bluuebunny/crossref_metadata_2025_split huggingface dataset:
Epstein‐barr virus‐specific antibodies in patients with adult T‐cell leukemia (ATL) and healthy ATL virus‐carriers
Authors: Imai Joko , Hinuma Yorio 
Published: February 2007

AbstractAntibodies to Epstein‐Barr virus (EBV)‐capsid antigen (VCA), early antigen (EA) and EBV‐associated nuclear antigen (EBNA) in the sera of 103 patients with adult T‐cell leukemia (ATL) and the sera of 243 age‐ and sex‐matched healthy adults, namely 99 anti‐ATLA‐positive (antibodies to ATL virus‐associated antigen) and 144 anti‐ATLA‐negative individuals, were determined by indirect immunofluorescence. The anti‐VCA titers in the sera from ATL patients were within the range observed in healthy controls. Anti‐EA was found in 27% of the sera from ATL patients, but in only 8% of the sera from anti‐ATLA‐negative healthy controls. Antibodies to EBNA, which were present in almost all healthy adults, were not found in 30% of the sera from ATL patients. Of the sera of anti‐ATLA‐positive healthy adult donors 11% were negative for EBNA antibody. These results suggest that functional impairment of the T‐cell system in most ATL patients, and also to a lesser extent in anti‐ATLA‐positive adults who might be healthy ATLV‐carriers, may cause an unusual immune response of antibodies to EBV‐associated antigens.
Seasonal variation in the junctional component of pigmented naevi
Authors: Holman C. D. J. , Heenan P. J. , Caruso V. , Glancy R. J. , Armstrong B. K. 
Published: February 2007

AbstractFrom an assessment of the presence of a junctional component in 8,380 pigmented naevi, and histological review of its extent and the presence of inflammation and regression in a sample of 216 junctional and compound naevi, it was determined that naevi excised in summer were more likely to have a junctional component and evidence of inflammatory response than those excised in winter. It is suggested that a short‐term promotional effect of sunlight on cells in the junctional zone of pigmented naevi may, in addition to increased case ascertainment in summer, explain reported seasonal variation in the incidence of malignant melanoma.
Immunodepression by the oncogen does not determine the relationship between tumor latency and immunogenicity
Authors: Prehn Richmond T. , Karcher Christine A. 
Published: February 2007

AbstractImmunogenic and non‐immunogenic tumor implants were made at varying intervals after administration of an oncogenic dose of 3‐methylcholanthrene to mice. The length of the interval did not detectably influence the growth of the implants, suggesting that immunodepression by the oncogen is probably not the cause of the relationship between the latencies and the immunogenicities of hydrocarbon‐induced tumors.
Effects of several species of human leukocyte interferon on cytotoxic activity of NK cells and monocytes
Authors: Ortaldo John R. , Mantovani Alberto , Hobbs Donna , Rubinstein Menachem , Pestka Sidney , Herberman Ronald B. 
Published: February 2007

AbstractTen species of purified human leukocyte interferon were tested for their ability to modulate the cytolytic activity of natural killer (NK) cells and the cytolytic and cytostatic activities of monocytes. The interferon species were tested at several antiviral tilers and examined for quantitative differences in their ability to modulate immunological function. At the higher doses of interferon (i.e., >500 units) all of the interferon species demonstrated significant augmentation of cytolysis and cytostasis. However, when low levels (i.e., 10‐50 units) of interferon were emplpyed, appreciable differences between the various interferon species were seen. A similar pattern of relative potency among the various species of pure leukocyte interferon was seen for augmentation of cytolysis by monocytes and NK cells. In contrast, a different pattern of relative potency was observed for augmentation of cytostasis. These results demonstrated substantial quantitative differences (as much as 100‐fold) in the ability of the various species of human leukocyte inperferon to induce significant levels of augmentation of these cellmediated functions. Such results should have significant impact in choosing a specific interferon species for appropriate clinical trials.
Natural killer cell activity during mouse hepatitis virus infection: Response in the absence of interferon
Authors: Stohlman Stephen A. , Brayton Peter R. , Harmon Richard C. , Stevenson Douglas , Ganges Roland G. , Matsushima Glenn K. 
Published: February 2007

