bluuebunny/crossref_metadata_2025_split huggingface dataset:
Armed human monocytes challenged with a sensitizing cancer extract release substances pharmacologically similar to leukotrienes
Authors: Thomson D. M. P. , Phelan Kerry , Morton Douglas G. , Bach Michael K. 
Published: February 2007

AbstractHuman peripheral blood monocytes were highly enriched by adherence to plastic, armed with serum from cancer patients, and challenged separately and simultaneously with the sensitizing and unrelated cancer extracts. The response of the monocytes was to release a factor that inhibited leukocyte adherence (LAI)4 to glass. The macrophage‐like cell line U937 released a similar factor when it was armed and challenged with the sensitizing cancer extract. The production of the factor was blocked by 10−6 M ETYA and 10−6 M NDGA but not by 10−6 M indomethacin. Moreover, a competitive inhibitor of leukotriene function, 10−6 M FPL55712, blocked the LAI reaction mediated by the factor. Arylsulfatase destroyed its activity while depletion of the monocytes' cellular glutathione pool with CyH or Et2Mal stopped production of the mediator. Pure leukotrienes (C and D) in a dose‐response fashion prevented the adherence of leukocytes to glass; the nonadherence of mononuclear cells was equal to that of polymorphonuclear cells. PGE2, if added to the leukocytes immediately before challenge with LTC or LTD, increased 1,000‐fold the leukocytes' sensitivity to the leukotrienes. Paradoxically, if leukocytes were washed and exposed to PGE2 15 min after being challenged with leukotrienes, their normal glass‐adherence property and the ability to respond again to LTD were restored. FPL 55712 blocked the effect of LTC and LTD from inhibiting the adherence of leukocytes to glass. The present study shows that human monocytes armed with cytophik antitumor antibody, when challenged with the sensitizing cancer extract, release leukotriene(s) as shown by pharmacologic evidence, implying that monocytes may play an important inflammatory role in human cancer.
Effect of retinoic acid on the spontaneous and interferon‐induced activity of human natural killer cells
Authors: Abb Jochen , Abb Hannelore , Deinhardt Friedrich 
Published: February 2007

AbstractNon‐toxic concentrations of retinoic acid (RA) inhibited the spontaneous activity of human natural killer (NK) cells. RA also inhibited the activation of human NK cells by treatment with partially purified human leukocyte interferon (HulFNα) or with inducers of IFNα and IFNγ. Full expression of the inhibitory action required prolonged exposure of human peripheral blood leukocytes to RA. Implications of these findings for the use of retinoids in the treatment of human malignancies are discussed.
Modulation of antigen‐induced leukocyte adherence inhibition by metabolites of arachidonic acid and intracellular nucleotides
Authors: Thomson D. M. P. , Phelan Kerry , Scanzano Rosemarie , Fink Aaron 
Published: February 2007

AbstractAfter binding a sensitizing tumor antigen, human leukocytes undergo a series of changes that lead to a loss of their glass‐adherent properties; a phenomenon called leukocyte adherence inhibition (LAI)1. After surgery or when patients have a large tumor burden, their test results become negative. This study shows that in vitro incubation of the leukocytes for 5 min with PGE2 converted to positive the negative test, in an immunologically specific manner. The effect was critically dose‐dependent, too little or too much did not alter the result. The same effect was achieved with PGE2, PGI2, aminophylline or other drugs that raise intracellular nucleotides, including dibutyryl cyclic AMP and dibutyryl cyclic GMP. Dibutyryl cyclic AMP stimulated a stronger response and 100 times less was needed than of dibutyryl cyclic GMP. Prostaglandins did not mediate LAI since Indomethacin failed to inhibit a positive test. Nonetheless, arachidonate metabolites were critical for the LAI phenomenon since BPB and mepacrine, inhibitors of phospholipase A2, negated the LAI response. Moreover, ETYA, phenidone and NDGA, inhibitors of the lipoxygenase metabolic pathway, all negated the positive LAI response. The positive response was especially sensitive to nullification by ETYA. Although the last‐named drugs inhibit other arachidonate metabolic pathways too, conclusive evidence that the matabolites of the lipoxygenase pathway, and leukotrienes in particular, mediate the LAI response was the fact that FPL 55712, a competitive antagonist of SRS, nullified a positive response at levels as low as 10−13 M. The results imply that prostaglandins were able to modulate the expression of LAI by affecting intracellular nucleotides, but leukotrienes, it seems, were the metabolites that mediated leukocyte nonadherence after monocytes recognized and bound tumor antigen.
Procoagulant and fibrinolytic activities of gastric and colorectal cancer
Authors: Szczepańaski Maciej , Lucer Cezary , Zawadzki Jakub , Tołłoczko Tadeusz 
Published: February 2007

