bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genetic deletions at specific loci by polycyclic hydrocarbons in relation to carcinogenesis
Authors: Fahmy O. G. , Fahmy Myrtle J. 
Published: February 2007

AbstractThe genetic properties of four benz[a]anthracene derivatives with varying carcinogenic potential were investigated on the stages of spermatogenesis in Drosophila melanogaster: two carcinogens, the 7,12‐dimethyl compound and its 7‐bromomethyl‐12‐methyl analogue; and two non‐carcinogens, methylated in the 1,7 or 3,9 positions. All proved virtually inactive with respect to the induction of point‐mutations: sex‐linked and autosomal recessive visibles and lethals. They were also ineffective in the production of chromosome breaks leading to major rearrangements, such as viable X‐fragments.Specific mutability tests confirmed the inactivity of all compounds on representative loci within the euchromatin of the X‐chromosome. In contrast, they were active to various degrees in the deletion of those loci involved in the transcription of r‐RNA, as measured by the effect on the heterochromatic X‐nucleolar organizer region, yielding bobbed mutations. The carcinogenic derivatives induced a high frequency of these mutations, whereas the non‐carcinogens were virtually inactive. The compounds which were active on the nucleolar organizer were also effective on the Minute loci.The mutagenic efficiency of the carcinogenic derivatives on the responsive loci proved to be differential, dependent on the chemical structure of the carcinogen and the metabolic activity of the target cells. The bearing of this phenomenon on specificity in carcinogenesis was discussed.
Development of resistance of novikoff hepatoma TO 5‐fluoro‐2'‐deoxyuridine
Authors: Wolberg William H. 
Published: February 2007

AbstractThree strains of Novikoff hepatoma were studied in tissue culture; the N1‐S1 or FUDR‐sensitive strain, N1‐S1/FUDR which is grown in and is resistant to 1 × 10−5M FUDR, and the cells which emerged as FUDR‐resistant after 10 generations when N1‐S1 was exposed to 1 × 10−7M FUDR. Inhibition of growth of N1‐S1 cells by FUDR was related to the concentration of the drug in the medium. The uptake of formate and serine into DNA‐thymine of these cells was inhibited by FUDR and the degree of inhibition was likewise proportional to the concentration of drug in the medium. The cells derived from N1‐S1 which were resistant to FUDR resembled the stable resistant strain, N1‐S1/FUDR, in that they lacked the ability to incorporate thymidine into DNA at 4.0 × 10−8M. Such cells apparently had less thymidine kinase activity and consequently also had a decreased ability to convert FUDR to the active monophosphate. Because of the decrease in thymidine kinase activity, the resistant strain, N1‐S1/FUDR, utilized thymidine as a source for DNA‐thymidine to a lesser extent than did the sensitive strain N1‐S1. However, both strains used serine and formate as the source of the 5‐methyl carbon of DNA‐thymidine to a similar extent.Growth studies in shaker flasks with a mixture consisting of 75% N1‐S1 and 25% N1‐S1/FUDR cells treated with FUDR demonstrated that rapid overgrowth by the 25% resistant cells obscured the significant killing of sensitive cells by the drug. Clonal studies revealed that a small portion of cells resistant to FUDR were present in the sensitive N1‐S1 strain of cells. The number of colonies which survived depended upon the concentration of the drug, but approximately 0.6% of the N1‐S1 cells grew in the presence of 1 × 10−5M FUDR. These studies led to the conclusion that the development of drug resistance in this system was actually a process of selection by which FUDR killed a certain percentage of cells determined by its concentration. Biochemically resistant cells which were present as a small proportion of the original “sensitive” tumor continued to proliferate and ultimately emerged as the dominant population.
Induction of lymphoma in BALB/c mice by Rowson‐Parr virus (RPV)
Authors: Carter R. L. , Chesterman F. C. , Rowson K. E. K. , Salaman M. H. , Wedderburn N. 
Published: February 2007