AbstractThe ability of the JHM3 strain of mouse hepatitis virus (MHV) to induce natural killer (NK) cells was examined. Infection of C57BU6 (86) mice with this virus resulted in the augmentation of natural cytotoxicity against YAC‐I target cells in the absence of a detectable interferon response. The cells responsible for this increased cytotoxicity were sensitive to complement‐mediated lysis with an anti‐Q‐5 reagent but not with a Thy 1.2 antiserum, indicating that they possess an NK‐like surface phenotype. Although variation in the NK response of individual B6 mice following JHM virus infection was found, even the animal with the most responsive NK cell population had no detectable interferon in the spleen. This finding contrasted with observations with an unrelated virus (lymphocytic choriomeningitis virus) and a serologically related strain of MHV. Infection with both of these viruses induced augmented NK cell activity and interferon responses. In addition, we found that neither the ability to mount an augmented NK cell response nor preferential lysis of virus‐infected targets correlated with resistance or susceptibility to JHM virus infection.
The presence of p53 transformation‐related protein in Ab‐MuLV transformed cells is required for their development into lethal tumors in mice
Authors: Rotter Varda , Abutbul Haya , Wolf David 
Published: February 2007

Abstractp53, a cellular‐encoded protein, is synthesized at elevated levels in a wide range of tumor cells. Ab‐MuLV‐transformed cells expressing both the viral‐encoded p120 oncogene and the cellular‐encoded p53 display a lethal tumor phenotype in syngeneic mice. L12 is an exceptional Ab‐MuLV‐transformed cell line that expresses the p120 oncogene and lacks the p53 cellular protein. Injection of L12 cells into syngeneic mice is followed by the development of local tumors that are subsequently rejected. Prolonged treatment of L12 cells with TPA, a tumor cell promoter, gave rise to L12T cells that synthesize the p53 protein and exhibit a lethal tumor phenotype. Comparison of one‐dimensional proteolytic partial peptide map of p53 obtained from L12T to that obtained from other Ab‐MuLV‐transformed cell lines confirmed their identity. These results suggest a correlation between the cellular expression of p53 in Ab‐MuLV‐transformed cells and their capacity to develop into lethal tumors in syngeneic mice.
Genetic control of the organ specificity of lymphoproliferative disease virus (LPDV) of Turkeys
Authors: Gazit Arnona , Yantv Abraham , Ilani Aviva , Ianconescu Marius , Perk Kalman , Zimber Amatzia 
Published: February 2007

AbstractIn a previous study based on the kinetics of virus replication and tumor formation (Gazit et al., 1982), it was shown that the organotropism of lymphoproliferative disease virus (LPDV) is confined to lymphoid tissues. The present paper demonstrates that this organ specificity is controlled at the level of infection and integration, that is, the lymphoid organs, which are the only organs sustaining virus replication, and also the only organs in whose cells integrated LPDV proviruses are detectable. At the same time, the efficiency of virus replication within the various target organs is regulated both at the level of infection and integration and at the level of viral gene transcription.
The mechanism of augmentation of natural killer cell activity by syngeneic tumor cells: Role of macrophage‐derived factor in NK boosting
Authors: Kawase Ichiro , Urdal David L. , Newman Walter , Henney Christopher S. 
Published: February 2007

AbstractThe role of natural killer (NK) cells in controlling tumor growth was investigated using an NK‐susceptible (cl27v‐IC2) and an NK‐insusceptible (c127av) subline of the lymphoma L5178Y. Syngeneic DBA/2 mice inoculated intraperitoneally with c127v‐IC2 tumor cells survived significantly longer than did c127av‐bearing mice. Similarly, c127v‐IC2, but not c127av tumor cells, were found to augment NK activity of spleen and peritoneal exudate cells in both DBA/2 and BALB/c nu/numice when inoculated into the peritoneal cavity. C127v‐IC2 tumor cells incubated with either DBA/2 or BALB/c nu/nu spleen cells in vitro boosted NK activity and induced the production of gamma‐type interferon (IFN), whereas incubation with c127av tumor cells induced neither NK activity nor IFN. Two kinds of cells cooperated in the production of IFN in response to c127v‐IC2 tumor cells, namely, cells which were nonadherent, bore asialo‐GM1, NK‐1.2 and a low level of Thy‐1.2 antigen and thus closely resembled NK cells, and those which were adherent and phagocytic and lacked both asialo‐GM1, and NK‐1.2 markers, presumably macrophages. Further analysis strongly suggested that c127‐v‐IC2 tumor cells stimulate macrophages to produce factor(s) which can induce the production of IFN by NK cells. The induced IFN was shown to be of the gamma type by its lability at ph 2.0 and insusceptibility to anti‐IFNα,β serum. This suggests a novel pathway for NK cell activation, and strongly supports the importance of macrophages and NK cells in natural resistance against certain tumors.
Selective inhibition by monosaccharides of tumor cell cytotoxicity mediated by mouse macrophages, macrophage‐like cell lines, and natural killer cells
Authors: Brunda Michael J. , Wiltrout Robert H. , Holden Howard T. , Varesio Luigi 
Published: February 2007

