bluuebunny/crossref_metadata_2025_split huggingface dataset:
Kinetics of the anti‐tumor delayed hypersensitivity response in mice with progressively growing tumors: Stimulation followed by specific suppression
Authors: Paranjpe Meera S. , Boone Charles W. 
Published: February 2007

AbstractAt various times during the progressive growth of transplanted SV40 and methylcholanthrene fibrosarcomas in mice the delayed hypersensitivity (DH) response to tumor cells was determined using a quantitative radioisotopic foot‐pad assay. For the first 7 days a close correlation was found between tumor size and the degree of DH reactivity. After this time, as the tumor grew larger, the DH response declined to non‐detectable levels. Following excision of the tumors the DH response returned to a high level. This suppression, or “eclipse”, of the anti‐tumor cellular immune response in animals bearing tumors beyond a certain size was specific for the types of tumor used. The spleen lymphocytes from unresponsive tumor‐bearing mice still supported a positive DH reaction when mixed with tumor cells and injected into the foot‐pads of normal mice.
Oncornavirus‐like particles in HeLa cells. II. Immunological characterization of the virus
Authors: Bauer Heinz , Daams Johan Hendrik , Watson Kenneth F. , Mölling Karin , Gelderblom Hans , Schäfer Werner 
Published: February 2007

AbstractAn oncornavirus‐like agent has been described in HeLa cells of human origin (Gelderblom et al., 1974). The investigation of its protein constituents revealed a pattern similar to but different from that of known oncornaviruses. Six polypeptides with molecular weights (mw) between 12,000 d and 28,000 d, and two glycopolypeptides of about 60,000 d and 80,000 d mw were detected by SDS‐polyacrylamide gel electrophoresis. No serological cross‐reaction was found between the HeLa virus and B‐ and C‐type oncornaviruses. Essentially, none of two interspecies‐specific antigenic determinants described in mammalian C‐type viruses has been detected in the HeLa virus. However a distinct serological relationship was found between the HeLa virus and the Mason‐Pfizer monkey virus in that these viruses share at least two antigens in the mw range of 16,000 d and 28,000 d, respectively. These results confirm the electron microscopic data described before (Gelderblom et al., 1974) and extend the evidence for a new group of oncornavirus‐like particles.
The importance of dose and proliferation of sv40‐transformed cells with different oncogenic potentials to the level of tumor immunity
Authors: Stillström J. 
Published: February 2007

AbstractThe immunizing effects of syngeneic SV40‐transformed mouse embryo cells derived from a cloned line, ME1 C9, were studied. The number of initially inoculated cells was of decisive importance for immunization when both irradiated and non‐irradiated (proliferative) cells were used. The 50% immunizing dose (ImD50) of highly oncogenic ME1 C9‐V15 cells against a weak challenge 3 weeks after immunization was found to be 104.1 irradiated or 102.7 non‐irradiated cells. Doses just below the ImD50 suppressed immunity; 104 irradiated cells had a tumor‐enhancing effect 3 weeks after but not 10 weeks after inoculation and 102 non‐irradiated cells did not significantly immunize until 6 weeks after inoculation, in spite of growing tumors. An immune state was reached more rapidly after resection of tumors induced by 102 cells, even when resections were performed at a time when the animals were still non‐immune. The immune suppression induced by a low dose of non‐irradiated (proliferating) cells seemed to be perpetuated and 10 weeks after inoculation there was still an immune deficit in comparison with the state of immunity in animals which had had their tumors resected. A second inoculation of a regularly non‐immunizing dose of 101‐102 cells 3 weeks after inoculation of 102 ME1 C9‐V15 cells enhanced the tumor incidence of the first inoculated cells. After inoculation of 105 irradiated or non‐irradiated ME1 C9‐V15 cells a one thousand‐fold increase in tumor resistance was obtained within 3 weeks. Before reaching a size of 12 mm the tumor mass did not affect the level of immunity in animals inoculated with ME1 C9‐V15 cells. Tumor resections 3 weeks after inoculation of 105 cells preserved the otherwise declining immunity. The ImD50s of weakly oncogenic (TPD50 > 105) and highly oncogenic (TPD50 < 104) non‐irradiated cells in irradiated animals against a weak challenge 10 weeks after immunization were 102.6 and 101.5 cells, respectively, measured in tumor‐free animals. Immunization doses of 101‐102 weakly oncogenic cells, i.e. below the ImD50, enhanced challenge tumor takes. Non‐tumor‐bearing animals inoculated with weakly oncogenic cells were less immune than non‐tumor‐bearing animals inoculated with highly oncogenic cells, when animals inoculated with equal numbers of cells or animals inoculated with greater than immunizing doses were compared. Animals with tumors induced by weakly oncogenic cells were less immune than animals with tumors of comparable size induced by highly oncogenic cells. The critical tumor size at which immunity against 105 ME1 C9‐V15 cells was broken was 11–12 mm for highly oncogenic and less than 4 mm for weakly oncogenic cells.
Malignant transformation in vitro of mouse fibroblasts by 7, 12‐dimethylbenz(A)anthracene and 7‐hydroxymethylbenz(A)anthracene and by their K‐region derivatives
Authors: Marquardt H. , Sodergren J. E. , Sims P. , Grover P. L. 
Published: February 2007

