bluuebunny/crossref_metadata_2025_split huggingface dataset:
Changes in the surface membrane of lymphocytes from patients with chronic lymphocytic leukemia and hodgkin's disease
Authors: Mintz Uri , Sachs Leo 
Published: February 2007

AbstractLymphocytes were isolated from the peripheral blood of 15 normal persons, 15 patients with chronic lymphocytic leukemia (CLL), 10 patients with Hodgkin's disease and 3 patients with CLL in remission. The cells were studied for cap formation and agglutinability by concanavalin A, and for cell attachment to the surface of a Petri dish. The percentages of lymphocytes with a cap were 25–34% for normal persons, 5–9% for CLL patients whether under treatment or not, 1–3% for untreated patients with Hodgkin's disease and about a normal percentage for CLL in remission. Vinblastine in all cases induced only about a 1.5‐ to 2‐fold increase in the percentage of cells with a cap. Agglutinability by concanavalin A was low for normal persons and high for all the patients including those with CLL in remission. Cell attachment to the Petri dish was low for normal persons and Hodgkin's disease patients, intermediate for CLL in remission and high for patients with CLL. Similar results for normal persons were obtained with peripheral blood lymphocytes that were predominantly T cells and with isolated normal B cells. Compared to lymphocytes from normal persons, lymphocytes from CLL patients were therefore different in cap formation, agglutinability and cell attachment; those from Hodgkin's disease in cap formation and agglutinability; and those from CLL in remission in agglutinability and cell attachment. These results indicate that there are different surface membrane changes in lymphocytes from patients with CLL, Hodgkin's disease and CLL in remission. It is suggested that these membrane changes may be useful as an aid in diagnosis.
Bcg therapy of pleural and peritoneal growth of transplanted rat tumours
Authors: Pimm M. V. , Baldwin R. W. 
Published: February 2007

AbstractGrowth of intrapleurally injected cells of immunogenic methylcholanthrene‐induced rat sarcomas was suppressed by intrapleural injection of viable or 1 × 106 R radiationsterilized BCG vaccine. As little as 10 μg moist weight of organisms was effective, and treatment could be given several days before or after tumour challenge. Pleural effusion growth of a moderately immunogenic ascitic hepatoma was also controlled by intrapleurally administered BCG. In contrast, BCG injected intravenously, subcutaneously or intraperitoneally was without influence on pleural tumour growths. Similarly, intraperitoneal growth of these tumours was suppressed only by intraperitoneal injection of BCG. With two other transplanted tumours, a chemically induced mammary carcinoma and a spontaneous sarcoma, both of which lack significant immunogenicity, BCG treatment of pleural and peritoneal growths was less successful and more variable. Nevertheless, these studies indicate the potential of this type of treatment of thoracic and peritoneal tumour deposits for possible clinical application in the treatment of malignant mesothelioma.
Oncogenesis by interspecific interaction of malignant murine and non‐malignant hamster cells in vitro
Authors: Goldenberg David M. , Pavia Rose A. 
Published: February 2007

AbstractA clone of Cloudman S91 murine melanoma 1 was fused in vitro with non‐malignant hamster cheek pouch cells by means of lysolecithin, and the putative hybrid progeny cells, HCP‐MM, were found to be highly malignant in hamsters, but not in appropriate mice. A malignant clone of HCP‐MM cells was shown to have hamster species‐specific surface antigens (as demonstrated by immunofluorescence and the cytotoxic antibody) and hamster‐like lactate dehydrogenase and NAD‐dependent malate dehydrogenase isoenzyme profiles. Nevertheless, chromosomes similar to those of both murine and hamster parental cells could be distinguished in cells of this malignant clone and in hamster tumor grafts by the method of trypsin‐Giemsa banding. A majority of the murine chromosomes, however, appeared to be lost. This study indicates that a murine melanoma previously found untransplantable in hamsters could produce a highly malignant and lethal tumor for hamsters after being mixed in vitro with non‐malignant hamster cells, in the presence of a fusing chemical. It is not as yet certain whether the production of transformed cells in vitro and of highly malignant tumors in the hamster (both with predominantly hamster properties) required heterosynkarion formation between the murine melanoma and hamster cheek pouch cells. Nevertheless, our results suggest that the presence of the murine melanoma, and possibly the interaction of its genome with non‐malignant hamster cells, was implicated in this process.
Cell‐mediated cytotoxicity to human pulmonary neoplasms
Authors: Vose B. M. , Moore M. , Jack G. D. 
Published: February 2007