AbstractThe long‐term pathological effects of Rowson‐Parr virus (RPV), injected intravenously into 84 young adult BALB/c mice, are described. In the main experiment, 70 test mice and 30 uninjected control mice were examined serially between 4 and 48 weeks. A second group of 14 injected animals were allowed to live out their life‐span. Four stages in the host response have been defined. Splenic hyperplasia predominates in Stages I and II: there is initially a short‐lived phase of moderate splenic enlargement and reactive hyperplasia (Stage I) which partly resolves, to be followed by a persistent period of slight splenomegaly and low‐grade (non‐specific) reactive hyperplasia (Stage II). Neoplastic changes (Stages III and IV) developed in almost 45% of test mice in the serial study. In most instances, the neoplastic process appears to arise in reticulum cells in the Malpighian follicles of the spleen and is initially confined to these structures (Stage III). Later (Stage IV) there is progressive replacement of the splenic pulp and increasing involvement of lymph nodes, liver and thymus; some animals develop a terminal leukaemia. A similar reticulum‐cell neoplasm was found in many of the RPV‐infected mice which were allowed to live out their life‐span; none of these animals survived for more than a year after infection. Four RPV‐infected mice developed lymphomas and leukaemias of other histological types. No reticulum‐cell neoplasms were found in the uninjected control animals.Certain features of the reticulum‐cell lymphoma associated with RPV are discussed. Emphasis is directed to two features; (1) the biphasic nature of the host response with respect to time, the lymphoma being preceded by long‐sustained reactive changes; and (2) the finding that reactive and neoplastic changes arise sequentially in the same organ, and perhaps involve the same cell‐type—splenic reticulum cells. In contrast to findings in several other murine lymphomas, the thymus is not apparently involved until late in the disease.It is clear that RPV can no longer be regarded as “a virus of minimal pathogenicity”.
Possible carcinogenic hazards of several tars and of locacorten‐tar ointment (spectro‐fluorescent investigations and experiments in animals)
Authors: Shabad L. M. , Khesina A. Ja. , Linnik A. B. , Serkovskaya G. S. 
Published: February 2007

AbstractThe content of benz (a)pyrene (BP) in some tars and the carcinogenic effect of the ointment, Locacorten‐Tar, has been investigated in our laboratory. The determination of BP was performed by the spectrofluorescence technique based on Shpolsky's effect in frozen crystalline solution of normal paraffins. The concentration of BP in wood tars varied from 0 to 338.2 μg/g, whereas that of BP in coal tars is about 15 times higher (5,000μg/g). In Locacorten‐Tar it was 225 μg/g. Locacorten‐Tar ointment was tested in C57 X CBA mice by skin application. By the end of the treatment (after one year) all surviving animals had malignant skin tumours (carcinomas and sarcomas), which metastasized and were transplantable. BP estimation can apparently serve as an indicator of the carcinogenicity of tars and ointments. The determination of its content may serve as one of the criteria for selecting constituent compounds for ointments.
Tumor‐associated immunogolobulins. The elution of IgG2 from mouse tumors
Authors: Ran Maya , Witz Isaac P. 
Published: February 2007

AbstractIn an attempt to detect and characterize immunoglobulins fixed in vivo onto tumor cells, a low pH buffer was used to dissociate the tumor cells from the bound immunoglobulins. IgG2 could be eluted from intact cells and from a membrane‐rich‐sub‐cellular fraction originating from primary muose banzo (a)pyrene‐indueced tumors and from spontaneous mammary tumors, indicating the association of this immunoglobulin with the surfac of the tumor cells. Significantly lower amounts of IgG2 were present in eluates of membrane‐rich fractioins originating from transplantable benzo(a) pyrene induced sarcomas. IgG1 was not detecetd in most of the tumor eluates. Membrane‐rich sub‐celluar fraction originating from normal mouse muscle did not contain any detectable immunoglobulin.On the basis of a semi‐quantitative estimation of IgG2 and IgGi in the serum of normal and tumor‐bearing mice, it was concluded that IgG2 is preferentially bound to tumor cells and is not a random contaminant of the cells or of the membrane‐rcih sub‐cellular fractions.
Detectioni and isolatinio of tumour‐specific antigen associated with a spontaneously arising rat mammary carcinoma
Authors: Baldwin R. W. , Embleton M. J. 
Published: February 2007

AbstractCell surface expressed tumour‐specific antigen was detected in one (Sp4) of eight spontaneously arising rat mammary carcinomas by membrane immnofluorescence tests with viable tumour cells in suspensioni and sera from syngeneic rats immunized against each tumour. These findings are consistent with the frequency of expression of significant tumour antigenicity as defined by transplantation methods. Also the tumour antigen detected by membrane immunofluorescence tests in mammary carcinoma Sp4 showed the individual characteristics as the tumour‐specific transplantation antigens, and no evidence was obtained of weak common antigens in these tumours.Tumour‐specific antigen in subcellular fractions of mammary carcinomas Sp4 was assayed by its capacity to absorb antibody from tumour‐immune sera. By this criterion, it was established that plasma membrane fractionis retained tumour‐specific antigen although recoveries were low, amounting to less than 5% of cell‐surface experssed antigen. In comparison, almost total recovery was obtained of alloontigen experessed on mammary carcinoma Sp4 cells. Plasma membrane fractioins from mommary carcinoma Sp4 lacked the capacity to induce tumour rejectino reactions in syngeneic rats although a weak humoral antibody response was obtained. These findings contrast with the more consistent immune response elicted by heavily irradiated mammary carcinoa Sp4 cells.
Transplantation immunity following immunization with extracts of adenovirus 12 tumour cells
Authors: Potter C. W. , Oxford J. S. 
Published: February 2007

