bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cytogenetic studies on an epithelial cell line derived from poorly differentiated nasopharyngeal carcinoma
Authors: Sizhong Zhang , Xiukung Gao , Yi Zeng 
Published: February 2007

AbstractAn epithelial cell line, CNE‐2, has been recently established from a poorly differentiated nasopharyngeal carcinoma, and it represents the first of its kind. Using chromosome banding techniques, cytogenetic analysis of the cell line was carried out. It was demonstrated that the chromosome numbers of the CNE‐2 cells varied from 87 to 107 and the modal number was 104‐103. All cells contained a series of structurally abnormal chromosomes, and most of them were either consistent or frequently found. Among these chromosomes there were two giant markers which, by banding pattern analysis, proved to be distinct from the so‐called giant group A marker chromosomes previously found in many lymphoblastoid cell lines from NPC. Comparison between the CNE‐2 and CNE, another epithelial cell line, which was established from well‐differentiated squamous NPC, showed that while they were quite different in many cytogenetic aspects, they had three marker chromosomes in common, namely, an iso8q, a t(?;3q) and a small acrocentric one. The question of whether chromosome markers specific for NPC exist is discussed in the light of the data presented.
Detection of epstein‐barr virus IgA/EA antibody for diagnosis of nasopharyngeal carcinoma by immunoautoradiography
Authors: Zeng J. , Gong C. H. , Jan M. G. , Fun Z. , Zhang L. G. , Li H. Y. 
Published: February 2007

AbstractAn immunoautoradiographic method was used for the detection of EB virus lgA/EA antibody in sera from NPC patients and other control groups. Ninety‐six percent of NPC patients had IgA/EA antibody with a high titer of GMT. The positive rates of IgA/EA antibody in patients with malignant tumours other than NPC and in normal individuals were only 4% and 0%, respectively. Eleven patients histologically diagnosed as having a chronic inflammation and who showed positive for IgA/EA antibody by immunoautoradiography were rebiopsied; six of them were discovered to have squamous cell carcinoma. Fourteen NPC patients had no IgA/EA antibody detected by immunofluorescence and immunoenzymatic testing, but 11 and six of them had IgA/VCA and IgA/EA antibodies detected by immunoautoradiography, respectively. These data indicate that the immunoautoradiographic method is more sensitive than either the immunofluorescence or immunoenzymatic test for the detection of IgA/EA antibody, and can be used for the detection of NPC in the early stages of development.
3H‐estradiol and 3H‐R5020 binding in cytosols of normal and neoplastic human ovarian tissue
Authors: Pollow K. , Schmidt‐Matthiesen A. , Hoffmann G. , Schweikhart G. , Kreienberg R. , Manz B. , Grill H.‐J. 
Published: February 2007

AbstractHigh‐affinity cytoplasmic estrogen and progesterone receptors in normal and abnormal ovarian tissues were studied. Estradiol receptor was detectable in 65% and progesterone receptor in 36% of the malignant tumors; 39% of all malignant ovarian tissues were estradiol‐ as well as progesterone‐receptor‐positive. Tumors were said to be receptor‐positive when the receptors bound >5 fM steroid/mg cytosol protein. No correlations were found between receptor status and histopathological diagnosis. In normal ovarian tissues collected at various phases of the menstrual cycle no changes in [<3>H]‐estradiol and [<3>H]‐R5020 binding could be detected. Analysis of the receptor concentration for both steroid hormones with regard to the menopausal status demonstrated highest levels in postmenopausal women. No significant difference could be found when two groups of patients with advanced ovarian carcinoma associated with the cytosol estrogen receptor status were compared in terms of two different therapeutic schemes (cytosolic chemotherapy with and without tamoxifen).
H‐2 control of the cytotoxic antibody response against a newly defined MuLV‐related cell‐surface antigen: G(B10.A)
Authors: Vlug Arjen , Zijlstra Maarten , DeGoede Ruud E. Y. , Hesselink Wim G. , Schoenmakers Harrie J. , Melief Cornelis J. M. 
Published: February 2007