AbstractProcoagulant activity (PA) and fibrinolytic activity (FA) were investigated in 14 specimens of gastric cancer (GC) and in 26 specimens of colorectal cancer (CC) and simultaneously, in samples of the normal mucosa obtained from the same organs. Histochemical localization of plasminogen activator was performed at the tumor borderline. The PA of the tumor extracts was in most cases lower than in the corresponding normal mucosa from GC as well as CC patients. The FA of the extracts of CC was also lower than that of normal mucosa. On the other hand, 11 of 14 cases with GC showed a significantly higher FA in the tumor extracts than that in the corresponding normal mucosa. The histochemical localization of plasminogen activator revealed that its activity is connected with small and medium‐sized blood vessels, but not with the cells of the two kinds of cancer investigated. Morphological and histochemical findings from both kinds of cancer demonstrate that the FA of their extracts depends on the vascularity of specimens of the respective tumors.
Correlation between the metastasizing activity of in vitro spontaneously transformed hamster cells and their natural resistance‐depressing activity
Authors: Deichman G. I. , Kluchareva T. E. , Kashkina L. M. , Matveeva V. A. , Vendrov E. L. , Zemtsova V. I. 
Published: February 2007

AbstractIn our previous experiments in Syrian hamsters the in vivo semiquantitative method of determination of the natural resistance‐depressing (NRD) activity of tumor cells was described. It was demonstrated that inactivated cells of different tissue culture cell lines derived from in vivo tumors in contrast to normal, or in vitro spontaneously transformed hamster embryo (STHE) cells, bear the NRD factor. It was suggested that NRD activity of tumor cells might be essential for the development of primary tumors and metastases (Deichman et al., 1979). Therefore, in this study we compared the NRD activity and metastatic activity (MA) of the parelal STHE cells never passaged in vivo and STHE in vivo sublines, obtained from subcutaneous tumor nodules and from individual spontaneous lung metastases (LM) after s.c. transplantation of STHE cells. Five LM sublines of STHE strain (out of eight investigated) were NRD active as well as the cells of one of two s.c. tumor nodules. Study of MA, i.e. the relation between the number of cells inoculated retroorbitally in the bloodstream of hamsters and the number of experimental metastases developed in the lungs of inoculated animals, demonstrated that the highest MA was observed with the cells of LM sublines possessing the highest NRD activity. Parental STHE cells did not depress natural anti‐tumor resistance and their MA was the lowest. The data presented demonstrate the heterogeneity of the population of constantly cultured in vitro STHE cells in relation to their NRD activity and the selection of NRD active cells during the development of lung metastases.
Papillary carcinomas of the thyroid have pore‐deficient nuclei
Authors: Johannessen Jan Vincents , Sobrinho‐Simöes Manuel , Finseth Inga , Pilström Lars 
Published: February 2007

AbstractA significant reduction in nuclear pore density observed in papillary carcinomas compared to normal thyroid, adenomas and follicular carcinomas probably disturbs the nucleo‐cytoplasmic transfer of ribonucleoproteins. This may contribute to the slow growth and indolent biological behavior of these tumors where even the presence of regional lymph node metastases does not worsen the prognosis. The signs of nuclear hyperactivity may result from an attempt to compensate for the nuclear membrane defect.
Social class risk factors among children with Hodgkin's disease
Authors: Gutensohn Nancy M. , Shapiro Daniel S. 
Published: February 2007

