for MA/IgA antibody, 58.3% of NPC patients were positive with a GMT of 1:7.3 and none of the normal individuals were positive. There was no difference in the detection of antibodies to EBV MA when other P3HR‐1 or B95‐8 cell lines, differing in their major membrane antigen, were used.
Measurement of a pancreatic cancer‐associated antigen (DU‐PAN‐2) detected by a monoclonal antibody in sera of patients with digestive cancers
Authors: Sawabu Norio , Toya Daishu , Takmori Yasuhiro , Hattori Nobu , Fukui Masanori 
Published: February 2007

AbstractDU‐PAN‐2 is a high‐molecular‐weight glycoprotein defined by a murine monoclonal antibody (MAb) against a pancreatic ductal adenocarcinoma cell line. In order to evaluate the usefulness of this antigen as a tumor marker, we determined the serum level of the antigen by competitive inhibition radioimmunoassay in sera from 139 patients with various malignant tumors, chiefly digestive cancers, 98 patients with different benign diseases and 11 healthy subjects. Values in the healthy subjects were less than 100 U/ml. Levels above 100 U/ml were frequently observed in sera from benign diseases, but levels above 400 U/ml were found in only 6 of the patients with benign diseases. In contrast, levels exceeding 400 U/ml were detected in 72% of patients with pancreatic cancer, 44% of patients with hepatocellular cancer and 40% of patients with biliary tract cancer. The positivity was low in other cancers such as gastric cancer (19%) and colorectal cancer (7%). Serum levels of CEA and CA 19–9 were rlso determined in cancer patients. Among the pancreatic cancer patients studied, values above 400 U/ml were found in 5 of the 8 CEA‐negative patients (< 5 ng/ml) and 2 of the 3 CA 19–9 negative patients (< 37 U/ml). These results indicate that determination of the serum DU‐PAN‐2 can aid in serological diagnosis of cancer of the digestive tract, more particularly of the pancreas.
Selective suppression of metastasis but not tumorigenicity of a mouse lung carcinoma by cell hybridization
Authors: Layton M. G. , Franks L. M. 
Published: February 2007

AbstractSomatic cell hybrids were produced by polyethylene glycol‐induced cell fusion between metastatic CMT167 (HGPRT−/OUAR) C57BL/Icrfat mouse lung carcinoma cells and 2 non‐metastatic cell lines: C3H/He mouse L‐M(TK−) cells of mesenchymal origin and EJ (OUAS) human bladder carcinoma cells. Fusion of 2 different CMT167 (HGPRT−) clones with L‐M(TK−) cells followed by selection in HMT medium gave rise to 14 intraspecific hybrids, which were shown to express H‐2 antigens specific for both the C57 and C3H mouse strains. Three interspecific hybrids arising from fusion of EJ(OUAS) and CMT167(HGPRT−/OUAR) cells were selected in HMT/ouabain medium and characterized by human isozyme analysis. All the hybrids produced large tumours after subcutaneous inoculation of 5 × 105 cells into adult athymic nu/nu mice. The intraspecific hybrid tumours were predominantly sarcomatous (mesenchymal) in structure but a few contained epithelial acini. Metastatic ability (as assessed by production of lung metastases) was completely suppressed in 13 of the 14 mouse/mouse hybrid cell clones. These results suggest that tumorigenicity, tumour structure and the ability to metastasize are expressed independently. The interspecific hybrids, which had not retained a full human chromosome complement, produced metastatic tumours that remained epithelial in structure.
A synergistic effect between anti‐idiotype antibodies and anti‐neoplastic drugs in the therapy of a murine B‐cell tumor
Authors: Hurwitz E. , Burowski D. , Kashi R. , Hollander N. , Haimovich J. 
Published: February 2007