AbstractK‐region epoxides derived from 7, 12‐dimethylbenz(a)anthracene and from 7‐hydroxymethlybenz(a)anthracene were tested for their ability to induce malignant transformation of the M2 clone of fibroblasts derived from C3H mouse prostate. The parent hydrocarbons, the corresponding K‐region dihydrodiols and a phenol were also tested with these cells. The K‐region epoxides induced transformation but were somewhat less active than the hydrocarbons; the ring‐hydroxylated derivatives were inactive. In other experiments, the addition of α‐naphthoflavone was found to inhibit the formation of water‐soluble metabolites from and the toxicity of 7, 12‐dimethylbenz(a)anthracene without affecting malignant transformation. The results are discussed in relation to current theories regarding the metabolic activation of polycyclic hydrocarbons.
EB virus‐associated antibodies in caucasian patients with carcinoma OE the nasopharynx and in long‐term survivors after treatment
Authors: de Schryver André , Klein George , Henle Werner , Henle Gertrude 
Published: February 2007

AbstractSera from 30 Swedish patients with nasopharyngeal carcinoma (NPC) collected before or shortly after commencement of therapy and from 24 long‐term survivors (LTS) were tested for antibodies to Epstein‐Barr virus (EBV) capsid antigens (VCA), to the O and R components of the EBV‐induced early antigen (EA) complex, and to EBV‐determined cell membrane antigens (MA). In the tumor‐bearing patients, all serologic reactivities increased overall from stage I to later stages of the disease: that is, with an increase in total tumor burden. In the LTS, who had remained apparently tumor‐free for 3 to 29 years, all reactivities were substantially lower than in the tumor‐bearing patients. While the data agreed in principle with those reported previously for Chinese NPC patients, there were considerable differences with respect to the incidence and titres of antibodies to the D component which, as discussed, might reflect a reduced responsiveness of Caucasian NPC patients or a difference in the distribution of various types of the disease among ethnic groups.
Cell‐mediated mutagenesis of mammalian cells with chemical carcinogens
Authors: Huberman Eliezer , Sachs Leo 
Published: February 2007

AbstractChemically non‐reactive carcinogens, such as polycyclic hydrocarbons, have to be metabolized by cellular enzymes in order to exert their biological effects including mutagenicity. Chinese hamster V79 cells can be efficiently mutated from 8‐azaguanine susceptibility to resistance by N‐methyl‐N‐nitro‐N‐nitrosoguanidine. But these cells do not metabolize polycyclic hydrocarbons and were therefore not mutated by these compounds. A system of cell‐mediated mutagenesis with carcinogenic hydrocarbons has been developed, by co‐cultivating V79 cells with lethally irradiated rodent cells that can metabolize the carcinogens. The number of mutations was dependent on the number of metabolizing cells and the carcinogens were not mutagenic when V79 cells were co‐cultivated with non‐metabolizing cells. Inhibition of the hydrocarbon metabolizing enzymes by 7,8‐benzoflavone, inhibited mutagenicity. Cell‐mediated mutagenicity was obtained with the carcinogenic hydrocarbons 7,12‐dimethylbenz (a)anthracene, benzo(a)pyrene and 3‐methylcholanthrene and there was no mutagenicity with the non‐carcinogenic hydrocarbon benz(a)anthracene. The degree of mutagenicity was related to the degree of carcinogenicity and the method detected mutagenicity with 0.1μg/ml. It is suggested that cell‐mediated mutagenesis with human cells should provide a useful system to test for environmental chemicals hazardous to humans that have to be metabolically activated.
Comparison of EBV neutralization tests based on abortive infection or transformation of lymphoid cells and their relation to membrane reactive antibodies (anti‐MA)
Authors: de Schryver André , Klein George , Hewetson John , Rocchi Giovanni , Henle Werner , Henle Gertrude , Moss Denis J. , Pope John H. 
Published: February 2007

