bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunological quantitation of phospholipid/CA2+‐dependent protein kinase of human mammary carcinoma cells: Inverse relationship to estrogen receptors
Authors: Borner Christoph , Wyss Rudolf , Regazzi Romano , Eppenberger Urs , Fabbro Doriano 
Published: February 2007

AbstractThe amounts of phospholipid‐and Ca2+‐dependent protein kinase (PKC) of various human mammary tumor cells containing (ER+) or lacking (ER‐) estrogen receptors were estimated by quantitative immunoblotting. According to several criteria the polyclonal anti‐PKC antibody raised in rabbits against porcine brain PKC specifically recognizes an 80‐kDa polypeptide on immunoblots. This 80‐kDa PKC presumably represents the autophosphorylated form of the holoenzyme. Immunological quantitation of PKC revealed that the levels of immunodetectable PKC varied widely among the various human mammary carcinoma cell lines but closely matched the amounts determined by enzyme activity and phorbol ester binding in the respective cell line. The largest amounts of immunodetectable PKC were found in the ER‐human mammary tumor cells (0.5 to 1.5 μg PKC/mg of cytosolic protein). These data indicate that ER‐human mammary carcinoma cell lines express significantly higher levels of PKC than their estrogen‐receptor‐containing counterparts.
Deferent behaviour of normal and neoplastic cells cultured in vitro in the presence of catalase and superoxide dismutase
Authors: Liotti F. S. , Bodo M. , Menghini A. R. , Guerrieri P. , Mariucci G. , Bruschelli G. 
Published: February 2007

AbstractChicken embryo fibroblasts and hepatocytes were studied in the presence of catalase and superoxide dismutase in order to establish whether these enzymes had the capacity to favour cell multiplication as previously shown for in vitro tumour ascites cells (ATP C+). The results indicate that, unlike ATP C+ cells, both fibroblasts and hepatocytes are inhibited in their multiplication by superoxide dismutase. Similar effects are exerted on hepatocytes by catalase, whereas the multiplication of fibroblasts is favoured by high doses of this enzyme. Enzyme determinations revealed high levels of catalase and superoxide dismutase in hepatocytes, whereas both enzymes were poor in fibroblasts and ATP C+.
Lysis of tumor cells by the retargeting of murine cytolytic T lymphocytes with bispecific antibodies
Authors: Barr I. G. , Macdonald H. R. , Buchegger F. , Von Fliedner V. 
Published: February 2007

AbstractThe specificity and efficiency of tumor‐cell lysis by the retargeting of murine cytolytic lymphocytes (CTL) with bispecific antibodies was examined. Bispecific antibodies (also known as heteroaggregated or hybrid antibodies) were produced by the chemical coupling of monoclonal antibodies (MAbs) against H‐2 antigens and the murine T‐cell receptor (TCR). Murine tumor cell lines which expressed on their plasma membrane an antigen reactive with one component of the bispecific antibody were efficiently lysed in the presence of polyclonal murine CTL. CTL capable of lysis were generated by stimulating spleen or lymph‐node cells with ConA and IL‐2, while unstimulated cells or cells incubated only with IL‐2 showed no lysis of target cells with bispecific antibodies. Furthermore, the lysis of target cells by bispecific antibodies and CTL did not cause the lysis of bystander cells (cells not expressing an antigen recognized by the antibody which are mixed with the target cells). The efficient CTL‐mediated lysis observed with these antibodies makes this a promising approach for the immunotherapy of human cancer.
Interleukin‐2 activated human killer lymphocytes: Lack of involvement of interferon in the development of IL‐2‐activated killer lymphocytes
Authors: Damle Nitin K. , Doyle Laura V. 
Published: February 2007