AbstractPeripheral blood leukocytes from patients with confirmed pulmonary neoplasia were tested for cytotoxicity against cultured cells derived from lung tumours of various histological types, foetal and normal adult lung tissue and tumours arising in organs other than the lung. Leukocytes from 73% of patients were cytotoxic for lung‐tumour derived cells compared with age‐ and sex‐matched normal donors, while the frequencies of reactivity against normal adult lung‐derived cells and cells from unrelated tumours (e.g. bladder, colon, breast) were 42% and 18% respectively. Leukocytes from lung cancer patients were also cytotoxic for cells derived from foetal lung but susceptibility to cytolysis was variable, cells from 13‐ and 14‐week embryos revealing greatest reactivity (88%). Leukocytes from patients with a variety of tumours of non‐pulmonary origin or with non‐malignant conditions (including respiratory disorders) were also reactive with lung‐tumour‐derived target cells but with a lower overall frequency (35%) than those from lung‐cancer patients. The significance of these cytotoxicity data for the existence of tumour‐specific host immunoreactivity in lung neoplasia is discussed.
Cell‐mediated cytotoxicity to moloney sarcoma in syngeneic and allogeneic rats
Authors: Veit B. C. , Feldman J. D. 
Published: February 2007

AbstractCell‐mediated cytotoxicity in the primary immune response to Moloney sarcoma tumor (MST) in allogeneic and syngeneic rats was found to be predominantly T‐cell‐dependent. A minor non‐T‐cell cytotoxic activity may also have been detected. CMC was presumably directed against tumor and viral related antigens in the syngeneic host and primarily against alloantigens in the allogeneic host. CMC was more vigorous in the allogeneic recipient than in the syngeneic host. This may be due to differences in quantities or immunogenicities of the various antigens involved. Two peaks of T‐cells in effector populations were observed during a 20‐day post‐inoculation period. The first peak corresponded to peak T‐cell‐mediated cytotoxicity on day 8 and the second peak occurred on days 13 or 14 when CMC was minimal or undetectable.
Regression of spontaneous mammary tumors in dogs after injection of neuraminidase‐treated tumor cells
Authors: Sedlacek H. H. , Meesmann H. , Seiler F. R. 
Published: February 2007

AbstractThe effect on tumor progression produced by the injection of VCN‐treated tumor cells in dogs with spontaneous mammary tumors was investigated. Untreated dogs of different races and different ages with at least two palpable spontaneous mammary tumors were selected. One of the tumors was left in the animal for further clinical examination whereas the other tumor (s) was (were) excised for preparation of a single‐cell suspension by mechanical disintegration and enzymatic digestion with collagenase and trypsin. (1) In the first group, each animal was injected with 2 × 107 similarly prepared autologous, mitomycin‐treated tumor cells: in 8 out of 12 dogs of this group the tumors progressed while so far 1 dog has died of metastasis. (2) In the second group, each animal received the same number of 2 × 107 tumor cells, which were mitomycin‐ and VCN‐treated: 13 out of 15 dogs had a significant regression of their tumors to less than 10% of the original volume; in 1 dog the tumor remained unchanged and in 1 dog it progressed. (3) In the third group, 8 dogs received 1 × 108 mitomycin‐ and VCN‐treated tumor cells: the application of this cell dose resulted in an accelerated tumor progression in all 8 dogs, 3 of which have already died of metastasis. The significance of these findings, with respect to potentiation and abrogation of the immunological response and with regard to immunotherapy in man, is discussed.
Human, rat and mouse liver‐mediated mutagenicity of vinyl chloride in S. typhimurium strains
Authors: Bartsch H. , Malaveille C. , Montesano R. 
Published: February 2007

AbstractExposure of S. typhimurium strains TA 1530, TA 1535 and G‐46 to vinyl chloride increased the number of His+ revertants/plate 16, 12 or 5 times over the spontaneous mutation rate. After 6 h of exposure to vinyl chloride, the mutagenic response for TA 1530 strain was enhanced 7‐, 4‐ or 5‐fold when fortified postmitochondrial liver fractions from humans, rats or mice were added. The enzyme‐mediated vinyl chloride mutagenicity was dependent on an NADPH generating system and the enzyme activity was localized in a liver microsomal fraction; 9,000 × g liver supernatant was three times more active than microsomes, while liver cytosol or alcohol dehydrogenase did not affect the mutagenicity. Phenobarbitone pretreatment of rats and mice increased the mutagenic response by up to 15–40% as compared to untreated controls. The relative mutagenic activities of VCM, taking the value from mouse liver as 100, for TA 1530 strain mediated by 9,000 × g tissue fractions were: rat liver, 80; mouse and rat kidney, 20 and 16; mouse and rat lung, less than 7; human liver (from four biopsy specimens), 170, 64, 70 and 46. Chloroacetaldehyde and chloroacetic acid, a urinary metabolite of VCM, showed toxic effects, while chloroethanol was weakly mutagenic for TA 1530 strain.
Tumor‐specific and forssman antigens of guinea‐pig hepatoma cells: Comparison of tumor cells grown in vivo and in vitro
Authors: Evans Charles H. , Ohanian Sarkis H. , Cooney Adele M. 
Published: February 2007