AbstractEpstein‐Barr virus (EBV)‐neutralizing (N) antibodies were determined in human sera by three techniques based on (1) early antigen (EA) synthesis in lymphoblasts (NEA); (2) inhibition of colony formation by lymphoblasts (NICF); and (3) cordblood lymphocyte transformation (NLT). A good correlation was noted between the NEA and NICF titres of 41 sera so tested (r = 0.73). The correlation between NEA or NICF and NLT titres was less pronounced (r = 0.54 and 0.56), possibly because only 22 sera were tested by the last method. Limited to concordant sera, i.e. sera with either both high or both low titres of antibodies to EB viral capsid antigens (VCA) and to EBV‐determined cell membrane antigens (MA), the N titres determined by the three methods showed a good correlation with anti‐MA titres (r = 0.83, 0.80 and 0.68, respectively) as did the few discordant sera with high anti‐MA but low anti‐VCA titres. However, some discordant sera with low anti‐MA and high anti‐VCA titres also showed substantial N titres. The mean anti‐VCA titres were equal in the concordant and discordant groups (553), the anti‐MA (BT) titres were 25 and ⩽ 1.4, respectively, whereas the neutralization titres were 209 (NEA), 204 (NICF) and 523 (NLT) in the concordant, as compared to 128, 74 and 99 in the discordant group. These findings support the view that lymphoblast transformation and EA induction and inhibition of lymphoblast colony formation are induced by the same type of viral particle.
Epstein‐barr virus: Transformation of non‐human primate lymphocytes in vitro
Authors: Falk Lawrence , Wolfe Lauren , Deinhardt Friedrich , Paciga June , Dombos Laszlo , Klein George , Henle Werner , Henle Gertrude 
Published: February 2007

AbstractContinuous lymphoblastoid cell cultures were established from marmoset (Saguinus sp.), squirrel (Saimiri sciureus), owl (Aotus trivirgatus) and cebus (Cebus apella) monkeys after culturing their peripheral lymphocytes with lethally X‐irradiated cells carrying Epstein‐Barr virus (EBV). Transformation also was achieved by exposing simian lymphocytes to infectious, cell‐free EBV derived from the simian lymphoblastoid cell cultures. Simian lymphocytes were not transformed after exposure to cell‐free EBV derived from HR‐1 cells. The simian cell cultures were similar to cell cultures derived from Burkitt's lymphoma or infectious mononucleosis patients. EBV‐induced early, viral capsid and membrane antigens, intranuclear inclusion bodies and herpesvirus virions were demonstrable in most cultures. Seven cultures were insusceptible to superinfection with EBV and treatment of the cultures with halogenated pyrimidines was relatively ineffective for inducing synthesis of early or viral capsid antigens. All cell cultures had B‐cell characteristics: they produced immunoglobulins but did not form spontaneous rosettes with sheep erythrocytes. Four of six marmoset monkeys, inoculated with EBV‐transformed marmoset lymphocytes, developed antibodies to EB viral capsid antigens and one marmoset inoculated with autochthonous transformed cells also developed heterophile antibodies. Seven marmosets, inoculated with cell‐free EBV derived from HR‐1 cell cultures, developed no detectable levels of antibodies to EBV‐specified antigens or heterophile antibodies. No overt clinical abnormalities were detected in any of the marmosets inoculated with HR‐1 or Kaplan EBV but one of five marmosets inoculated with B95hyphen;8 EBV developed a lymphoma.
Characteristics of murine C‐type viruses. IV. The virus produced by ehrlich tumor cells and its hybrids with mouse L cells
Authors: Grundner Gertrud , Fenyö Eva Maria , Klein Eva 
Published: February 2007

AbstractThe infectious properties of viruses produced by Ehrlich tumor cells (E), the A9 subline of mouse L cells (L), their hybrids (EL0 and EL) and high‐malignant sublines of the low‐malignant hybrid line (ELm) were investigated. The infectivity assays were antigen induction on JLS‐V9 cells, antigenic conversion and focus induction on S + L ‐ cells (D56 subline) and focus formation on BALB/3T3 cells. The E and L viruses, produced by the parental cells, were detected in the JLS‐V9 test but were distinguished in S + L ‐ and BALB/3T3 cells. The L virus was focus‐positive, the E virus focus‐negative (BALB/3T3). For antigenic conversion, the L virus was negative and the E virus positive (D56). The hybrid cell line, tested on several occasions after the hydridization event, produced viruses with characteristics similar to both E and L viruses, regardless of the complete or reduced chromosome numbers. The malignant sublines selected from the hybrid showed preferential loss of the A9 parent‐derived biarmed chromosomes. One of these lines produced virus (ELm) with infective properties similar to those of the E virus. This suggests that the virus produced by a particular cell line is determined by the cell genome. Another malignant subline was found to be negative for production of infectious virus in all three indicator systems.
Neoantigens on spontaneous and carcinogen‐induced rat tumours defined by in vitro lymphocytotoxicity assays
Authors: Baldwin R. W. , Embleton M. J. 
Published: February 2007

