bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects on in vitro tumor growth of macrophages isolated from human ascitic ovarian tumors
Authors: Mantovani Alberto , Peri Giuseppe , Polentarutti Nadia , Bolis Giorgio , Mangioni Costantino , Spreafico Federico 
Published: February 2007

AbstractMacrophages were isolated from 22 human ascitic ovarian epithelial tumors and their growth‐inhibitory capacity was tested using as targets the following in vitro tumor cell lines: murlne TLX9 lymphoma and FS6 sarcoma; human myeloid K562 leukemia and human E cell line derived from an ovarian carcinoma. Macrophage preparations were heterogeneous in their interaction with tumor target cells, and assay conditions, such as the type of target cell, incubation time, and attacker to target cell (A:T) ratio critically affected the evaluation of the cytotoxic potential of tumor‐associated macrophages. At an A:T ratio of 7:1 no cytostatic activity on TLX9 and K562 cells was ever observed, but in the presence of specific antibody 8 out of 12 macrophage preparations tested showed significant antibody‐dependent cytotoxicity on TLX9 lymphoma cells. Macrophage preparations from two patients significantly inhibited growth of the FS6 sarcoma and a cytostatic activity on E cells was observed in five additional patients. Significant stimulation of the proliferative capacity of at least one of the target cell lines was observed in 11 subjects at an A:T ratio of 7:1. In 12 patients, macrophage cytostatic activity on E cells was also tested at an A:T ratio of 35:1; eight out of 12 preparations showed significant cytotoxicity under these conditions. When the same subject was repeatedly tested at short intervals the same pattern of inhibition or stimulation of tumor growth was observed.
A comparison of the prognostic value of antibody‐dependent lymphocyte cytotoxicity and other ebv antibody assays in Chinese patients with nasopharyngeal carcinoma
Authors: Chan S. H. , Levine P. H. , De‐Thé G. B. , Mulroney S. E. , Lavoue M. F. , Glen S. P. P. , Goh E. H. , Khor T. H. , Connelly R. R. 
Published: February 2007

AbstractAntibody titres to EBV‐associated antigens in Chinese NPC patients were analysed according to length of survival after diagnosis and to disease stage. Geometric mean titres of ADLC antibody were highest in the long‐term survivors, whereas VCA, EA and EBNA antibody titres showed an inverse relationship to survival. High VCA, EA and EBNA titres were less frequent, and high ADLC titres were more frequent in long‐term survivors than in intermediate or short‐term survivors. The association of geometric mean titres of EBV antibodies with prognosis could not be entirely explained by stage of disease. A functional role for the ADLC antibody is suggested by the association of a high ADLC antibody titre with a good prognosis regardless of stage of disease.
Azathioprine‐induced lymphocytic neoplasms of NZB mice lack ecotropic murine leukaemia virus
Authors: Harvey Jennifer J. , East June , Katz Fay E. 
Published: February 2007

AbstractNZB mice injected intramuscularly throughout a 6‐month period with the immunosuppressant azathioprine (Imuran) developed lymphocytic lymphomas 6–7 months after treatment was initiated. These malignancies were quite distinct from the reticulum‐cell neoplasia which occurs spontaneously in the strain, and were readily transplantable to NZB or histocompatible BALB/c recipients. Xenotropic, but not ecotropic murine leukaemia virus (MuLV) was detected in leukaemic tissues of some donor and recipient NZBs when tested in vitro by co‐cultivation with permissive cell lines, genome rescue, XC and viral polymerase assays. Virus filtrates prepared from donor leukaemic tissues were non‐pathogenic when injected into newborn C3H mice. These results are evidence against a mandatory ecotropic MuLV genome in lymphocytic neoplasia.
A quantitative assay for tumor antigen based on inhibition of cytotoxicity of sensitized lymphocytes
Authors: Huber Sally , Lucas Zoltan J. 
Published: February 2007

AbstractSpecific inhibition of cell‐mediated cytotoxicity can be used as a quantitative measure of soluble tumor antigen if highly cytolytic cells are obtained. In vitro secondary stimulation of spleen cells sensitized in vivo to the syngeneic 13762A mammary adenocarcinoma results in a lymphocyte population consistently more cytolytic than lymphocytes after primary stimulation. Maximal cytolysis requires removal of dead lymphocytes from the effector population. Soluble tumor antigen (STA) is detected only in supernatant: of 13762A mammary tumor cultures grown in the presence of the proteolytic enzyme inhibitor, ε‐amino caproic acid. Soluble MTM antigen preparations block lymphocytes immune to the mammary tumor but not lymphocytes immune to a second mammary adenocarcinoma (R3230) or to allogeneic spleen cells. Soluble antigen preparations from other tumors do not inhibit lymphocytes specifically cytolytic to the 13762A tumor. Additional evidence that the STA preparation contains tumor antigen is its ability to induce specific cytolytic lymphocytes and partial protection from challenge with live MTA tumor cells.
Interactions of murine leukemia virus (MuLV) with isolated lymphocytes. Iv. The role of mitogen‐induced cellular dna synthesis in virus infection and replication
Authors: Cerny Jan , Isaak Dale D. 
Published: February 2007