AbstractWhen cultured with native or recombinant interleukin‐2 (IL‐2) human small agranular lymphocytes acquire the ability to kill various tumor targets. The development of these IL‐2 activated killer (IAK) cells, also known as LAK, is observed in the absence of antigen or mitogen. Interferons are known to augment the lytic effects of natural killer cells and cytolytic T lymphocytes. Our study was undertaken to examine the effect of human α, β, and γ interferons on the induction and the effector phase of IAK function. When cultured with small lymphoid cells IFN alone did not induce anti‐tumor cytolytic activity in those lymphocytes. Despite their known anti‐proliferative effects, none of the 3 IFN species at any concentrations tested inhibited the development of IAK activity when present during the entire culture period. IFN neither inhibited nor augmented the development of IAK cells under suboptimal conditions. Furthermore, activation of IAK cells was not affected by the presence of neutralizing antibodies to either α or γ IFN. Post‐activation exposure of IAK cells to IFN also failed to either augment or inhibit their lytic activity. Thus, neither endogenously generated nor exogenously added IFN had any effect on the IAK system, in contrast to their augmenting effects on NK cells and CTL.
Lymphogenous and hematogenous metastasis of Lewis lung carcinoma in the mouse
Authors: Weiss L. , Ward P. M. 
Published: February 2007

AbstractQuantitative and temporal comparisons were made between lymphogenous and hematogenous metastasis in the non‐immunogenic model system of mice bearing transplanted 3LL tumors in their hind feet. The experimental evidence indicates that cancer cells disseminate from clinically detectable primary cancers by non‐exclusive routes in the bloodstream and in the lymphatics. Following a delay of approximately 2 weeks after injection of 3LL cancer cells into the foot, local lymph‐node micrometastases occur, together with the first appearance of overt hematogenous metastases in the lungs. The anatomic extent of lymph‐node involvement, determined by bioassays of orthotopic grafts, of ipsilateral popliteal, inguinal and lumbar nodes, provides an accurate indicator of hematogenous metastasis, even though lymphogenous and hematogenous metastasis are operationally independent in this tumor/host system.
B‐cell lymphomas of high‐grade malignancy frequently lack HLA‐DR, ‐DP and ‐DQ antigens and associated invariant chain
Authors: Momburg Frank , Herrmann Barbara , Moldenhauer Gerhard , Möller Peter 
Published: February 2007

AbstractThe expression of HLA‐DR, HLA‐DP and HLA‐DQ antigens was studied in an unselected series of 66 B‐cell lymphomas by means of immunohistology using monoclonal antibodies against non‐polymorphic determinants in a sensitive immunoperoxidase technique. In addition, the expression of the MHC class‐II antigen‐associated invariant chain (li) was examined, The tumors were classified according to the Kiel classification, 30 being of high‐grade and 36 being of low‐grade malignrancy. Only 6 lymphomas of high‐grade and 16 lymphomas of low‐grade malignancy showed coordinate strong expression of all HLA class‐II antigens and invariant chain as observed in the normal peripheral B cell. Six further tumors of high‐grade and 8 tumors of low‐grade malignancy contained tumor‐cell subsets with reduced expression of one or several of the antigens. Eighteen lymphomas of high‐grade and 12 lymphomas of low‐grade malignancy contained varying tumor‐cell subsets that were negative for HLA‐DR, ‐DP, ‐DQ and li in a selective or combined manner. Three highly malignant tumors were devoid of all class‐II antigens and li; 2 highly malignant tumors expressed invariant chain only. The presence of high‐grade malignancy was significantly correlated with the occurrence of tumor cells lacking HLA‐DR (p = 0.004), HLA‐DP (p = 0.013), HLA‐DQ (p = 0.007) or 11 (p = 0.024).
Interferon treatment of human genital papillomavirus infection: Importance of viral type
Authors: Schneider Achim , Papendick Uwe , Gissmann Lutz , De Villiers Ethel‐Michele 
Published: February 2007