AbstractH‐2‐congeneic C57BL mice with milk transmission of B‐tropic murine leukemia virus (V+ mice) have a much higher lymphoma incidence than the same strains without milk‐transmitted virus (V—mice). Gene(s) within the major histocompatibility complex (H‐2) influence virus titers, lymphoma incidence, lymphoma type and the anti‐MuLV envelope antibody response. In this paper, we report that the prevalence of cytotoxic antibodies to virus‐induced lymphomas is also regulated by the H‐2 complex. Milk transmission of MuLV resulted in the formation of cytotoxic antibodies against primary virus‐induced C57BL lymphomas. These antibodies detect an antigen that is also present on the RADAI tumor‐cell line, and on normal spleen cells of young adult B10.A (H‐2a) mice of both V+ and V‐ sublines, but not on spleen cells of young adult B10 (H‐2b) mice of either subline. These cytotoxic antibodies were detected in the sera of B10V+ and B10.A(5R)V+ animals, but not in the sera of B10.AV+ mice. This indicates that the prevalence of these antibodies is controlled by a gene in the K‐and/or I‐A region of the H‐2 complex. The presence of these cytotoxic antibodies in serum is recessively inherited. The specificity of the cytotoxic antibodies was investigated with a standard panel of transplantable tumor‐cell lines. Of these, only the RADAI cells expressed the target antigen in direct cytotoxicity tests and by absorption. The ability of B10V+ sera to lyse the B10.AV+ and RADAI tumor cells is ascribed to antibody activity against a new MuLV‐related cell‐surface protein: G(B10.A). Immunochemical analysis and absorption experiments with different types of purified MuLV and MuLV‐infected cell lines indicate that the cytotoxic antibodies belong to low‐avidity IgM antibodies that are directed to MuLV.
Characterization of the surface proteins of SV40‐transformed mouse and human cells: Absence of SV40‐specific proteins
Authors: Rose Timothy M. , Weil Roger 
Published: February 2007

AbstractThe proteins of a number of SV40‐ and spontaneously transformed mouse and human cell lines were compared in an effort to identify a surface protein which would correspond to the SV40 tumor‐specific transplantation antigen (TSTA). Analysis of the one‐ and two‐dimensional electrophoretic patterns of 35S‐methionine‐labelled total proteins and 125I‐labelled surface proteins of several of these cell lines failed to reveal the presence of proteins specific to transformation by SV40. Antisera were prepared against SV40‐ and spontaneously transformed mouse cells in syngeneic mice. In serological assays, these antisera reacted with surface antigens common to both SV40‐ and spontaneously transformed mouse cell lines. Electrophoretic analysis of the 125I‐surface‐labelled proteins which these antisera immunoprecipitated from extracts of SV40‐ and spontaneously transformed mouse and human cells identified a set of common surface proteins with apparent molecular weights of 15, 44, 50, 72, 77, 105, 150 and 230 kdal. No SV40‐specific surface proteins were detected. Two of the transformed cell surface proteins (105 and 150kdal) were present as well in membrane fractions of 35S‐methionine‐labelled primary mouse kidney cultures. The proteins of the primary cultures could not be iodinated by lactoperoxidase suggesting that these proteins were present at a “cryptic” location at the surface of normal cells. We were not able to obtain serological or immunochemical evidence for the presence of SV40 large T‐antigen at the surface of any of the SV40‐trans‐formed cell lines tested using either hamster anti‐SV40 tumor sera, a rabbit antiserum against SDS‐denatured gel‐purified large T‐antigen or antisera against SV40‐transformed mouse cells. In conjunction with the report that large T‐antigen released from disrupted SV40‐transformed cells will bind to cell surfaces (Lange‐Mutschler and Henning, 1982), we consider the possibility that the specific rejection of SV40‐induced tumors by sensitized animals is the result of immunological reactions against both common transformation‐related surface antigens and SV40 T‐antigen from disrupted cells that has bound to the surface of other tumor cells.
Antitumor effects of interferon in mice injected with interferon‐sensitive and interferon‐resistant friend leukemia cells. III. Inhibition of growth and necrosis of tumors implanted subcutaneously
Authors: Belardelli F. , Gresser I. , Maury C. , Duvillard P. , Prade M. , Maunoury M.‐T. 
Published: February 2007