AbstractA series of monosaccharides were tested for their ability to inhibit the effector phase of macrophage‐mediated cytolysis against two susceptible murine tumor target cells, L5I78Y and RL♂I. Two monosaccharides, D‐mannose and N‐acetyl‐D‐galactosamine, were found to decrease cytotoxicity consistently in a dose‐dependent manner. However, D‐mannose preferentially inhibited lysis of RL♂I target cells with little effect on lysis of L5I78Y target cells, while the reverse was found with N‐acetyl‐D‐galactosamine. Neither monosaccharide interfered with the activation of macrophages by polyinosinic:polycytidylic acid. Natural killer cell activity was decreased by a 25 mM concentration of D‐mannose but not by N‐acetyl‐D‐galactosamine, although increasing concentrations of N‐acetyl‐D‐galactosamine were inhibitory. Neither monosaccharide affected cytotoxicity by alloimmune T cells. Cytotoxicity of macrophage‐like cell lines against tumor target cells was also decreased by monosaccharides but the pattern of inhibition was different from that seen with activated macrophage effector cells. Both D‐mannose and N‐acetyl‐D‐galactosamine inhibited glucose oxidation by activated macrophages but only D‐mannose significantly decreased protein synthesis of activated macrophages. These results indicate that monosaccharides can inhibit macrophage‐mediated cytotoxicity in a selective manner with the pattern dependent on the tumor target cell used in the assay.
Dietary habits and lung cancer risk
Authors: Kvåle Gunnar , Bjelke Erik , Gart John J. 
Published: February 2007

AbstractA previously reported negative association between a high index of dietary vitamin A and lung cancer incidence was confirmed in an extended follow‐up, covering 11 1/2 years, of 13,785 men and 2,928 women. Responses to a postal questionnaire provided the dietary information. Relationships between the major dietary items and lung cancer were explored for various diagnostic subsets of the 168 lung cancer cases diagnosed among the study subjects. Analyses were stratified for sex, age, residence characteristics, cigarette smoking and, at times, socioeconomic group. Although the data do not permit a firm interpretation in terms of risk enhancement by a marginal retinoid deficiency, we found that the apparent protection afforded by higher intakes of vitamin A or its provitamins was particularly strong for lung cancer appearing as squamous‐cell carcinoma and among those with higher alcohol intakes. The individual food items which showed the strongest negative association with lung cancer were carrots and milk. These two items made a major contribution to the vitamin A index and its variation among the respondents.
Mortality patterns among embalmers
Authors: Walrath Judy , Fraumeni Joseph F. 
Published: February 2007

AbstractIn view of recent findings of nasal cancer in rats exposed to formaldehyde vapors, we investigated the proportionate mortality experience of embalmers licensed to practice in New York State. Mortality was significantly elevated for cancers of the skin and colon and for arterio‐sclerotic heart disease, whereas significant deficits were seen in mortality from respiratory diseases and accidents. Respiratory cancer mortality was not excessive and no deaths were attributed to nasal cancer. Mortality was significantly elevated for cancers of the skin, kidney, and brain among those licensed only as embalmers, whereas mortality patterns were unremarkable among those licensed also as funeral directors (and presumably less exposed to formaldehyde). These preliminary results indicate the need for occupational cohort studies to clarify the carcinogenic potential of formaldehyde.
Prospective study of “early” gastric cancer
Authors: Tsukuma Hideaki , Mishima Takashi , Oshima Akira 
Published: February 2007

AbstractIn order to elucidate the natural history of early gastric cancer, we followed up non‐concurrently certain patients who had been diagnosed endoscopically as having “early” gastric cancer and who had histological evidence of cancer by biopsy, but on whom surgical resection had been delayed or had not been conducted. At the Center for Adult Diseases, Osaka, 56 cases were eligible for this study. Out of these, 27 cases progressed to advanced cancer and 16 remained at the early stage during the follow‐up period (6‐88 months, mean: 29 months). The remaining 13 cases had had neither surgical resection nor examinations. The survivorship function for the duration of “early” gastric cancer was estimated by the life‐table method of Kaplan and Meier. The median of the duration was estimated as 37 months. The 5‐year survival rate of the 34 cases on whom surgical resection had not been conducted was estimated as 64.5%. These results suggest that early diagnosis and early treatment may lead to a reduction of mortality from stomach cancer.
A new mechanism for tumor‐induced platelet aggregation. Comparison with mechanisms shared by other tumors with possible pharmacologic strategy toward prevention of metastases
Authors: Lerner William A. , Pearlstein Edward , Ambrogio Cynthia , Karpatkin Simon 
Published: February 2007