AbstractLymph‐node cells from rats bearing tumours apparently lacking in tumour rejection antigens were cytotoxic in vitro for cultured tumour cells. The specificities of these reactions differed, however, from those demonstrated with immunogenic chemically‐induced rat tumours since cross‐reactivity was observed, especially between tumours of the same histological type. This was most clearly demonstrated in tests with rat mammary carcinomas where tumour‐bearer lymph‐node cells were cytotoxic for a range of mammary carcinomas including spontaneously arising and chemically‐induced tumours. The reactivities of tumour‐bearer lymph‐node cells could be blocked by pre‐treating target cells with serum of tumour‐bearing rats and also by sera of multiparous rats. Conversely, tumour‐bearer sera were highly effective in blocking embryo cells from attack by sensitized LNC from multiparous rats. The results suggest that antigens detected on these tumours by the in vitro assay were embryonic components which were immunogenic in the tumor‐bearing host, although they were not capable of inducing tumour‐rejection reactions in immunized rats.
In vitro inhibition of tumour cell growth and DNA synthesis by peritoneal and lung macrophages from mice injected with corynebacterium parvum
Authors: Olivotto M. , Bomford R. 
Published: February 2007

AbstractPeritoneal and lung macrophages from CBA mice injected with Corynebacterium parvum were tested for in vitro inhibition of growth and DNA synthesis of syngeneic tumour cells. Peritoneal macrophages inhibited the growth of RI leukaemia cells, and the DNA synthesis of RI leukaemia and T3 fibrosarcoma cells. Maximum inhibition of DNA synthesis was at 5 days after C. parvum injection. Inhibition was most effective when contact between macrophages and target cells was allowed, since medium from macrophage cultures was only slightly inhibitory. Macrophages maintained alone in culture for 48 h lost their ability to inhibit RI cell DNA synthesis. Lung macrophages inhibited the DNA synthesis of RI cells most effectively 14 days after C. parvum injection.
A bank of frozen peripheral blood lymphocytes for In vitro immunological studies on east African cancer patients
Authors: Steel C. M. , Levin A. G. , Tsu T. , Gross R. L. 
Published: February 2007

AbstractA bank of peripheral blood lymphocytes, frozen in liquid nitrogen, has been established from East African cancer patients and from control donors including healthy individuals and patients with non‐malignant disorders. The techniques of collection, lymphocyte separation and cell freezing are simple enough to have been applied successfully in an isolated mission hospital. In the first year of operation samples have been stored from over 400 individuals. On recovery, the cells have high viability, will respond to PHA in culture, are suitable for determination of HL‐A phenotype and react with sheep red blood cells in the spontaneous rosette test. It is predicted that lymphocyte banks of this type will have a useful place in the study of immunological factors in cancer, particularly in developing countries.
Ethylhydrazine hydrochloride as a tumor inducer in mice
Authors: Shimizu Hidesuke , Nagel Donald , Toth Bela 
Published: February 2007

AbstractThe lifetime administration of 0.0125% ethylhydrazine hydrochloride in drinking water to randomly bred Swiss mice, beginning at 7 weeks of age, induced tumors of the lungs and blood vessels. Eighty‐eight percent of the treated females and 62% of the treated males developed lung tumors, whereas among the controls, the incidence was 21% in the females and 23% in the males. In addition, the incidence of blood‐vessel tumors rose from 5 to 60% in the females and from 6 to 16% in the males, as compared with the controls. The gross and light microscopic investigation of the tumors showed adenomas and adenocarcinomas of the lungs and angiomas and angiosarcomas of the blood vessels of characteristic appearance. This investigation proves for the first time the tumorigenicity of this chemical. The environmental significance of hydrazine derivatives is discussed in the light of the obtained results.
Rat α1F. XI. Immunological control of cell proliferation: Increased growth rate and α1F production by morris hepatoma 5123tc in rats treated with anti‐thymocyte serum
Authors: Bernstein P. , Wepsic H. T. , Sell S. 
Published: February 2007