AbstractAntibodies directed against idiotypic determinants of the cell‐surface IgM of a B lymphoma, 38c, were effective in delaying development of the tumor and in some instances in preventing its growth. The efficacity of the anti‐idiotype antibodies was markedly increased when they were injected in combination with anti‐neoplastic drugs. Since chemotherapy, as such, is limited by the general toxicity of the drugs it was of advantage to apply them in low doses. The drug doses used were mostly ineffective by themselves, yet were active in combination with the antibody in a more than additive fashion. We performed studies designed to elucidate the mechanism of the synergy between the anti‐idiotype antibodies and the drugs. The data suggest that the activity of the antibody is partly indirect and is mediated through the host's effector cells. In the case of one drug, daunomycin, the activity is also, at least in part, mediated through peritoneal exudate cells (PEC). Daunomycin injected intraperitoneally activated PEC. Such activated PEC, when injected into recipient mice, could replace the drug in its synergy with the antibody. In conclusion, it was shown that it is possible to increase the effectiveness either of antibodies to tumor cells or of cytotoxic drugs by combination therapy.
Lectin binding glycoproteins in human melanoma cell lines with high or low tumorigenicity
Authors: Berthier‐Vergnes Odile , Réano Alain , Doré Jean‐François 
Published: February 2007

AbstractLectin binding glycoproteins of 5 human malignant melanoma cell lines (HMMCL), differing in their ability to grow subcutaneously in athymic nude mice, were compared by electrophoresis of total cellular proteins and subsequent incubation of SDS‐poly‐acrylamide gel with 125I‐labelled lectins. Despite the similarity between the protein profiles of the different HMMCL, Concanavalia ensiformis agglutinin (ConA), wheat‐germ agglutinin (WGA) and peanut agglutinin (PNA) revealed differences in their glycoprotein expression, in contrast with Ulex europaeus agglutinin I (UEA 1). A great diversity was observed in the electrophoretic mobilities and/or staining intensities of ConA and WGA binding glycoproteins of HMMCL. However, neither ConA‐reactive glycoproteins nor WGA‐reactive glycoproteins could be detected that were characteristic of HMMCL with high tumorigenicity (HT) or low tumorigenicity (LT). In contrast, the expression of two cell‐surface PNA binding glycoproteins appeared to be related to the tumorigenic phenotype of HMMCL. One of them, with an apparent molecular weight of 190 kDa, was only detected in the LT cell lines. The other, with an apparent molecular weight of 60 kDa, was detected in all HMMCL but became strongly labelled after neuraminidase treatment only in the HT cell lines. Thus, the expression of glycoproteins rich in terminal galactose residues may characterize human melanoma cells with different tumorigenic behavior.
Metabolic and morphologic changes in brown adipose tissue from non‐growing mice with an isogeneic sarcoma. Evaluation with respect to development of cachexia
Authors: Edström Staffan , Kindblom Lars‐Gunnar , Lindmark Lars , Lundholm Kent 
Published: February 2007

AbstractBrown adipose tissue plays a thermoregulatory role influencing energy balance in experimental animals and possibly also in humans. In the present study we have reevaluated whether brown adipose tissue may contribute to the development of cancer cachexia in non‐growing mice bearing an isogeneic tumor. Interscapular brown adipose tissue mass decreased by 20% in freely‐fed sarcoma‐bearing mice housed at room temperature. Increased mitochondrial density and increased oxidation rate of acetate at low acetate concentrations were found in brown fat from sarcoma‐bearing mice, while the oxidation capacity was unchanged compared with that of freely‐fed controls. Metabolic and morphologic changes in brown fat from sarcoma‐bearing mice were similar to those found in weight‐paired controls, which had experienced the same loss of body weight as the tumor‐bearing mice. Selective and non‐selective B‐receptor blockade and surgical removal of interscapular brown fat before tumor implantation did not influence the nutritional state of freely‐fed tumor‐bearing mice. Injections of noadrenaline caused a proportionately lower increase in oxygen uptake in tumor‐bearing animals than in freely‐fed controls. Exposure to cold (+5° C) doubled food intake and led to hypertrophy of brown fat in both sarcoma‐bearing mice and control animals. Tumor growth was lower although not statistically different in animals housed at +5°C compared with animals housed at +25°C. It is concluded that brown adipose tissue from sarcoma‐bearing mice could not account quantitatively for the host wasting in tumor‐bearing mice housed at room temperature.
Establishment of a new myeloid leukemia cell line (TK‐1), and isolation of cells having a translocation involving a band 17q23
Authors: Ohno Hitoshi , Doi Shoichi , Fukuhara Shirou , Yamasowa Michihiko , Kannagi Mari , Ishikura Hiroto , Nishikori Masaru , Uchino Haruto 
Published: February 2007