AbstractExtracts were prepared from transplanted adenovirus‐12 tumours of both hamsters and CBA mice by freezing and thawing and centrifugation at 100,000 x g/1 h. Extracts from CBA mice were also filtered through Millipore filters. These extracts were found to induce immunity to tumour cell challenge. Immunization with similar extracts of hamster tumours induced by SV40 of CELO virus did not induce immunity in CBA mice to tumour development. The results indicate that a possibly soluble extracts of adenovirus 12 tumour transplantation antigen can be obtained, and this antigen can be assayed in the adenovirus‐12‐induced CBA mouse tumour system.
Humoral responses to tumour xenografts in ALS‐treated mice
Authors: Beverley P. C. L. , Simpson Elizabeth 
Published: February 2007

AbstractAn isotopic antiglobulin technique was used to study the humoral response to a hamster tumour grafted into ALS‐treated or normal mice. Approximately 50% of ALS‐treated animals fail to reject the tumour after cessation of ALS treatment. All ALS‐treated animals show a delayed humoral response compared to controls but in those animals which fail to reject tumours, a high level of serum antibody is maintained even in the presence of a large tumour mass.
Lethal reticuloproliferative disease induced in Cebus albifrons monkeys by Herpesvirus saimiri
Authors: Meléndez L. V. , Hunt R. D. , Daniel M. D. , Fraser C. E. O. , García F. G. , Williamson M. E. 
Published: February 2007

AbstractFour cinnamon ringtail monkeys (Cebus albifrons) inoculated intramuscularly with Herpesvirus saimiri died between 18 and 20 days after inoculation. Each of the four monkeys presented an extensive infiltration of reticulum cells in various organs (liver, lungs, kidney, pancreas, spleen, thymus, lymph node). The character of the infiltrate closely resembled reticulum cell sarcoma thus providing further evidence of the high oncogenic capacity of Herpesvirus saimiri.
Epstein‐Barr virus (EBV)‐associated antibody patterns in malignant lymphoma and leukemia. I. Hodgkin's disease
Authors: Johansson Bo , Klein George , Henle Werner , Henle Gertrude 
Published: February 2007

AbstractSera from Swedish patients with Hodgkin's disease as well as control sera from donors without known disease were titrated for antibodies to the Epstein‐Barr virus (EBV) by the indirect immunofluorescence technique. In the same sera antibodies capable of blocking the direct membrane immunofluorescence reaction obtained between Epstein‐Barr virus carrying lymphoblastoid cell lines and a fluorescein‐conjugated reference serum from a patient with Burkitt's lymphoma (F‐Mutua conjugate) were tested. The serological reactivity of the control sera was very similar to that described in previous reports. In contrast, sera from Hodgkin's disease patients showed an increased reactivity in both tests. When the donors were grouped in relation to clinical and histological data of prognostic importance, an inverse relationship was found between the frequency of lymphoid cells and EBV‐associated serological reactivity. Whereas paragranuloma cases did not exceed the reactivity level of the controls, patients with Hodgkin's sarcoma were highly reactive in both tests, reaching levels comparable to those seen in Burkitt's lymphoma and nasopharyngeal carcinoma. The granuloma group was intermediate with regard to serological reactivity.
Effects of prolactin or growth hormone on growth of carcinogen‐induced mammary tumors of adreno‐ovariectomized rats
Authors: Nagasawa Hiroshi , Yanai Reiko 
Published: February 2007