AbstractAdministration of highly purified interferon to DA/2 mice inhibited the growth of interferon‐sensitive or interferon‐resistant Friend erythroleukemia cells implanted subcutaneously. Injection of interferon at the site of tumor inoculation was more effective than injection of interferon intraperitoneally. Histologic examination of tumors in interferon‐treated mice showed extensive areas of tumor‐cell necrosis in the absence of an obvious host‐cell infiltrate. Interferon inhibited the growth of established subcutaneous tumors and induced complete tumor regression in some mice. Interferon treatment also resulted in an inhibition of tumor metastases in the liver and spleen.
Characterization of “H‐2K,D‐like structures” on MM2 × mouse L cell hybrids. II. An “H‐2Kd‐like” structure on C3H‐derived tumor
Authors: Kubota Koichi , Manson Lionel A. 
Published: February 2007

AbstractAnti‐MM2 serum, which had been prepared by immunizing C3H/He mice with syngeneic MM2 mouse mammary ascites tumor, immunoprecipitated “H‐2K,D‐like” molecules on DBA/2 and C3H.H‐2° lymph node cells as well as on somatic cell hybrids between MM2 tumor and mouse L cells. Preclearing of lysates from C3H.H‐2° lymph node cells with anti‐H‐2.31 serum removed all “H‐2K,D‐like” molecules reactive with anti‐MM2 serum, indicating that the molecules detected by anti‐MM2 serum are H‐2Kd antigens. The anti‐H‐2.31 serum detected an “H‐2K,D‐like structure” on the hybrid cells and absorption of the anti‐H‐2.31 serum with the hybrid cells deprived the serum of anti‐H‐2Kd reactivity. The hybid cells could induce antibodies against the H‐2Kd antigen in C3H/He mice. These results indicate that on the hybrid cells, whose parental cells were both derived from C3H mice, there is an “H‐2K,D‐like structure” that has the H‐2Kd private specificity. Absorption of anti‐MM2 serum with EL4 cells did not affect the capacity of the serum to detect the H‐2Kd antigen on C3H.H‐2° lymph node cells, indicating that the “H‐2Kd‐like structure” is distinct from “H‐2K,D‐like structure A” which was previously reported. Nine isozymes were examined and MM2 cells, mouse L cells, and the hybrids were found to have the same isozyme markers as those of the C3H/He mouse.
Emergence of low‐mobility t lymphocytes in cancer patients and its clinical significance
Authors: Nakajima Toshifusa , Mori Takeo , Iwaguchi Takao 
Published: February 2007

AbstractElectrophoretic mobility of lymphocytes from healthy individuals and cancer patients was analyzed by means of a fully automated cell electrophoresis apparatus (Parmo‐quant). Electrophoretic mobility histograms showing two distinct peaks were obtained with peripheral blood lymphocytes from normal subjects. A border line was placed at the mobility of 0.95 μm/sec/V/cm, and cells slower than this were designated as low‐mobility cells (LMC) and faster cells as high‐mobility cells (HMC). LMC, constituting the slower peak, consisted mainly of B cells and a small number of T cells (LMT). HMC, the constituent of the faster peak consisted of two types of T cells (HMT). In patients with malignant tumors, analysis revealed lowered electrophoretic mobility of T cells, with T/B ratios comparable to those in normal subjects. An increase in the percentage of LMT seemed characteristic of suppressed immunity in cancer patients since it showed a strongly positive correlation with the percentage population of IgG‐FcR‐positive T lymphocytes and with the serum level of immunosuppressive substance. The incidence of abnormal LMT/HMT ratios was highest in patients with recurrent cancer, and it was also high in the advanced stages of gastrointestinal cancer. This index could provide useful information for the early detection of cancer relapse during postoperative follow‐up. A fully automated electrophoresis apparatus greatly facilitated the measurement (5 min/100 cells) and permitted quantitative and statistical analysis of mobility histograms of cell electrophoresis.
Excretion of a tumor‐associated trypsin inhibitor (TATI) in urine of patients with gynecological malignancy
Authors: Huhtala Marja‐Liisa , Kahanpää Kari , Seppää Markku , Halila Hannu , Stenman Ulf‐Håkan 
Published: February 2007