AbstractWe compared the social class characteristics of 66 families with children diagnosed with Hodgkin's disease (HD) from 1959 through 1977 in a defined population with that of 182 “control families” identified by a random process from the population base. The 14 youngest cases (<10 years at diagnosis) were from somewhat lower social‐class backgrounds than their 37 controls as evidenced by the distribution of median income, single‐unit housing, and poverty level of their census tract of residence, as well as by the occupational class of head‐of‐household. In contrast, the social class characteristics of the 52 older children with HD (10–14 years) were quite similar to that of their 145 controls. This apparent shift from lower to average social class between younger and older children with HD Hodgkin's disease may reflect a shift in their age of exposure to common infections. If true, these findings are consistent with the hypothesis that HD may develop as a rare consequence of a common infection. However, these findings are based on small numbers of cases and on indirect measures of social class.
Induction of avidin in chickens infected with the acute leukemia virus OK 10
Authors: Korpela Jukka , Kulomaa Markku , Tuohimaa Pentti , Vaheri Antti 
Published: February 2007

AbstractThe presence of avidin, a progesterone‐dependent oviductal glycoprotein, was studied in viral tumors. Newborn chickens were infected with the acute leukemia virus OK 10, and the first tumors occurred within 2–3 weeks. Avidin was assayed using a [14]biotin‐binding method and radioimmunoassay. In the control chickens, avidin concentrations were <0.3 μg/g in the plasma and <1.5 μg/g in various tissues including the immature oviduct. In the OK 10 virus‐infected chickens, no significant induction was observed during the acute infection or any time thereafter if no tumors were seen. In chickens that developed tumors, avidin concentrations were significantly increased in tumorous tissue only located in the mesenterium and occasionally in the oviduct. In tumors occurring elsewhere (kidney, ovary, muscle, testis, liver, colon) avidin concentrations were not elevated. Tumor‐associated avidin had extraordinary biotin‐binding capacity after treatment at +90° C similar to the progesterone‐dependent avidin, whereas antibody‐binding properties suggested that tumor‐associated avidin may have a some‐what altered antigenic structure.
Anti‐tumor activity of daunorubicin linked to poly‐L‐aspartic acid
Authors: Zunino Franco , Giuliani Fernando , Savi Giuseppina , Dasdia Teresa , Gambetta Romolo 
Published: February 2007

AbstractDaunorubicin was bound to poly‐l‐aspartic acid via the methylketone side chain of the drug to avoid reaction of the sugar amino group believed to be essential for optimal drug activity. Attachment of the drug to the poly‐amino acid by an ester linkage was achieved by nucleophylic substitution reaction of 14‐bromo‐daunorubicin. Compared with free daunorubicin, the polymeric derivative was less cytotoxic to HeLa cells in vitro, but more effective against all tumor models tested (P388 leukemia, Gross leukemia, MS‐2 sarcoma). The binding to the poly‐peptide markedly reduced drug toxicity but only slightly decreased drug potency. The daunorubicin‐poly‐L‐aspartic acid conjugate demonstrated antitumor activity comparable to that of doxorubicin in leukemia models, but superior to that of doxorubicin in a solid tumor model (MS‐2 sarcoma).
Non‐random duplication of chromosome 15 in T‐cell leukemias induced in mice heterozygous for reciprocal and robertsonian translocations
Authors: Wiener Francis , Spira Jack , Babonits Magda , Klein George 
Published: February 2007