AbstractThe effects of exogenous administration of bovine prolactin and bovine growth hormone (GH) on 7,12‐dimethylbenz(a)anthracene (DMBA)‐induced mammary tumor were investigated in female Sprague‐Dawley rats. Rats were bilaterally adrenoovariectomized 15 days after the appearance of the first palpable mammary tumors and were treated with either prolactin or GH beginning the next morning. Marked stimulation of incidence and growth of mammary tumor and of normal mammary gland growth followed subcutaneous injections of 1.25 or 2.5 mg prolactin twice daily for 20 days. GH had no effects on mammary tumor, whereas it accelerated the growth of normal mammary gland and increased the body weight. The administration of 2.5 mg prolactin twice daily for 10 days, beginning 20 days after adreno‐ovariectomy, raised the number and size of regressed mammary tumors to the pre‐operative levels, while the half dose of prolactin had no effects.These results indicate that prolactin is the principal hormone responsible for the growth of DMBA‐induced mammary tumor of the rat, whereas GH has only a minimal role in the growth of the tumor.
The relation of metabolism to macromolecular binding of the carcinogen benzo[a]pyrene, by mouse embryo cells in culture
Authors: Duncan Margaret E. , Brookes P. 
Published: February 2007

AbstractThe metabolism of tritiated benzo[a]pyrene (B[a]P) by primary mouse embryo cells in culture was studied. At concentrations of B[a]P in the medium below about 2–3 mμ moles/ml, metabolism was exponential with time, but at higher concentrations a period of rapid metabolism was followed by a progressive decline. The extent of binding of the hydrocarbon to DNA, RNA and protein was studied under the above conditions. It was found that at low doses of hydrocarbon the binding to macromolecules was proportional to the overall metabolism, with the result that the binding index, i.e. the amount of hydrocarbon bound divided by the amount metabolized, was constant. At higher dose levels, overall metabolism did increase with dose whereas macromolecular binding reached a plateau value. This resulted in a fall in the “binding index” below the constant value found at low doses of B[a]P.As a consequence of these results and those of other workers, a model scheme is proposed for the enzymic metabolism of B[a]P which accords with the known facts of metabolism and macromolecular binding.
Effect of neuraminidase on electrophoretic mobility and immune cytolysis of human uterine cervix carcinoma cells
Authors: Vasudevan D. M. , Balakrishnan K. , Talwar G. P. 
Published: February 2007

AbstractThe electrophoretic mobility of human uterine cervix carcinoma cells at pH 7.2 was found to be 0.89 μ/sec/v/cm at 25®C, while normal human cervix cells had a mobility of 0.58 μ/sec/v/cm. Treatment of the carcinoma cells with neuraminidase for 30 min reduced the electrophoretic mobility to 0.46 μ/sec/v/cm. Neuraminidase liberated more N‐acetyl‐neuraminic acid from carcinoma cells than from normal cells. Immune cytolysis of carcinoma cells by lymphocytes was studied by means of.51.Cr‐release technique. Autologous and homologous lymphocytes from carcinoma cervix patients had a lytic effect on carcinoma cervix cells; and the cytolysis was increased about two‐fold when the malignant cells were treated with neuraminidase. Homologous lymphocytes from healthy donors had comparatively little cytolytic action on malignant cells. Autologous lymphocytes had virtually no effect on normal cervical cells and neuraminidase treatment did not affect their susceptibility to lymphocytes. Autologous and homologous serum from cancer patients had a cytolytic influence on malignant cells; but normal serum was without effect. Although calcium chloride reduced the negative surface charge on the malignant cells, as gauged by their electrophoretic mobilities, no increase in the cytolysis of carcinoma cells by autologous lymphocytes was observed in the presence of charge‐reducing concentrations of calcium chloride.These results suggest the possibility that in the case of cervical carcinoma, sialic‐acid‐containing moieties partially mask tumor‐specific antigens on cell surface and prevent their recognition by immunologically competent cells of the host.
Modifications ultrastructurales de la surface des cellules BHK 21/13 transforméES, DÉPENDANT DE NUCLÉOTIDES DE L'ADÉNINE
Authors: Torpier G. , Montagnier L. 
Published: February 2007

AbstractULTRASTRUCTURAL CHANGES OF THE SURFACE OF BHK 21/13 TRANSFORMED CELLS, DEPENDING ON ADENINE NUCLEOTIDESBHK 21/13 cells transformed by either RNA or DNA oncogenic viruses have a modified surface, as shown, at the ultrastructural level, by an increase in the affinity of this surface for the dye ruthenium red. This increase takes place only when the cells have been grown in the presence of adenine nucleotides. Since the same nucleotides are required for the growth of these cells in agarose medium containing sulfated polysaccharides, it is suggested that this transformation character is related to the observed surface changes.
Demonstration of cell‐mediated immunity to human neoplasms of various histological types
Authors: Hellström Ingegerd , Hellström Kark Erik , Sjögren Hans Olov , Warner Glenn A. 
Published: February 2007