AbstractThe requirement for lymphocyte activation with mitogen during in vitro infection with murlne leukemia virus (MuLV) of Friend virus complex (FV) and the suppressive effects of MuLV on mitogen‐induced lymphocyte activation were studied in short‐term suspension cultures. Lymphocytes were infected with FV in vitro and then resuspended in culture medium with or without mitogens. Cells releasing infectious MuLV were enumerated as infectious centers (IC) on sarcoma virus+, leukemia virus‐fibroblasts. The accumulation of IC in cultures followed a Diphasic curve characterized by a plateau between days 1 and 4 and by a 10‐fold increase in IC between days 5 and 7. Stimulation with a B‐cell mitogen, bacterial lipopolysaccharide (LPS), following infection increased the number of IC 10‐to 40‐fold. On the other hand, stimulation with concanavalin A (Con A), a T‐cell mitogen, did not appreciably increase the number of 1C detected on day 5 post infection. Further studies on the role of LPS‐induced DNA synthesis in the enhancement of MuLV replication revealed two points: (1) a comparable enhancement of 1C was observed In cultures stimulated with LPS 2 days prior to or immediately after FV infection and in those which were not stimulated until 2 days after infection; (2) treatment of FV‐infected, LPS‐stimulated lymphocytes with 5,6‐bromodeoxyuridine (BrdUrd) and visible light at 2 days abolished cellular DNA and RNA synthesis but did not diminish subsequent MuLV replication; however, cellular DNA and RNA synthesis as well as MuLV replication were inhibited in LPS‐stimulated cells treated with BrdUrd and light prior to infection with FV. The uptake of both [3H]thymidine and [14C]uridine by LPS‐stimulated lymphocytes was inhibited by about 50% in the presence of infectious FV whereas uptake in Con‐A‐stimulated lymphocytes was not inhibited. Kinetic studies showed that the inhibition of LPS stimulation was not detectable until 24 h and later; the uptake of [3H] thymidine during the first 12 h after infection and mitogen activation was the same in infected and non‐infected cultures. Collectively, the results indicate that MuLV‐Friend infects normal B cells but that the subsequent virus replication and secondary infection remain low unless the cells are activated with a mitogen. Virus replication, however, eventually become independent of cellular DNA synthesis and the virus itself inhibits the cellular nucleic acid synthesis at a later stage in the infection.
Effector and suppressor lymphoid cells in tumor‐bearing guinea‐pigs
Authors: Berczi I. , Sehon A. H. 
Published: February 2007

AbstractThe immune reaction of guinea‐pigs against their growing tumors was studied. Strain 13 guinea‐pigs were killed 2 weeks after SC implantation of the transplantable methylcholanthrene‐induced sarcoma (MC‐D), when the tumor was 2–3 cm In diameter. Spleen, lymph‐node, bone‐marrow and peripheral blood leukocytes (PBL), and subsets of spleen cells and PBL were mixed with lethal doses (105) of tumor cells and inoculated SC into normal recipients. Spleen, lymph‐node and bone‐marrow cells either enhanced or did not influence tumor growth, while PBL exerted a strong inhibitory effect. Normal spleen and normal PBL did not affect tumor growth. The spleen cells of tumor‐bearing animals were separated on nylon wool columns: the first fraction containing T cells was responsible for tumor enhancement, the second fraction containing predominantly non‐T (Ia+) cells inhibited tumor growth. Adherent cells had no effect. Similarly, after removal of T cells from the spleens with a specific rabbit antiserum or of non‐T cells plus a minor portion of T cells with an anti‐la serum (produced in strain 2 guinea‐pigs), the remaining cell population had, respectively, an inhibitory or an enhancing effect on tumor growth. By contrast, removal of either T or la+ cells from PBL eliminated their anti‐tumor effect. The major portion of splenic T cells formed EA rosettes. EA rosette‐positive cells were restricted to a minor portion of peripheral T lymphocytes. Thus, splenic and peripheral T cells from tumor‐bearing animals were different both functionally and according to their surface markers. It is hypothesized that Fc+ T cells are suppressors which are triggered by immune complexes.
Uninhibited growth and metastases of herpes simplex virus‐transformed cells in virus‐sensitized hosts
Authors: Hay Kathleen A. , Lausch Robert N. 
Published: February 2007