AbstractEighteen women and 6 of their male sexual partners with lower genital tract infections caused by various human papil‐iomavirus (HPV) types were treated with systemic or topical interferon (IFN) application. All patients with vulvar or penile lesions had a history of podophyllin or surgical treatment. In the female group, 9 patients showed complete response, 8 patients partial response and 1 patient no response. In the male patients complete response was seen in all patients. The response rate appears to depend on the HPV type present. Women with an HPV 16/18 infection showed a lower response rate to IFN treatment (complete response in 5 out of 14 patients), whereas lesions caused by HPV 6(11) showed com‐ plete response in all 4 cases. During follow‐up examinations (mean 7.5 months) no recurrence of disease was observed. Systemic treatment showed tolerable and temporary side‐ effects. Topical treatment yielded identical efficacy and no side‐effects.
Patterns of seminoma tissue markers and deletions
Authors: Yamamoto H. , Rudén U. , Ljungdahl‐Ståhle E. , Brehmer‐Andersson E. , Hirano K. , Hisazumi H. , Stigbrand T. , Wahren B. 
Published: February 2007

AbstractSeminomas and control tissues were analyzed for several tumor markers. Very high levels of placental alkaline phosphatase (PLAP)‐like enzyme levels were found in all 18 seminomas studied. The majority of the seminomas were of phenotype I, thus differing from placental FLAP. The mean amount of enzyme protein as measured by monoclonal antibodies, was 100 times higher than in non‐malignant tissues and 10 times lower than in placental tissue. The specific enzymatic activity in seminomas was about half of that observed in placenta. Similarly, the specific activity of PLAP‐like enzymes in sera of patients with seminoma was only about half of that found in pregnancy sera. HCG was strongly elevated in 3 seminomas, but not obviously related to FLAP. Thirteen of the 17 pure seminomas had HCG over 100 IU/g, which was not seen in normal testes. Liver alkaline phosphatase (LAP) and intestinal alkaline phosphatase (IAP) were high in seminomatous tissues, the mean increases being 60‐fold and 20‐fold, respectively. The highest IAP levels were found in 2 yolk‐sac tumors. Ferritin was moderately elevated in seminomas, but high in several control tissues. Carcinoembryonic antigen (CEA) was not elevated and alpha‐fetoprotein (AFP) was not detected at all in pure seminomas. A decrease in carbohydrate antigen 50 (CA‐50) content was noted in seminomas as compared to normal testes, yolk‐sac tumors and choriocarcinomas. Defects in tumor‐related enzymes may account for increase of PLAP and decrease of CA‐SO.
Altered HLA antigens expressed on T and B lymphocytes of adult T‐cell leukemia/lymphoma patients and their relatives
Authors: Sonoda Shunro , Yashiki Shinji , Takahashi Kazuo , Arima Naomichi , Daitoku Yasuhisa , Matsumoto Makoto , Matsumoto Tadashi , Tara Mitsutoshi , Shinmyozu Koichi , Sato Kaoru , Inoko Hidetoshi , Ando Asako , Tsiji Kimiyoshi 
Published: February 2007

AbstractThe HLA types of peripheral blood lymphocytes (PBL) of 36 adult T‐cell leukemia/lymphoma (ATLL) patients were examined and compared with those of 45 healthy relatives of these patients, and with those of 10 non‐ATLL families including 80 healthy members. Thirty‐one percent of ATLL patients showed either a gain or a loss of HLA antigens determined by the presence of alien HLA antigens or the absence of inherent HLA antigens deduced from familial haplotype analysis. The antigen specificity of HLA gained or lost was variable and differed from case to case among ATLL patients. Although the gain of HLA was detected only in ATLL patients, the loss of HLA was found both in ATLL patients and in asymptomatic healthy relatives. The rate of HLA loss in ATLL patients (8.4%) and their relatives (17.8%) was much higher than in relatives of non‐ATLL patients (1.1 %). The HLA gain and loss revealed in the PBL of ATLL patients were confirmed by altered HLA phenotypes in the cloned T and B cells established from ATLL patients. Our results suggest that latently infecting HTLV‐1 may induce altered HLA phenotypes in T and B cells, primarily with loss of HLA antigens in a population of asymptomatic virus carriers, and secondarily with a gain of HLA antigens after the development of ATLL.
Alternative methods of selecting rat hepatocellular noduli resistant to 2‐acetylaminofluorene
Authors: Semple‐Roberts Esther , Hayes M. Anthony , Armstrong Dianna , Becker Richard A. , Racz William J. , Farser Emmanuel 
Published: February 2007