AbstractIn earlier studies we reported the finding of a tumor‐associated peptide that also occurred at high concentrations in early amniotic fluid. Determination of the N‐terminal sequence of this peptide revealed that it is closely related or identical to the pancreatic secretory trypsin inhibitor. Therefore, the peptide is called tumor‐associated trypsin inhibitor (TATI). The concentration of TATI was determined by radioimmunoassay in the urine of 148 patients with various forms of gynecologic malignancy and in a reference population consisting of 98 patients with non‐malignant gynecologic disease, and also in 40 patients with severe infections or inflammatory disease. In the reference population, the median urinary concentration of TATI was 22 μg/g creatinine and the central 95 % reference interval was 7‐50 μg/g creatinine. Elevated urinary levels were observed in 53 % of all patients with gynecologic cancer, in 63 % of those with active disease and 26% of those in clinical remission. The highest urinary TATI level (11,000 μg/g creatinine) was over 200 times the upper limit of the reference range. Patients with cervical cancer had the highest frequency of elevated values. Increased excretion of TATI was also observed in patients with severe bronchopulmonary infections and pancreatitis. Although increased excretion of TATI is not cancer‐specific, the distinction by elevated levels of TATI between malignant and nonmalignant gynecologic disease is better than by most other putative tumor markers, and the increased excretion of TATI in patients with active disease can be important for the understanding of tumor biology.
Site‐directed chemotherapy with a drug bound to anti‐idiotypic antibody to a lymphoma cell‐surface IgM
Authors: Hurwitz Esther , Kashi Rina , Burowsky Daphna , Arnon Ruth , Haimovich Joseph 
Published: February 2007

AbstractXenogeneic antibodies against the cell‐surface IgM of a B‐cell lymphoma (38C‐13) were coupled through a dextran bridge to the anti‐neoplastic drug, daunomycin. The conjugate maintained both its antibody and its drug activity. The effectiveness of the conjugate was tested in vivo in mice challenged with the 38C‐13 lymphoma. Drug conjugates of the idiotypic antibodies injected intraperitoneally 2 days after tumor transplantation almost completely inhibited tumor development. The controls, daunomycin‐dextran‐goat anti‐DNP, free daunomycin, or the antibodies alone had no effect or only delayed the tumor development.
Characterization of T lymphocytes mediating in vivo protection against RSV‐induced murine sarcomas
Authors: Prat Maria , Di Renzo Maria Flavia , Comoglio Paolo M. 
Published: February 2007

AbstractTumors induced by Rous sarcoma virus (RSV) in different mouse strains share a common tumor‐associated transplantation antigen, whose expression is controlled both by the viral transforming srcgene and by cellular gene(s) (Prat et al., 1981). The mechanism(s) responsible for the in vivo protective immune response against two RSV‐induced sarcomas has now been investigated. In the “Winn assay” the growth of both tumors was specifically prevented or significantly reduced by the simultaneous administration of lymphocytes isolated from immunized donors. The effector cells were radiosensitive (2,500 rad), Lyt‐l+, Lyt‐2,3+ Thy.l+ cells. Better protection was afforded by transfer of immune spleen cells from mice pre‐treated with cyclophosphamide, which is known to abrogate T‐cell suppressor activity. In a 5‐day mixed lymphocyte/tumor cell culture specific anti‐RSV‐induced sarcoma cytotoxic activity was barely detected, while a good production of interferon‐gamma (IFN‐y) was observed. The cells involved showed the same functional and surface phenotype as displayed by the effectors of the “Winn” assay. It is concluded that in the immune rejection of RSV‐induced sarcomas, Lyt‐l+, Lyt‐2,3+ T cells, rather than cytotoxic T lymphocytes, and lymphokines such as IFN‐γ are involved.
In vitro induction of tumor‐specific immunity by highly purified vsv grown in SV40‐transformed cells and tumor glycolipids incorporated into liposomes
Authors: Ansel Sandra 
Published: February 2007