AbstractTwo translocation – carrying stocks of mice, T(7;15)9H and Rb(4;15) were resistant to chemical leukemogenesis by 7,12‐dimethylbenz(a)‐anthracene (DMBA) or methyl‐nitroso‐ N‐urea (MNU). Lymphomas were induced in F1 hybrids derived from crossing these two stocks with various susceptible strains. In T‐cell leukemias originating from F1 hybrids with Rb(4;15) as one parent and strain CBA or ASW as the other, the translocation chromosome was present in two copies. In trisomic tumors derived from Rb(4;15) X AKR F1 cross, the AKR‐derived chromosome 15 was duplicated regularly. In contrast, all trisomic lymphomas of the T(7;15)9H F1 outcrosses showed duplication of the non‐translocated chromosome 15 and not of the (7;15) translocation chromosome. It is suggested that the resistance of the T(7;15)9H stock to chemical induction of T‐cell leukemia may be related to the position of the translocation on chromosome 15 (band D2). Our previous studies (reviewed by Klein, 1981) have indicated that this area may contain an oncogene that needs to be activated and subsequently undergo duplication in the course of leukemia development. In our previous studies on trisomic leukemias induced in heterozygotes (Wiener et al., 1979, 1980b), we have found that duplication was nonrandom in all investigated crosses, unless the normal and the translocation marker carrying chromosomes were derived from the same inbred strain. A “duplication preference” scale could be established between chromosomes No. 15 derived from different strains. This suggested that the likelihood of leukemia development was different, depending on the genetic origin of chromosome 15. In the present study, we have found that the duplication of chromosome 15 occurred at random in the CBAT6T6 × C3H F1 cross. This is attributed to the close genetic relationship between the two strains, as indicated by their shared isoenzyme and other markers.
Epstein‐Barr virus induction by a serum factor: IV. Ubiquitous occurrence of the factor within vertebrates and its interaction with defined lymphoid cell lines
Authors: Wittmann Peter , Höfler Petra , Bauer Georg 
Published: February 2007

AbstractWe have recently reported the existence of a serum factor that induces Epstein‐Barr virus antigens in Raji cells (Bauer et al., 1982b, c). Here we demonstrate the ubiquitous presence of this factor in sera of vertebrates of all five classes. Furthermore, we tested 48 EBV‐genomepositive lymphoid cell lines of different origins for responsiveness to the serum factor. Only cells from lines of two groups, i.e. Burkitt's lymphoma and EBV‐transformed marmoset lines, responded to the factor, whereas human lymphoblastoid cell lines were not induced by the serum factor.
Tumor localization of CEA‐containing human tumors in nude mice by means of monoclonal anti‐CEA antibodies
Authors: Hedin Anders , Wahren Britta , Hammarström Sten 
Published: February 2007

AbstractThree different monoclonal antibodies (mabs) directed against conformation‐dependent protein determinants in carcinoembryonic antigen (CEA) were evaluated for tumorimmunolocalization of CEA‐containing human tumors grown in nude mice. The antibodies were of high affinity and of the IgG1 subclass. They did not react with non‐specific cross‐reacting antigen (NCA), biliary glyco‐protein 1 (BGP 1) or orosomucoid. 10–20 μCi(1–2 μg) of 131I‐labelled mab was injected intraperitoneally into mice bearing heterografts of the CEA‐containing human tumor cell lines LS 174T, Detroit 562 or HT‐29 or into mice bearing grafts of the non‐CEA‐containing human tumor cell line RD. The concentration of radiolabelled mab in the tumor compared with the mean concentration in the mouse increased up to day 4 after injection. In contrast, the concentration ratios of radioactivity in the other tissues decreased with time. Excellent tumor localization was obtained with mab 38SI in mice bearing LS 174T tumors. The concentration of radioactivity (cpm/g) tissue wet weight) was 24–390 times higher in the tumor than in the muscle. The difference between tumor and liver and between tumor and blood was 4–89 times and 2–25 times, respectively. A mean value of 40% of the total radioactivity in the mouse at day 4 was localized to the tumor. Mab 38SI also showed positive tumor localization in mice carrying Detroit and HT‐29 tumors. Means of 22% and 18% of the total radioactivity in the mouse at day 4 were found in these tumors, respectively. Mab 38SI was, however, not enriched in the tumor of mice bearing the non‐CEA‐containing sarcoma RD. Furthermore, when LS 174T tumor‐bearing mice were injected with normal mouse IgG, no enrichment of radioactivity in the tumor was seen. Positive tumor localization with mab 48 was obtained while mab 9 was not enriched in the tumor. Scanning pictures of LS 174T‐grafted mice on day 4 after injection of 131I‐mab 38SI showed a definite radioactive spot corresponding to the tumor and in addition a spot corresponding to the liver or the heart.
Antibody responses to epstein‐barr virus‐specific DNase in relation to the prognosis of juvenile patients with nasopharyngeal carcinoma
Authors: Tan Reng‐Seng , Cheng Yung‐Chi , Naegele Robert F. , Henle Werner , Glaser Ronald , Champion John 
Published: February 2007