AbstractCloned tumor‐cell lines were derived from two antigenically distinct ascites variants of diethylnitrosamine‐induced guinea‐pig hepatomas (designated line 1 and line 10). Cell‐surface antigens on the ascites and in vitro‐grown tumor cells were analyzed with immunofluorescence, C1 fixation and transfer, and antibody‐complement‐mediated cytotoxicity tests. Tumor‐specific and Forssman antigens continued to be expressed during 3–6 months of in vitro cultivation. Differences between ascites and cultured cells were noted in the degree of antigen expression and sensitivity to antibody‐complement‐mediated cytotoxicity. Cells grown in vitro exhibited a greater number of Forssman and tumor‐specific antigen sites than in vivo grown cells as determined by the quantitative C1 fixation and transfer test. Immunofluorescent staining indicated that some cloned lines were considerably more homogeneous in terms of antigen expression than were the cultured, non‐cloned parent cells or ascites‐grown cells. Cloned lines were frequently more sensitive to the cytotoxic action of antibody and complement than were the in vivo grown and cultured non‐cloned parent tumor cells. Sensitivity to cytotoxicity did not necessarily correlate, however, with the degree of antigen expression. These results suggest that; (1) the expression of Forssman and tumor‐specific antigens does not diminish on cells cultivated in vitro and (2) ascites hepatoma cells in vivo are a heterogeneous population of cells differing in their degree of antigen expression and sensitivity to antibody‐complement‐mediated cytotoxicity.
The detection of the epstein‐barr virus (ebv) nuclear antigen (ebna) by anti‐complement immunofluorescence. Immunoglobulin class of antibodies and role of complement
Authors: Liabeuf A. , Nelson R. A. , Kourilsky F. M. 
Published: February 2007

AbstractThe Epstein‐Barr virus (EBV)‐associated nuclear antigen (EBNA) was detected by anti‐complement immunofluorescence (ACIF) in Raji lymphoblastoid cell line, and the mechanism of the reaction explored, using Ig fractions of anti‐EBNA sera and purified components of complement. Following fractionation of serum from 13 donors, anti‐EBNA antibodies were always found to be associated with IgG, but were also detectable in the IgM fraction of four sera. Sequential addition of functionally pure complement components in the ACIF reaction showed that the classical sequence of complement activation is involved. Anti‐EBNA antibody reactions in Raji cell nuclei can also be detected by anti‐Ig immunofluorescence with a low level of sensitivity. The same pattern of granular fluorescence was observed when C3 (β1A/β1C), or C4 or IgG anti‐EBNA antibodies were revealed with the corresponding fluorescein‐conjugated reagents. Blocking of the ACIF reaction was achieved with Fab'2 anti‐EBNA antibody fragments, which therefore provided an appropriate specificity control for the detection of EBNA.
Immunofluorescence and anti‐complement immunofluorescence absorption tests for quantitation of epstein‐barr virus‐associated antigens
Authors: Reedman Beverley M. , Hilgers J. , Hilgers F. , Klein G. 
Published: February 2007

AbstractImmunofluorescence absorption methods are described which permit quantitative estimation and differentiation of Epstein‐Barr virus (EBV)‐associated antigens (virus capsid antigen, VCA, early antigen, EA and EBV‐determined nuclear antigen, EBNA) in cell extracts. EBNA was present in all cell lines (producer and non‐producer) which carried the EBV‐genome, while VCA and EA were present in producer lines only. All the antigens were absent from a lymphoid cell line (MOLT‐4) which lacked the EBV‐genome, as well as from leukemia cells from peripheral blood. The techniques demonstrated antigenic identity of the various antigens when prepared from different cell lines.
Leukaemogenesis and regeneration of lymphoid system in (C3H × AKR/tiald)F1 hybrids restored with parental bone marrow and thymic cells
Authors: Legrand E. , Duplan M. C. Kressmannet J. F. 
Published: February 2007