AbstractPeripheral blood lymphocytes from a total of 373 tumor patients were tested by either a colony inhibition or a cytotoxicity test for cell‐mediated immunity against human neoplasms of various histological types. Lymphocytes from 51 of 59 patients studied (88%) either reduced colony numbers formed by plated autochthonous tumor cells or were cytotoxic to them, and lymphocytes from 78 of 87 patients tested (89%) had a similar effect on allogeneic tumor cells of the same histological type as those of the lymphocyte donors. Evidence indicating antigenic cross‐reactivity between tumors of the same histological type was obtained for the following seven groups of neoplasms: malignant melanomas, carcinomas of the colon, breast, testis, endometrium and ovary, and various sarcomas. Lymphocytes affecting tumor cells had no effect on normal cells from the same patient, or on cells from other types of neoplasms than the target cells under study.The degree of cell‐mediated immunity, as detectable with the techniques employed, was approximately the same in patients having active neoplastic disease as in patients who were clinically symptom‐free. Eleven of 12 patients who were tested after having been symptom‐free for more than 2 years had a lymphocyte‐mediated anti‐tumor immunity.
Lysosomal changes and enhanced metastatic growth: An experimental study of the effects of some non‐ionic surfactants
Authors: Carter R. L. , Birbeck M. S. C. , Stock J. A. 
Published: February 2007

AbstractThe effects on metastatic growth of Triton WR‐1339 and three chemically related non‐ionic detergents have been investigated in 40 hamsters bearing subcutaneous transplants of a metastasizing lymphoma (ML). Ten further untreated animals with tumour grafts and 20 normal animals without tumour grafts acted as controls. In hamsters without tumours, the four detergents commonly produced three hepatic changes: an increase in the liver/body weight ratio, an increase in stainable acid phosphatase, and an increase in the number and size of the lysosomes, together with ultrastructural changes. In tumour‐bearing animals, the detergents all produced a paradoxical effect, partially inhibiting growth of the tumour graft but markedly facilitating metastatic spread. More organs contained secondary tumours in the test groups, and the pattern of involvement in certain organs (liver, kidneys) was strikingly altered, with diffuse rather than focal metastatic growth. Detailed investigations of the liver established that treated animals all showed the same (but more profound) changes as those seen in detergent‐treated hamsters without tumours‐i.e., high liver/body weight ratios, high acid phosphatase scores, and lysosomal damage. No lysosomal lesions were found in untreated tumour‐bearing hamsters.In the discussion, it is stressed that the detergents tested acted principally on host (cf. tumour) tissues, and it is suggested that local lysosomal damage in lysosome‐rich organs such as the liver may be one factor whereby these detergents facilitate local tumour spread. Ways in which lysosomal lesions may affect local tumour growth are discussed, and analogies are drawn from previous work relating to lysosomal changes and the (associated) enhanced growth of mycobacteria. The implication of the present findings in relation to the old “soil” hypothesis of metastatic growth are indicated but the fallacies of premature generalizations about lysosomal changes and metastasis are stressed.
Malignant transformation induced by 7,12‐dimethylbenz(a)anthracene in rat embryo cells infected with rauscher leukemia virus
Authors: Rhim Johng S. , Vass William , Cho Han Y. , Huebner Robert J. 
Published: February 2007

AbstractThis report describes morphological transformations observed approximately 6 weeks after treatment of Rauscher leukemia virus (RLV) infected rat embryo (RE) cells with various levels of 7,12‐Dimethylbenz(a)‐anthracene (DMBA) for 7 days. Uninfected cells treated with DMBA and RLV‐infected RE cells untreated with DMBA failed to show any evidence of transformation. When stained with Giemsa, the foci of transformed cells consisted of randomly oriented criss‐crossing spindle‐shaped cells, having much more rapid replication rates than the untreated and untransformed RE cells. The transformed cells were more resistant to the toxicity of DMBA than were the untransformed RE cells. Local subcutaneous sarcomas were produced when the transformed cells were transplanted into newborn rats, whereas the infected or DMBA‐treated untransformed cells produced no tumors. Cells derived from the tumors, when re‐established in tissue culture, like the tumor tissue itself contained group‐specific (GS) complement‐fixing antigens characteristic of the murine leukemia‐sarcoma virus complex and the C‐type RNA particles. These results, which showed that both chemical and virus were required for transformation, suggest that the C‐type RNA viral genome of RLV provided specific oncogene information for the malignant transformation.