AbstractThe administration of anti‐thymocyte serum (ATS) to rats bearing transplantable Morris hepatoma 5123tc resulted in an increase in the growth rate of the tumor and in the rate of alpha1fetoprotein (α1F) production by the tumor. ATS‐treated rats not only had faster growing tumors and correspondingly higher serum α1F concentrations than untreated 5123tc tumor‐bearing rats, but also the amount of α1F per gram of tumor tissue was significantly greater. In addition, the mitotic index of tumors in ATS‐treated animals was twice that of the tumors in control animals. The results indicate that the rate of α1Fa production by hepatomas that have the capacity to synthetize α1Fa is directly related to the number of proliferating cells present at any given time. In addition, this report clearly demonstrates that the rate of growth of a tumor is not a fixed property of the tumor but may be accelerated by immunosuppression of the tumor‐bearing animal.
Reduced transplantability of syngeneic tumors in rats immunized with allogeneic tumors
Authors: Kobayashi Hiroshi , Gotohda Eiki , Kuzumaki Noboru , Takeichi Noritoshi , Hosokawa Masuo , Kodama Tadao 
Published: February 2007

AbstractThe growth of transplanted syngeneic tumors in Wistar/KA (WKA) rats was inhibited by three immunizations with tumors from allogeneic Donryu rats which possibly are unrelated antigenically. Inhibition of syngeneic tumor growth was not associated with the source or type of the tumors (carcinoma and sarcoma) used. A slight inhibition was also observed in rats immunized with a large amount of xenogeneic tumor or allogeneic normal spleen, liver and kidney cells. Inhibition was also observed after immunization with syngeneic tumors artificially infected with murine leukemia virus. However, the inhibition was strongest in rats immunized with allogeneic tumors. The mechanism of inhibition may be immunological, and it may be associated with an increase in the non‐specific immunity of the host.
Immunosuppressive and immunostimulatory factors produced by malignant cells In vitro
Authors: Wong Alfred , Mankovitz Ralph , Kennedy James C. 
Published: February 2007

AbstractThe addition of small numbers of irradiated mouse fibrosarcoma cells to cultures containing syngeneic mouse spleen cells and sheep erythrocytes resulted in almost complete inhibition of the expected anti‐sheep hemolytic plaque‐forming cell responses; the addition of even smaller numbers resulted in stimulation rather than inhibition. This same pattern was reproduced when various other types of syngeneic or allogeneic malignant cells were tested under similar conditions; the presence of strong (H‐2) histocompatibility differences had no apparent effect. Metabolically active irradiated malignant cells were required to produce inhibition; dying cells or soluble extracts of cells were ineffective. However, serum‐free supernatants from healthy cultures of non‐irradiated fibrosarcoma cells were found to be inhibitory at high concentrations and stimulatory at low concentrations, in a pattern similar to that found when intact irradiated fibrosarcoma cells were used. High‐speed centrifugation of such supernatants sedimented the stimulatory material but left the inhibitory material in solution. When syngeneic fetal fibroblasts were substituted for the fibrosarcoma cells, it was found that both the intact fibroblasts and their culture supernatants were stimulatory, and that the stimulatory material could be sedimented as before by high‐speed centrifugation. However, very little inhibitory effect was produced by either intact fibroblasts or their culture supernatants, except when unusually high concentrations were used. It is concluded that at least some types of healthy malignant cells release soluble material capable of inhibiting immune responses: their non‐malignant counterparts produce little if any inhibitor.
Virus‐augmented tumor transplantation antigens: Evidence for a helper antigen mechanism
Authors: Boone Charles W. , Paranjpe Meera , Orme Thomas , Gillette Ronald 
Published: February 2007

AbstractWhile the homogenate of a transplantable SV40‐transformed fibrosarcoma of BALB/c mice was without tumor transplantation antigen (TTA) activity, a homogenate of the same tumor cells after infection with influenza virus or vesicular stomatitis virus retained TTA activity to a degree approaching that of whole cells. Ultraviolet inactivation of the virus in the homogenate did not affect its TTA activity. Strong evidence for a helper antigen mechanism was provided by two findings: (1) Mice made tolerant to influenza virus could no longer be made tumor‐immune with the virus‐infected tumor homogenate, and (2) priming mice with three weekly injections of egg‐grown influenza virus abrogated the ability of the virus‐infected tumor homogenate to produce tumor immunity when it was given during the fourth week. Although tumor‐cell homogenates would not induce tumor immunity, they would elicit a delayed hypersensitivity reaction in the foot pad. A working hypothesis that correlates all of the findings is proposed.