AbstractLeukaemogenesis and repopulation of the lymphoid system have been studied in sub‐lethally irradiated (C3H × AKR/TIALD) F1 hybrids which have been restored with parental Bone Marrow (BM) cells with or without thymic cells. The metacentric marker of the TIALD sub‐strain made it possible to identify the host or donor origin of leukaemias. Leukaemias occur either in the thymus (lymphosarcomas) or in the other lymphoid tissues (extra‐thymic leukaemias). After irradiation, the percentage of lymphosarcomas increases from 5 to 95%. The rate of leukaemias in hybrids which have been restored only with BM cells is 55, 56 and 100% respectively depending on the origin of BM: syngenic, C3H and AKR. In this last group 75% of the lymphosarcomas originate from donor cells. The inhibitory efficiency of the three kinds of BM on leukaemogenesis seems to be related to their respective abilities to spontaneous malignant transformation. When AKR or C3H thymic cells are injected together with BM cells, leukaemogenesis is altered. The effect is indirect as these cells are not actually concerned by the malignant transformation. The percentage of LS is significantly reduced and the mean survival improved in hybrids restored with C3H thymic, mixed with AKR or C3H BM cells. AKR thymic cells are less efficient. In both cases, the percentage of extra thymic leukaemias increases at the expense of lymphosarcomas. Thymic cells do not change the kinetics of repopulation in thymus and lymph‐node by the BM cells, except when C3H thymic cells are mixed with TIALD BM cells; in this case, the lymph‐node repopulation is temporarily enhanced. Different hypotheses might explain the effect of thymic cells on leukaemogenesis: enhanced recovery of the post‐irradiation immunological deficiency, transfer of virus by the AKR thymic cells, and more probably influence of the thymic cells on the maturation or/and differentiation of the lymphoid cells.
Enhancement by drugs of metastatic lung nodule formation after intravenous tumour cell injection
Authors: Van Putten L. M. , Kram L. K. J. , Van Dierendonck H. H. C. , Smink T. , Füzy M. 
Published: February 2007

AbstractIn studies on a model of induced pulmonary metastasis in mice a tumour host system was analysed which was not affected by immunogenicity of the tumour for the host; neither intensive immunosuppression nor immunization caused a significant change in the quantity of pulmonary metastatic nodules. In contrast the application of cytostatic drugs and of Corynebacterium parvum could modify the pulmonary resistance to the formation of tumour nodules by a factor greater than 100 in either direction. This finding confirms the observation of others that major modification of the resistance to metastatic tumour formation can occur independently of classical immunological mechanisms. Special attention is drawn to the fact that cyclophosphamide enhances the formation of metastatic nodules in this model by factors of 100 to more than 1,000, whereas other cytostatic drugs including the cyclophosphamide congeners iphosphamide and trophosphamide are active only by factors between 2 and 12. The possible practical significance of these findings is discussed.
Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices
Authors: Armstrong Bruce , Doll Richard 
Published: February 2007

AbstractIncidence rates for 27 cancers in 23 countries and mortality rates for 14 cancers in 32 countries have been correlated with a wide range of dietary and other variables. Dietary variables were strongly correlated with several types of cancer, particularly meat consumption with cancer of the colon and fat consumption with cancers of the breast and corpus uteri. The data suggest a possible role for dietary factors in modifying the development of cancer at a number of other sites. The usefulness and limitations of the method are discussed.
The mechanism of carcinogenic action of 1,2‐dimethylhydrazine (sdmh) in rats
Authors: Pozharisski K. M. , Kapustin Yu. M. , Likhachev A. J. , Shaposhnikov J. D. 
Published: February 2007