AbstractA myeloid leukemia cell line (TK‐1) was established from the peripheral blood of a patient with lymphoblastic lymphoma whose leukemia cells were composed of T‐lymphoblasts and immature myeloid cells. The established TK‐1 cell line consisted of immature myeloid cells with heavy azurophilic granulation in the cytoplasm. The TK‐1 cells were positive for peroxidase, and exhibited a strong positive reaction for α‐naphthyl acetate esterase and naphthol AS‐D chloroacetate esterase. The cells were weakly positive for Fcγ‐receptors, showed no phagocytosis and did not reduce NBT. With the treatment of 1α, 25‐dihydroxy‐vitamin D3, they exhibited morphological and functional differentiation. The TK‐1 cell line contained normal diploid cells and pseudodiploid cells, and the two populations were successfully cloned; the clone with a normal karyotype was designated the TK‐1D cell line, and the clone with a pseudodiploid karyotype, which had a translocation involving chromosomes 14, 17 and one other chromosome, was designated the TK‐1B cell line. These cloned cells lacked Epstein‐Barr virus nuclear antigens and had almost the same myelomonocytic characteristics as the parent TK‐1 cells. The breakpoint of chromosome 17 involved in the translocation of the pseudodiploid cells was identified to be a band 17q23.
Transformation of hamster spleen lymphocytes by human T‐cell leukemia virus type I
Authors: Akagi T. , Takata H. , Ohtsuki Y. , Takahashi K. , Oka T. , Yano S. , Miyoshi I. 
Published: February 2007

AbstractCo‐cultivation of spleen cells of Syrian golden hamsters with lethally irradiated MT‐2 cells harboring human T‐cell leukemia virus type I (HTLV‐I) resulted in the establishment of lymphoid cell lines, HCT‐1 and HCT‐2, which exhibited the normal karyotype of golden hamsters. Cells of both the HCT‐1 and HCT‐2 lines lacked surface immunoglobulins and reacted with a monoclonal antibody (MAb) specific for hamster T cells. Some were positive for OKIal. None of them expressed HTLV structural antigens (p19 and p24) or virus particles, but they contained HTLV‐1 proviral DNA monoclonally. By immunochemical analysis of the labelled cell antigens, sera from adult T‐cell leukemia (ATL) patients reacted with the two polypeptides, p37 and p40, which may not be viral structural proteins and still remain to be characterized. HCT‐1 and HCT‐2 cells were transplantable into newborn hamsters, pre‐treated with anti‐hamster thymocyte serum and non‐treated, respectively, producing diffuse malignant lymphoma. These findings indicated that HTLV‐1 not only immortalized but also transformed hamster T cells non‐productively.
Interaction of recombinant interferons with recombinant interleukin‐2: Differential effects on natural killer cell activity and interleukin‐2‐activated killer cells
Authors: Brunda Michael J. , Tarnowski Deborah , Davatelis Viveca 
Published: February 2007