AbstractFour established tumour lines of hamster cells transformed by herpes simplex virus (HSV) but not shedding the virus were examined for continued expression of virus‐associated antigens. Hamster or rabbits, appropriately immunized to the tumour cells, produced virus‐neutralizing antibody. The serum titres were invariably low, suggesting that only small quantities of virion antigen were present in the cells. Hamsters sensitized to HSV and resistant to virulent virus challenge did not reject low numbers of tumour cells, nor was the incidence of lung metastases significantly reduced. Virus‐sensitized lymph‐node cells, readily cytotoxic for HSV‐infected hamster embryo fibroblasts, did not lyse any of three transformed lines tested in an 18‐h 51chromium release test. Animals that had their tumour excised demonstrated no or only modest resistance to tumour rechallenge. Thus, virus‐specific transplantation rejection antigen could not be detected in the HSV tumour lines although low levels of virus structural antigens were present.
Dissociation of anti‐tumor immune responses in rats immunized with solubilized tumor‐associated antigens from a methylcholanthrene‐induced fibrosarcoma
Authors: Minami Akio , Mizushima Yutaka , Takeichi Noritoshi , Hosokawa Masuo , Kobayashi Hiroshi 
Published: February 2007

AbstractSoluble tumor antigens were prepared from chemically‐induced rat fibrosarcoma KMT‐17 cells by various methods [Na‐deoxycholate (DOC), 3 M‐KCI extraction, and crude membrane preparations by mechanical disruption]. Soluble tumor antigens prepared by DOC extraction (DOC‐STA) could be detected by a radioisotopic footpad assay (FPA) and they showed the strongest antigenic activity in KMT‐17 immune rats. Anti‐tumor immune responses in rats previously immunized with DOC‐STA were measured by FPA, Winn assay, and transplantation resistance. Significant responses detected by the FPA and Winn assay were demonstrated in rats immunized with DOC‐STA. However, rats previously immunized with DOC‐STA showed a significant enhancement of tumor growth when challenged with KMT‐17 cells. This enhancement was specific for the tumor line used. Normal rats which received adoptive transfer of thymus and spleen cells from rats immunized with DOC‐STA produced specific enhancement of tumor growth as compared with non‐treated rats. Administration of cyclophosphamide before immunization with DOC‐STA abrogated the enhanced tumor growth in the host. These results suggest that immunization with soluble tumor antigens specifically enhanced tumor growth by the induction of immunosuppressor cells. Dissociation between the anti‐tumor immunity detected by the FPA and Winn assay and the enhanced tumor growth detected by transplantation resistance in rats immunized with DOC‐STA is discussed.
Age as a modifying factor of 7, 12‐dimethylbenz(a)‐anthracene‐induced mammary carcinogenesis in the lewis rat
Authors: Haslam Sandra Z. 
Published: February 2007

AbstractThe influence of age at DMBA administration on (1) susceptibility to mammary tumor development, (2) the proportion of tumors which are ovary‐dependent, and (3) the frequency of spontaneous tumor regression was examined in female Lewis rats between 25 and 200 days of age. Tumor development was monitored for a 12‐month period after carcinogen administration. Age at carcinogen administration affected (1) the number of tumors induced, (2) the latent period of tumor development, and (3) the number of tumors which regressed spontaneously. More tumors developed in young rats; however, a large fraction of these tumors regressed spontaneously. The frequency of spontaneous tumor regression was strongly age‐related, being highest in rats treated up to 70 or after 150 days of age. Mean latent period of development of tumors which regressed spontaneously (SRT) was significantly shorter than that of tumors which grew progressively (PGT). Furthermore, mean latent period of SRT development was significantly shorter in rats treated at 25 or 50 days of age. In contrast, all age‐groups were equally susceptible to the development of progressively growing tumors (PGT). PGT incidence, mean latent period of PGT development, mean numbers of PGT per PGT‐bearing rat and the relative proportion of PGT which were ovary‐dependent were similar for all age‐groups at the end of 12 months. These results indicate that, in the Lewis rat strain, age does not confer significant or permanent refractoriness. Furthermore, spontaneous tumor regression is a frequent and strongly age‐related phenomenon.
Influence of the mouse hepatitis virus (MHV) infection on the growth of human tumors in the athymic mouse
Authors: Kyriazis Andreas P. , Dipersio Linda , Michael J. Gabriel , Pesce Amadeo J. 
Published: February 2007