AbstractBecause tumor‐induced platelet aggregation appears to play a role in the development of certain experimental tumor metastases, we examined the mechanism(s) of tumor‐induced platelet aggregation as well as the effect of various anti‐platelets agents. Two mechanisms for tumor‐induced platelet aggregation have been previously described: (1) a mechanism which requires complement, a stable plasma factor, divalent cation and a sialo‐lipo‐pro‐tein vesicular component of the tumor membrane for platelet aggregation; and (2) a mechanism which operates via the generation of thrombin and requires a phos‐pholipid component of the tumor membrane. We now report a new mechanism of tumor‐induced platelet aggregation which is shared by three different tumors: a spontaneously metastatic human melanoma, HM29, a murine melanoma, B16F10, and a carcinogen‐induced metastatic murine colon carcinoma, CT26. These tumors do not require cell‐surface sialic acid or serum complement as does the first mechanism. They do not require cell‐surface phospholipid, as do the tumors representing the other two mechanism. They do not aggregate platelets via the generation of thrombin as do tumors representing the second mechanism. These tumors are unique in that they require a trypsin‐sensitive surface protein for activity. The ability of the thrombin‐generating tumors to aggregate platelets is uniquely sensitive to two highly specific, synthetic thrombin‐competitive inhibitors: DAPA and No. 805. The other two groups of tumors are at least 10 times more sensitive to inhibition of platelet aggregation by elevation of cyclic AMP levels (prostacy‐clin, 6‐keto‐PGE1, dibutyryl cyclic AMP) and at least 10 times more sensitive to inhibition of prostaglandin synthesis (indomethacin, ibuprofen). Thus, tumor‐induced platelet aggregation is heterogeneous with respect to mechanism of action as well as inhibition by anti‐platelet pharmacologic agents. Sensitivity to anti‐platelet agents correlates with the mechanism by which tumor cells aggregate platelets.
The mutational origin of serum independence in Chinese hamster cells in vitro
Authors: Varshaver Nina B. , Marshak Marina I. , Shapiro N. I. 
Published: February 2007

AbstractThe genetic mechanisms determining the ability of transformed cells to grow in a medium with a low serum content (ser+) were studied in a clone of Chinese hamster cells with normal serum requirements. The fluctuation test has shwon that serum independence occurs as a random spontaneous event. Its rate of occurrence is about 10−5. The concomitant study of a gene mutation (resistance to 6‐mercaptopurine ‐ 6MP) revealed similar characteristics with respect to the distribution of the number of mutants in replicate cultures. N‐methyl‐N1‐nitro‐N‐nitrosoguanidine (MNNG) and SV40 significantly increased the frequency of ser+ colonies. Induction was detected after an expression time of 3‐4 days, which is typical of gene mutations. In 16 out of 18 ser+ clones of independent origin the ser+ character remained stable. The results suggest that the ser+ character originates in most cases from a mutation event.
Systemic adoptive immunotherapy of a highly immunogenic murine lymphoma growing in the brain
Authors: Romani L. , Blanchi R. , Puccetti P. , Floretti M. C. 
Published: February 2007

AbstractSystemic adoptive immunotherapy with specifically immune lymphocytes was successfully performed in immunodepressed mice challenged intracerebrally with L5178Y/DTIC lymphoma cells, a tumor subline rendered highly immunogenic through In vivo exposure to 5‐(3,3‐dimethyl‐1‐triazenyl)‐1H‐imidazole‐4‐carboxamide (DTIC)1. The systemic immunotherapy relied on the infusion of in vitro‐generated primary cytotoxic T‐lympho‐cytes (CTL), the anti‐tumor activity of which was evaluated by measuring tumor‐cell proliferation In the brain in terms of radiolabel uptake and by recording survival times of recipient leukemic mice. The protection afforded by CTL appeared to be specific and was largely conditioned by dose and time of CTL administration. The levels of protection correlated well with the in vitro killing of L5178Y/DTIC tumor cells.
In vitro detection of cell‐mediated immunity to individual tumor‐specific antigens of chemically induced BALB/c fibrosarcomas
Authors: Carbone Giusi , Colombo Mario P. , Sensi M. Luisa , Cernuschi Antonio , Parmiani Giorgio 
Published: February 2007