AbstractDietary 2‐acetylaminofluorene (2‐AAF) coupled with a stimulus for cell proliferation such as a 2/3 partial hepatectomy (PH) or a necrotizing dose of carbon tetrachloride is frequently employed to generate nodules of resistant (“initiated”) rat hepatocytes. This regimen is a useful model for experimental analysis of alterations in hepatocytes during carcinogenesis, and also as an assay for initiation by various carcinogens. Because of the decreasing availability of carcinogen‐containing diets from commercial sources, we have developed alternative methods of 2‐AAF administration to generate nodules in rats initiated with N‐nitrosodiethylamine. This study compared the nodule‐selecting and cancer‐promoting efficacy of 2‐AAF administered by the Solt‐Farber procedure (0.02% in diet for 2 weeks) with 2‐AAF administered by gavage, as a suspension in 1% aqueous carboxymethyl‐ cellulose (CMC). Three or 4 daily administrations of 2‐AAF by gavage (20 mg/kg/day) followed by PH on day 4 were equivalent to the dietary regimen in generating early resistant nodules, late persistent nodules and hepatocellular carcinomas. These regimens were similar to the dietary regimen of 2‐AAF in inhibiting virtually all normal hepatocyte proliferation. These regimens permit control over the duration and level of 2‐AAF exposure and the resulting size of selected nodules.
Effects of ouabain on NIH/3T3 cells transformed with retrovirai oncogenes and on human tumor cell lines
Authors: Tagliaferri Pierosandro , Yanagihara Kazuyoshi , Ciardiello Fortunate , Talbot Neil , Flatow Ursula , Benade Leonard , Bassin Robert H. 
Published: February 2007

AbstractBoth murine and human cell lines transformed by the v‐Ki‐ras gene have been shown to be much more sensitive to the toxic effects of the cardiac glycoside ouabain than their respective controls. This differential toxicity has previously been used in the isolation of flat revertant clones from populations of Kirsten murine sarcoma virus transformed NIH/3T3 cells. Here, we have undertaken a further characterization of this phenomenon in murine and human tumor cells. Two different techniques, a 51Cr‐release assay and a quantitative Crystal violet elution assay, have been employed to compare the sensitivities to ouabain of normal and v‐Ki‐ras‐transformed NIH/3T3 cells. In each assay, ras‐transformed NIH/3T3 cell lines displayed an increased sensitivity to ouabain as compared to the parental NIH/3T3 cell line, both in dose‐response and in time‐course experiments. In a separate study, ouabain was also able to inhibit the growth in semi‐solid medium of 2 v‐Ki‐ras‐transformed NIH/3T3 cell lines (DT and K‐NIH) in a dose‐dependent fashion. The same concentrations of ouabain were effective in both the 51Cr‐release and Crystal violet assays. To address the question of whether increased sensitivity to ouabain is a specific result of transformation with the ras oncogene or is a common event which accompanies transformation by other oncogenes, we have screened a variety of transformed NIH/3T3 derivatives. All of these lines displayed an increased sensitivity to ouabain when compared to the parental NIH/3T3 cell line.
Interferon‐induced alterations in metastatic capacity, class‐1 antigen expression and natural killer cell sensitivity of melanoma cells
Authors: McMillan T. J. , Rao J. , Everett C. A. , Hart I. R. 
Published: February 2007