AbstractCytotoxic effector lymphocytes (CL) were induced by in vitro immunization of spleen cells from normal Syrian hamsters to syngeneic tumor cells, either SV40‐transformed (EH‐SV) or spontaneously transformed (EH‐N). The lymphocyte reactivity was measured in a direct 15Cr release cytotoxic effector lymphocytes with EH‐SV‐ and EH‐N‐labelled targets. A specific cytotoxic effect against tumor cells carrying the sensitizing antigens was observed. Cytotoxic effector lymphocytes were also induced by in vitro immunization of hamster spleen cells to highly purified vesicular stomatitis virus (VSV) grown either in syngeneic SV40‐transformed fibroblasts or in “normal” fibroblats. Purified virus possessing an intact envelope or virus subparticles devoid of their glycoprotein spikes stimulated the cellular immune responses against host tumor antigens present within the viral envelope. Cytotoxicity assays have revealed two tumor‐specific antigens (TSA), one induced by SV40 and present in SV40‐transformed cell lines and the other present in “normal” cells. CL were also induced by in vitro sensitization of spleen cells from normal hamsters to liposomes containing the polar glycolipid fraction from EH‐SV and/or EH‐N cells. A specific cytotoxic effect against tumor cells that have supplied the glycolipid extract was observed, suggesting specific recognition of glycolipid antigens characteristic for each tumor line. This study supports the view that surface glycolipids act as tumor‐specific antigens implicated in the destruction of SV40‐induced tumors in Syrian hamsters.
A leukocyte adherence inhibition (LAI) assay of anti‐tumor immunity in rats using selective radioimmunological assessment of adherence of T lymphocytes and monocytes
Authors: Morizane Toshio , Sjögren Hans Olov 
Published: February 2007

AbstractA new, highly sensitive micro‐glass‐tube leukocyte adherence inhibition (LAI) assay has been developed to detect anti‐tumor sensitization in a rat colon carcinoma system. This technique requires fewer cells and smaller amounts of antigen preparations than the previous glass tube method. The microscopic enumeration of adherent cells is replaced by a cellular radioimmunoassay (CRIA) which utilizes antibodies binding to mononuclear cells (MNC) and 125I‐labelled protein A. Antigen preparations were shown to be adsorbed to glass. Precoating of glass vials with fetal calf serum or antigen preparations was shown to cause a major increase in nonspecific LAI. The new LAI technique is designed to minimize such nonspecific LAI. By applying an anti‐T‐cell monoclonal antibody (McAb), an anti‐lg antiserum and an anti‐monocyte (MC) antiserum it became possible to assess selectively the change of adherence of T cells, B cells and monocytes. The specificity of the assay was demonstrated with anti‐T‐cell and anti‐MC reagents in criss‐cross experiments using two defined antigens and different tissue extracts as test antigens. The LAI response of peripheral blood MNC was examined after the subcutaneous isografting of 1 × 107 X‐irradiated DMH‐W49 colon carcinoma cells. Six days after sensitization all the rats showed an LAI response detectable with anti‐T‐cell and anti‐MC reagents, which gave considerably higher LAI indices than anti‐MNC antiserum. After the subcutaneous isografting of 1 × 105 viable DMH‐W49 cells, 12 of 24 rats (50%) showed an LAI response detectable with the anti‐MNC antiserum during a 3‐week follow‐up period. On the other hand, an LAI response was detected in all the 14 tumor‐inoculated rats tested when the adherence of T lymphocytes and monocytes was assessed selectively.
Concentration and time‐dependent inter‐relationships for antitumour drug cytotoxicities against tumour cells in vitro
Authors: Rupniak H. Thomas , Whelan Richard D. H. , Hill Bridget T. 
Published: February 2007

AbstractCryopreserved tumour cells obtained from the ascitic fluid of a patient with an ovarian carcinoma were employed to determine the effect on in vitro drug cytotoxicities of varying both drug concentration and exposure time. Four antitumour drugs, in common clinical usage, were selected for study. Tumour‐cell survival following drug treatment was measured by colony‐forming ability in the soft‐agar assay developed by Courtenay et al. (1978). Treatment with cis‐platinum, adriamycin or vinblastine generated exponential survival curves with increasing cell kill resulting from either increasing drug concentrations or prolonging exposure times. In contrast, no detectable cell kill was elicited by treatment with hydroxyurea for short exposure times of 1 or 6 h, even at concentrations as high as 1 mg/ml, although continuous drug exposure resulted in a steep exponential survival curve. These results, obtained directly from biopsy material, are in close agreement with data from parallel studies employing a continuous human tumour‐cell line (COLO 205 derived from a colon carcinoma). Duration of exposure is therefore an important determinant of drug‐induced cytotoxicity under these assay conditions. The results with hydroxyurea, however, imply that prolonged incubation times are necessary to evaluate the cytotoxicity of certain agents and so the routinely employed 1 h exposure in most current human tumour drug sensitivity tests is inadequate for such drugs. These data therefore provide evidence that employing a single set of standard conditions of drug exposure to evaluate all antitumour drugs may be inappropriate.