AbstractThe ability of recombinant interferons (IFNs) to modulate recombinant interleukin‐2 (rIL‐2) augmentation of natural killer (NK)‐cell activity and to modulate the generation of activated killer (AK) cells was examined. Incubation of murine spleen cells for 18 hr with either human rIL‐2 or a human hybrid recombinant IFN alpha, rHuIFN‐αA/D, which is active on murine cells, resulted in a dose‐dependent increase in NK activity; however, recombinant murine IFN gamma, rMuIFN‐γ, had little activity. A more than additive augmentation of cytotoxicity was obtained when spleen cells were incubated with the combination of rIL‐2 and rHuIFN‐αA/D. Incubation of murine spleen cells with rIL‐2 for 3 days resulted in a dose‐dependent induction of AK cells which were cytotoxic to an NK‐resistant tumor target cell. In contrast to the results observed on NK activity, incubation of spleen cells with rHuIFN‐αA/D and rIL‐2 inhibited AK‐cell activity. Partially purified murine IFN‐α had inhibitory activity comparable to that of rHuIFN‐αA/D. The addition of rHuIFN‐αA/D at the initiation of culture of spleen cells with rIL‐2 (day 0) resulted in maximal inhibition of cytotoxicity; inhibition was reduced or absent if rHuIFN‐αA/D was added on day 1 or 2 of culture. The proliferation of spleen cells incubated with rIL‐2 was also inhibited by rHulIFN‐αA/D. Addition of rMuIFN‐γ to spleen cells and rIL‐2 increased the cytolytic activity of AK cells and did not inhibit rIL‐2‐induced proliferation of spleen cells. Similar data were also obtained with human peripheral blood lymphocytes and recombinant cytokines. Incubation of human peripheral blood lymphocytes with rIL‐2 and recombinant human IFN‐α (rHuIFN‐αA) or recombinant human IFN‐γ (rHuIFN‐γ) resulted in a more than additive increase in NK activity. Human AK‐cell cytotoxicity was inhibited by rHuIFN‐αA but enhanced by rHuIFN‐γ. Thus recombinant IFNs have differential effects on rIL‐2‐induced cytotoxic cells, resulting in augmentation or inhibition of activity, which is dependent on both the type of IFN and the cytotoxic activity examined. These results may have important implications for the potential therapeutic use of combinations of these cytokines.
in vitro studies with melphalan and pediatric neoplastic and normal bone marrow cells
Authors: Worthington‐White Diana A. , Graham‐Pole John R. , Stout Susan A. , Riley Christopher M. 
Published: February 2007

AbstractChemotherapeutic agents are used in increasingly high dosages to treat patients with refractory cancers. An in vitro clonogenic assay was used to investigate the effects of melphalan on cultures of human neuroblastoma, Ewing's sarcoma, and osteosarcoma cells, as well as on normal bone marrow cells. A I‐hr incubation with 10−5 m melphalan significantly inhibited tumor colony growth of both fresh neuroblastoma and osteosarcoma cells (p < 0.01) while Ewing's sarcoma cells and normal bone marrow appeared resistant to melphalan even at a 100‐fold higher concentration. Incubation with melphalan for 8 hr did not significantly increase the sensitivity of neuroblastoma and osteosarcoma or the relative resistance of Ewing's sarcoma cells; however, normal bone marrow which had remained resistant to melphalan after I hr of incubation, showed significant inhibition of colony growth after an 8‐hr incubation with the agent. Repeated exposure to melphalan increased the degree of inhibition of both tumor and normal marrow colonies. Fresh neuroblastoma cells were significantly more sensitive than long‐term cultured neuroblastoma cells at all drug doses tested. HPLC studies demonstrated that the loss of melphalan followed first‐order kinetics with a half‐life of 69 min, and that in addition to the 2 known breakdown products, mono‐ and dihydroxymelphalan, several other peaks were present which were not attributable to the tissue culture medium or the buffer solutions.
Lung cancer risk associated with cigar and pipe smoking
Authors: Benhamou Simone , Benhamou Ellen , Flamant Robert 
Published: February 2007

AbstractA case‐control study of 1,529 histologically confirmed male lung cancer cases and 2,899 controls matched for sex, age, hospital of admission and interviewer was conducted in France between 1976 and 1980. The results presented concern the effects of smoking habits, especially cigar and pipe use, on the occurrence of lung cancer, in a total of 38 exclusive cigar smokers, 61 exclusive pipe smokers and 586 mixed tobacco smokers. Exclusive cigar or pipe use (RR = 5.6 and 1.6 respectively) has been shown less harmful than exclusive cigarette smoking (RR = 13.3), mixed cigar and cigarette smoking (RR = 8.5) and mixed pipe and cigarette smoking (RR = 8.0). Different inhalation practices were observed according to smoking habits: while among exclusive cigarette smokers 29.8% never inhaled the smoke, among exclusive cigar and exclusive pipe users these percentages were 89.5% and 86.9 respectively. No significant increase with greater exposure to cigar was found among mixed cigar and cigarette smokers after adjustment for exposure to cigarettes, defined by duration and daily consumption of cigarettes (RR = 1.20), and by type of cigarettes smoked–light or dark, filter or nonfilter (RR = 1.13). Similar results were observed among mixed pipe and cigarette smokers after adjustment for cigarette exposure (RR = 0.95 and 1.04).