AbstractPre‐treatment of B16 melanoma cells with recombinant interferon‐γ (IFN‐γ) markedly increased their lung‐colonising capacity following i.v. injection into syngeneic mice as compared with control cells. A similar enhancement was observed following the injection of treated cells into athymic nude mice but not in athymic mice carrying the beige mutation. Pre‐treatment of syngeneic mice with anti‐asialo GM1 antibody effectively abrogated any interferon‐induced increase in experimental metastatic activity. The same IFN‐γ treatment significantly increased resistance of B16 cells to splenic natural killer (NK) cell activity as determined by in vitro assays. IFN‐α/β pre‐treatment of B16 cells decreased sensitivity to NK‐cell‐mediated lysis to a lesser extent than IFN‐γ and had no detectable effect upon the subsequent metastatic activity of the tumour cells. Class‐1 antigen expression was altered by these IFN treatments, with IFN‐γ causing dramatic increases in expression of H‐2Db antigen, in a pattern consistent with the possibility that increased H‐2 antigen expression on B16 cells led to decreased NK‐cell sensitivity which was reflected by an increase in experimental metastatic capacity.
Metastatic but not primary melanoma cell lines grow in vitro independently of exogenous growth factors
Authors: Rodeck Ulrich , Herlyn Meenhard , Menssen Hans D. , Furlanetto Richard W. , Koprowski Hilary 
Published: February 2007

AbstractFive out of 6 cell lines derived from metastatic melanoma lesions grew in a chemically defined base medium consisting of a mixture of calcium‐supplemented MCDB 153 and L 15 media in the absence of any polypeptide growth factors. In contrast, under these conditions no growth was seen in any of 5 primary melanoma cell lines tested, including 2 cell lines from patients whose metastatic cells proliferated well in base medium. Growth stimulation of all 11 melanoma cell lines by epidermal growth factor (EGF), transferrin, insulin, and insulin‐like growth factor (IGF)‐I alone and in various combinations was studied. Insulin represented the strongest single growth factor for primary and metastatic melanoma cell lines. The metastatic cell lines remained growth‐responsive to EGF, insulin and transferrin and responded more vigorously to these exogenously provided mitogens than the primary cell lines. No synergistic or additive growth effects of insulin, transferrin, or EGF for primary and metastatic cell lines were observed. Cross‐linking studies with 125I‐IGF‐I demonstrate surface expression of the type‐1 IGF receptor on melanoma cells. Growth stimulation by insulin and IGF‐I was inhibited by adding to the culture medium a monoclonal antibody to the type‐1 IGF receptor. Our studies indicate that IGF‐I and Insulin are major growth factors for melanoma cells and act via the type‐1 IGF receptor.
Paired Epstein‐Barr virus (EBV)‐negative and EBV‐converted Burkitt lymphoma lines: Stimulatory capacity in allogeneic mixed lymphocyte cultures
Authors: Avila‐Cariño J. , Torsteinsdottir S. , Ehlin‐Henriksson B. , Lenoir G. , Klein G. , Klein E. , Masucci M. G. 
Published: February 2007

AbstractEpstein‐Barr virus (EBV)‐negative Burkitt lymphoma lines (BLE‐) and their in vitro EBV‐converted sublines (BLEc), obtained by infection with the P3HR1 and B95‐8 strains of EBV, were compared for their capacity to induce T‐lymphocyte proliferation in allogeneic mixed lymphocyte cultures (MLC). Regardless of the virus strain used for conversion, the BLEc lines induced a considerably stronger primary MLC response than their EBV‐negative parentals. Only the BLEc lines were able to maintain T‐lymphocyte proliferation in repeated stimulations. The low proliferative response observed in cultures stimulated with BLE−cells was not due to the generation of suppressor cells or to the release of inhibitory factors. The increased stimulatory capacity of BLEc lines was unrelated to changes in expression of MHC class‐I and class‐II antigen, or of B‐cell activation markers, and was not due to the reactivation of EBV‐specific memory T cells, since lymphocytes from EBV‐seropositive and seronegative donors responded similarly. The results indicate that the capacity of BL cells to elicit cellular immune responses may be influenced by their EBV‐carrying status.
Complementation of anti‐CEA and anti‐TAG‐72 monoclonal antibodies in reactivity to human gastric adenocarcinomas
Authors: Ohuchi Noriaki , Simpson Jean F. , Colcher David , Schlom Jeffrey 
Published: February 2007