AbstractThe growth characteristics and histological appearance of tumors resulting from transplantation of the tumor lines HEp‐2 and SW480 into pathogen‐free and mouse hepatitis virus infected athymic mice were studied. Subcutaneous or intra‐peritoneal implantation 1 × 106 neoplastic cells into pathogen‐free animals resulted in tumor growth. Subcutaneous transplants grew locally, surrounded by a capsule of connective tissue. The fibrovascular stroma supporting the neoplastic tissue was minimal and infiltration of tumor capsule was observed. Intraperitoneal tumors grew in a multifocal pattern, were not encapsulated, showed marked invasiveness and metastasized. The same number of neoplastic cells (1×106) transplanted into hepatitis‐positive animals failed to develop into grossly visible tumors. When the number of transplanted cells was increased to 2×107, tumors appeared in a few animals. All tumors, regardless of the site of transplantation, were characterized by the presence of severe fibrohistiocytic reaction at the site of implantation that possibly influenced the tumor growth. No evidence supporting T‐cell‐mediated tumor rejection was observed. It is concluded that the state of health of the athymic mice is critical for the growth of human tumors and may account for the variations in reporting successful transplantation of such tumors in nude mice.
Neutralization of pseudotypes of vesicular stomatitis virus by sera from avian retrovirus‐infected hosts
Authors: Mandeville Rosemonde , Rohan Peter , Wainberg Mark A. 
Published: February 2007

AbstractWe investigated the capacity of lymphocytes and sera from chickens bearing tumors induced by avian sarcoma viruses (ASV) to interact with phenotypically mixed particles of vesicular stomatitis virus (VSV) and ASV. Immune chicken sera were able to specifically neutralize such VSV pseudotypes. This ability could be absorbed out, however, on purified preparations of avian retro‐viruses, suggesting that reactivity was primarily against avian retrovirus envelope components. Supernatant fluids containing phenotypically mixed particles were unable to stimulate division of lymphocytes of tumor‐bearing hosts, an ability possessed by culture fluids containing native ASV particles. Polyacrylamide gel analysis was unable to resolve any distinct pseudotype protein, which was not present in either of the parental virus types. Treatment with crude preparations of ultraviolet (UV)‐irradiated VSV pseudotype material did not afford immunity against subsequent challenge with live ASV.
A new virion precipitation test for oncovirus envelope antigens which detects common antigenic determinants in mammalian type‐C viruses and mason‐pfizer monkey virus
Authors: Altstein A. D. , Zakharova L. G. , Zhdanov V. M. 
Published: February 2007

AbstractA method for the study of oncovirus envelope antigens was developed, based on the precipitation of intact virions by a double antibody technique. The amount of precipitated virus was then measured as reverse transcriptase activity. The method was designated the virion precipitation test (VPT). It has been used for titration of antibodies to envelope antigens of oncoviruses. The study of envelop antigens of 11 different oncoviruses permitted their differentiation into the following groups: (1) murine type‐C viruses: (2) feline type‐C viruses; (3) simian type‐C viruses; (4) the RD‐114/BEV group; (5) Mason‐Pfizer monkey virus (M‐PMV); (6) bovine leukemia virus; (7) avian type‐C viruses; (8) mouse mammary tumor virus. No common antigenic determinants were detected in the last three groups. Mammalian type‐C viruses (RD‐114, NIH‐MuLV, G‐MuLV) had common antigenic determinants in the envelope, as demonstrated with an anti‐RD‐114 serum. Mammalian type‐C viruses also shared antigenic determinants with M‐PMV. The relationship of type‐C viruses to M‐PMV decreased in the follwoing order: RD‐114—NIH‐MuLV—G‐MuLV. It was also shown that the endogenous xenotropic feline RD‐114 virus was more closely related to xenotropic NIH‐MuLV than to ecotropic G‐MuLV. The nature of the common antigenic determinants, as demonstrated by VPT on the surface of mammalian type‐C viruses and M‐PMV, and their significance for the concept of oncovirus evolution are discussed.
Cell surface glycoprotein changes in Epstein‐Barr virus‐positive and ‐negative human hematopoietic cell lines
Authors: Van Beek Wim P. , Nilsson Kenneth , Klein George , Emmelot Peter 
Published: February 2007