AbstractThe radioactivity level in blood, bile, urine and contents of parts of the gastro‐intestinal tract in rats was studied after subcutaneous administration of 3H‐1,2‐dimethylhydrazine (3H‐SDMH) which induces colonic tumours. The alkylation of DNA, RNA and protein in the intestinal mucosa, liver and kidneys was estimated 1 h to 28 days after 3H‐SDMH treatment from the 3H‐incorporation into these macro‐molecules. Administration of 3H‐1,2‐diethylhydrazine (3H‐SDEH) which does not induce intestinal tumours was made as a control. Fifteen to 30 min after 3H‐SDMH treatment, marked radioactivity was found in blood, bile, urine and in contents of all regions of gastro‐intestinal tract. After 3H‐SDMH administration no label occurred in the contents of localized segments of gastro‐intestinal tract although it was present in blood, bile and urine. 3H‐SDMH methylated DNA, RNA and proteins of intestinal mucosa, liver and kidney to a high degree. One hour after 3H‐SDMH treatment the incorporation of label into protein of intestinal mucosa was higher than into liver and kidneys. 3H‐SDEH did not alkylate macromolecules in these organs but did so in thymus, spleen and brain, which are target organs for this carcinogen. After total hepatectomy. 3H‐SDMH did not methylate macromolecules of the intestinal mucosa. The following mechanism for the carcinogenic effect of SDMH is suggested. A carcinogenic metabolite of SDMH forms, in the liver, a conjugate with glucuronic acid. This glucuronide enters the gut both with bile and directly via the circulation. Microbial β‐glucuronidase releases the active metabolite which, in turn, alkylates tissue macro‐molecules.
Rat cell line 3y1 and its virogenic polyoma‐ and SV40‐transformed derivatives
Authors: Kimura Genki , Itagaki Asao , Summers Jesse 
Published: February 2007

AbstractCell lines were established from cultures derived from Fischer rat embryos according to the transfer schedule described by Todaro and Green (1963) for mouse 3T3 cells where cell crowding and serum exhaustion were kept to a minimum. Cell growth rate did not decline greatly during the course of successive 3‐day transfers. Like 3T3 cells, the rat cell lines possess very low saturation densities under standard culture conditions. A clonal cell line with a relatively high plating efficiency was obtained from one of the cell lines, 3Y1. In these cloned cultures, virus growth was not detectable upon infection with SV40, while a small amount of virus was produced upon infection with polyoma virus. Morphological transformation of the cloned 3Y1 cells by SV40 and polyoma virus could be assayed with single‐hit kinetics and with efficiencies comparable to those of the previously available transformation systems for each virus. Independent cell lines transformed by SV40 were consistently virus‐free and all the lines tested produced SV40 upon fusion with permissive monkey cells. Most of the independent transformed cell lines isolated after polyoma infection appeared to be virus‐free, although the cultures of some lines produced a small amount of polyoma virus spontaneously after a prolonged cultivation. Most of the virus‐free polyoma‐transformed lines produced virus upon fusion with permissive mouse cells.
Induction of specific changes in the surface membrane of myeloid leukemic cells by steroid hormones
Authors: Lotem Joseph , Sachs Leo 
Published: February 2007

AbstractNormal mature macrophages and granulocytes have surface membrane receptors for specific immunoglobulin and immunoglobulin complement, which can be detected by rosette formation with erythrocytes coated with antibody (EA) or with antibody and complement (EAC). There are three types of myeloid leukemic cells, IR+D+, IR+D− and IR−D−. IR+D+ cells were induced to form receptors for EAC but not for EA by the steroid hormones prednisolone, dexamethasone and estradiol. Induction required protein synthesis and was not inhibited by cordycepin or vinblastine. Optimum induction required the continued presence of the hormones. IR+D+ cells were also induced by these hormones to migrate in agar, attach to the surface of a Petri dish and form macrophages. IR+D− cells showed a lower inducibility by these hormones and no formation of macrophages. There was no induction of any of these changes with IR−D− cells. The steroid hormones progesterone, testosterone and cortisone did not induce these changes in any of the leukemic cells and inhibited induction by prednisolone, dexamethasone and estradiol. The results indicate that specific surface membrane changes in myeloid leukemic cells can be induced by certain steroid hormones.
Oncogenic transformation of primary hamster cells by herpes simplex virus type 2 (HSV‐2) and an HSV‐2 temperature‐sensitive mutant
Authors: Kimura Susumu , Flannery Virginia L. , Levy Barnet , Schaffer Priscilla A. 
Published: February 2007

AbstractSix oncogenically transformed cell lines were obtained following infection of hamster embryo fibroblasts with UV‐irradiated herpes simplex virus type 2 (HSV‐2) or with an HSV‐2 temperature‐sensitive mutant. All lines produced undifferentiated fibrosarcomas in newborn hamsters, four of the six lines produced metastatic tumors in the lung, and sera from tumor‐bearing hamsters contained neutralizing antibody to HSV‐2. HSV‐specific cell‐surface antigen (s) was detected by immunofluorescence tests in all six of the lines established from primary tumors. Antibody to an early, HSV‐specific, non‐structural polypeptide (VP134) reacted by immunofluorescence with antigen (s) in fixed preparation of three of the six tumor‐cell lines.