AbstractMonoclonal antibody (MAb) B72.3 and MAb COL‐4 are reactive with the high‐molecular‐weight (Mr > 106) tumor‐as‐sociated glycoprotein (TAG)‐72, and the Mr 180,000 carcino‐ embryonic antigen (CEA), respectively. Antibody competition radioimmunoassays (RIAs) using 1251‐MAb B72.3 or 1251‐COL‐4 have demonstrated that each MAb also recognizes a distinct antigenic determinant. Solid‐phase RIAs using MAbs B72.3 and COL‐4, however, demonstrated similar reactivity for each MAb with gastric carcinomas versus normal gastric mucosa. Tissue sections from ail of 17 gastric adenocarcinomas also reacted with both MAb B72.3 and MAb COL‐4 when immunoperoxidase techniques were used. Double‐staining techniques using both MAbs on the same section were performed on formalin‐fixed, paraffin‐embedded gastric tissue sections using the combination of avidin‐biotin peroxidase complex and avidin‐biotin alkaline phosphatase complex immunohis‐tochemical methods. The double‐staining technique revealed that some carcinoma cells react with MAb B72.3, some react with MAb COL‐4, and others react with both MAbs. This technique has demonstrated that more carcinoma cells can be detected by both MAbs as compared to the number of stomach carcinoma cells shown to be reactive with either one or the other MAb. These studies thus define the rationale for the use of combinations of MAbs which recognize different tumor‐associated antigens as immunological adjuncts for detection and perhaps therapy of gastric carcinoma.
Inhibition of homotypic aggregation of a human Burkitt‐lymphoma cell line
Authors: Wolf Michael F. , Koerner Ulrike , Klumpp Britta , Schumacher Kurt 
Published: February 2007

AbstractThi molecules involved in homotypic aggregation of the human Burkitt‐lymphoma cell line Raji were investigated by inhibition of reaggregation with carbohydrates and glycoconjugates, by inhibition of glycosylation, and enzyme treatment of the cell surface. Complete inhibition of reaggregation was achieved with bovine submaxillary mucin. Asialomucin, on the other hand, was not effective in this assay. Another potent inhibitor of reaggregation was the ganglioside GMI. The common carbohydrate structure of these molecules is NeuNAc‐(gal)‐galNAc. Lactosamine, fucosyllactosamine, sialyllactosamine, complex mannose type, or Thomsen‐Friedenreich antigen sequences are not involved in aggregation. Neuraminidase and chloroquine also abolished agglutination of cells. The finding that mucin, but not asialomucin, inhibits the reaction, demonstrates the importance of sialic acid in this process. Homotypic aggregation was shown to be resistant to trypsin. Using the glycosylation inhibitor tunicamycin we show that N‐glycosidically linked carbohydrate chains are involved in aggregation. Swainsonine or castanospermine, which inhibit processing of terminal sialyllactosamines to the mannose core, did not interfere with the reaction supporting the results of the inhibition assay. The data presented suggest the involvement of 2 molecules in homotypic aggregation of human Burkitt‐lymphoma cells. One component is a lectin‐like molecule containing N‐linked carbohydrate chains. The other component carries the neuraminidase‐sensitive and trypsin‐resistant determinant NeuNAc‐(gal)‐galNAc and, therefore, appears to be a glycolipid. This proposed lectin‐carbohydrate interaction in homotypic aggregation is further supported by the frequently observed dependence of lectins on divalent cations as indicated by inhibition of aggregation with EDTA and EGTA.