AbstractIt has previously been shown that differential fucose labelling of many normal and homologous tumor cells, followed by proteolytic release and degradation, yields glycopeptides which upon gel filtration shown an increase in fast‐eluting glycopeptides for the tumor cells. This technique has now been applied to cell‐surface glycoproteins of different human hematopoietic cell lines. These lines included Epstein‐Barr virus (EBV)‐carrying lymphoblastoid cell lines of presumed non‐neoplastic origin, and malignant EBV‐genome‐positive Burkitt lymphoma and EBV‐negative non‐Burkitt lymphoma, leukemia and myeloma lines. As compared with normal peripheral lymphocytes, both the lymphoblastoid type of cell lines and the different types of lines of proven malignant ancestry contained the fast‐eluting glycopeptides on their cell surface with very few exceptions. It is therefore concluded that (I) malignant conversion of human lymphoid cells in vivo is commonly, but not obligatorily, associated with a specific change in the composition of the fucosyl glycopeptides, and (2) EBV infection of B lymphocytes does not lead only to the well‐documented immortalization in vitro but also, as a rule, to the same type of alteration in fucosyl glycopeptides as was demonstrated for the neoplastic cell lines. It proved possible to distinguish several categories of hematopoietic cell lines due to the effect that pretreatment of the glycopeptides with neuraminidase or mild acid exerted on their subsequent chromatographic behavior.
Moloney lymphoma cells express a polyprotein contanining the GAG gene‐coded p15 and the moloney leukemia virus‐induced cell surface antigen (MCSA)
Authors: Karande Anjali , Yefenof Eitan , Fenyö Eva Maria , Klein George 
Published: February 2007

AbstractThe relationship between MCSA and the viral structural proteins in YAC Moloney lymphoma cells was further investigated by using membrane immunofluorescence and immunoadsorbent columns. As previously observed, MCSA showed only minimal capping and thereby differed In behaviour from gp70, p30 and p12 virion antigens. Whereas antibody‐induced capping of gp70 did not change the membrane distribution of MCSA, co‐capping was observed between MCSA and p30 and p12 gag protein antigens. This indicated that, whereas MCSA is distinct from gp70, it is linked to p30 and p12 on the membrane of living cells. It was then attempted to isolate MCSA on anti‐p30 and anti‐pIS immunoadsorbent columns from solubilized YAC cells. Contrary to what was expected, no MCSA was bound to the anti‐p30 column. On the other hand, a part (10–15%) of the MCSA was bound to the anti‐pIS column, indicating that MCSA is linked to the gag p15.
Expression of Fv‐4r allele in hematopoietic cells from g mice resistant to friend leukemia virus
Authors: Ikeda Hidetoshi , Odaka Takeshi 
Published: February 2007

AbstractG mice carrying the Fv‐4 resistant allele supported virus growth neither at an early nor a later (Kai et al., 1976) stage of infection with NB‐tropic FLV. This resistance could not be abolished by treatment of G mice with cyclophosphamide or cortisone acetate. By bone‐marrow or spleen‐cell transplantation into irradiated mice, the resistance of G mice could be transferred to Fv‐4‐susceptible mice. Conversely, transfer of bone‐marrow or spleen cells of Fv‐4‐susceptible mice rendered G mice susceptible. It could be concluded that, as assessed by the virus content in the spleen, helper LLV grows mainly in radiosensitive, bone‐marrow‐derived cells, and the Fv‐4 gene is expressed in these cells.
Antiserum to murine leukemia virus recognizes novel cell surface molecules associated with growth control and transformation
Authors: Rieber Manuel , Rieber Mary , Alonso Mina 
Published: February 2007

AbstractAntiserum directed against murine leukemia virus also reacts with several external proteins present in rat cells transformed by a temperature‐sensitive Rous sarcoma virus. Reaction of iodinated cell extracts with anti‐MLV (murine leukemia virus) serum revealed the presence of a 200,000 dalton iodinated component detectable also by metabolic labelling with glucosamine only in serum‐starved cultures restricted in the expression of transformation. A similar assay with iodinated cells that express the transformed phenotype revealed the preferential recognition of two components with an approximate molecular weight of 100,000 daltons as well as an additional 65,000‐dalton external component. Growth of the transformed non‐producer NT3‐KR cells in the presence of inducers of C‐type viruses leads to an increased synthesis of a 100,000‐dalton glycoprotein (gp100) recognized by the anti‐MLV serum, which is also recognized by the antiserum in NRK‐MSV‐MLV transformed producer cells, in addition to a virus‐like glycoprotein of 71,000 dalton (gp71). Absorption of the anti‐MLV serum with monolayers of NT3‐KR cells eliminated the ability of the serum to recognize the gplOO but not the gp71 from NRK‐MSV‐MLV‐transformed producer cells. The mediation of post‐translational changes in growth control is suggested by the transformation‐dependent alteration in the molecular weight of the non‐virion surface proteins recognized by anti‐MLV serum in the rat cells used in this study.