AbstractIn this study we have analyzed the in vitro cell‐mediated cytotoxicity of immune peritoneal exudate cells (PEC), elicited in syngeneic mice against the MCA‐induced, TSTA‐bearing BALB/c fibrosarcomas CA‐2, GI‐17 and C‐3. The 4 h 51Cr‐release assay showed the immune PEC effectors to be specifically cytotoxic to fibrosarcoma used for the immunization, but not to other syngeneic MCA‐induced tumors or normal fibroblasts. Cold target inhibition experiments on CA‐2 cells confirmed the specificity of the reaction. When PEC, lymph‐node and spleen cells from BALB/c anti‐CA‐2 mice were compared for anti‐tumor activity, only PEC were found to kill tumor cells significantly. PEC effectors did not have a significant level of NK or NC activities since they were unable to destroy YAC‐1 target and the PEC‐mediated anti‐tumor activity was not inhibited by unlabelted YAC‐1 or WEHI‐164 tumor cells. PEC anti‐CA‐2 were analyzed for the expression of T‐cell markers by anti‐Thy 1.2, anti‐Ly 1.2 and Ly 2.2 monoclonal antibodies. Anti‐tumor specific effector cells were identified as mature T cells since they were not adherent to plastic and showed Thy l.2+, Ly 1.2− and Ly 2.2+ phenotypes. In addition, anti‐H‐2Kd but not anti‐H‐2Dd alloantiserum added to target cells, blocked CA‐2 tumor lysis, thus supporting the conclusion that the T‐cell response against TSTA is H‐2 restricted.
Formation and growth of multicellular spheroids of human origin
Authors: Carlsson J. , Nilsson K. , Westermark B. , Pontén J. , Sundström C. , Larsson E. , Bergh J. , Påhlman S. , Busch C. , Collins V. P. 
Published: February 2007

AbstractDifferent types of human cells which normally grow as monolayers or suspension cultures were tested for their capacity to form and grow as spheroids. Sixteen out of the 27 tested tumour cell lines formed spheroids. Nearly all of these spheroids also grew. With only two exceptions the doubling times were longer when the tumour cells grew as spheroids than when they grew in conventional mass culture. Eleven out of 13 tested human non‐tumour cells formed small spheroids but of these only the spheroids of lymphoid origin could grow. These lymphoid cells grew faster when aggregated to spheroids than when in single‐cell suspension culture. None of the other non‐tumour cells, which normally grew as monolayers, could grow as spheroids. The normally monolayer‐cultured tumour cells formed symmetrical spheroids with smooth surfaces while the normally suspension‐cultured cells formed irregular spheroids with rough surfaces. All large spheroids had a necrotic centre surrounded by a shell of viable cells. The thickness of the viable cell layer varied depending on cell type. The shape and organization of cells within the spheroids also varied largely. The results show that many types of human cells can be cultured as spheroids and that a wide spectrum of morphological appearances and growth rates can be obtained.
Differential reactivity of monoclonal antibodies with human colon adenocarcinomas and adenomas
Authors: Stramignoni Daniela , Bowen Robert , Atkinson Barbara F. , Schlom Jeffrey 
Published: February 2007

AbstractMonoclonal antibodies have been generated using membrane‐enriched extracts of human metastatic mammary carcinoma lesions (Colcher et at., 1981), some of which demonstrated binding to the surface of human colon carcinoma cell lines. We report here an analysis of the reactivity of three of these monoclonal antibodies with formalin fixed tissue sections of human colon adenocar‐cinomas and adenomas. The three monoclonals employed were B72.3, which is reactive with a 220‐400 kdal high molecular weight glycoprotein complex; B6.2, reactive with a 90 kdal glycoprotein, and B1.1, which is reactive with the 180 kdal glycoprotein CEA. B1.1 was least selective in its reactivity to colon carcinoma versus adenoma lesions. When 10 μg/ml of purified B1.1 IgG were used per slide, 94% (15 of 16) of carcinomas and 83% (15 of 18) adenomas showed reactivity. Monoclonal B72.3 demonstrated the most selective reactivity for carcinomas. Eighty‐two percent (14 of 17) of carcinomas were positive while none of 18 adenomas examined showed reactivity with more than a few percent of adenoma cells positive. When a low concentration of purified B72.3 immunoglobulin was used per slide, 8 of 16 carcinomas and none of 46 adenomas or normal colon epithelium samples scored positive. Monoclonal B72.3 also reacted with cells in areas of “atypia” within adenomas. The reactivity of monoclonal B6.2 was intermediate as compared to B1.1 and B72.3 in its selectivity of reactivity for carcinoma cells. A heterogeneity in the populations of tumor cells showing reactivity with the three monoclonals was observed within many of the tumor masses. Both colon adenocar‐cinomas and adenomas can now be placed in several distinct groups based on their expression of antigens reactive with the three monoclonal antibodies employed.