AbstractWe have examined serial sera from 17 juvenile patients with nasopharyngeal carcinoma (NPC) for their capacity to neutralize the activity of Epstein‐Barr virus (EBV)‐specific DNase. The results revealed that NPC patients who became long‐term survivors (LTS) without evidence of the disease either never possessed significant levels of antibodies to the enzyme or showed a gradual decline in the number of EBV DNase units neutralized from an elevated level at diagnosis to an insignificant figure several years later. All the 10 LTS neutralized less than 4, and some neutralized less than 2 units of the enzyme 3 or more years after the initial diagnosis. In contrast, serial sera from juvenile patients who died of NPC neutralized over 10 and as many as 25 units of EBV DNase either persistently until death occurred or with transient declines during unmaintained remissions. Rises and declines in the neutralizing activity were, with few exceptions, accompanied by corresponding changes in the titers of IgA and IgG antibodies to EB viral capsid antigen and to the diffuse component of the early antigens. Although the number of juvenile NPC cases available for study was small, the observations suggest that the EBV DNase neutralization test may serve to provide information on the prognosis of the patients.
Hybridization between a human epithelial line, infectable by Epstein‐Barr virus, and burkitt lymphoma lines: Membrane properties, superinfectability, inducibility and tumorigenicity
Authors: Mitrani‐Rosenbaum Stella , Ber Rosalie , Goldblum Natan , Povey Susan , Gamliel Haim , Ben‐Bassat Hannah 
Published: February 2007

AbstractThe human epithelial line U, which is partially infectable with EBV, was hybridized with the EBV‐genome carrying Burkitt lymphoma lines P3HR‐1 and Daudi. Authenticity of the hybrids U‐Put and U‐Dut was established by isoenzyme studies. Although the two hybrids carried the EBV genome derived from the lymphoma parent, being 100% positive for Epstein‐Barr‐virus‐associated nuclear antigen (EBNA), they resembled the U parent in many respects: they were deficient for membrane immunoglobulins and Fc receptors, and had a lower concentration of EBV‐C1 receptors than either parent. Unlike the P3HR‐1 parent, U‐Put hybrid was nonpermissive for both the EBV cycle antigens, early antigen (EA) and viral capsid antigen (VCA). The inducing agent 12‐O‐tetra‐decanoyl‐phorbol‐13‐acetate (TPA) caused distinct viral early antigen synthesis (EA) in U‐Put, lower, however, than that of the parental P3HR‐1. U‐Dut was completely nonpermissive and noninducible for early and viral capsis antigens. Thus, even an epithelial parent infectable by EBV restricted, although not completely, expression of EBV antigens, with the exception of EBNA. It has been suggested that EBNA is an autonomous function of the viral genome, independent of host cell control; the latter regulates expression of antigens related to viral cycle. The hybrids U‐Put and U‐Dut resembled the U parent also in regard to growth in soft agar and tumorigenicity in nude mice, although in this respect the lymphoma parental properties were not completely eclipsed.
Interferon treatment of murine meth‐a sarcoma cells: Effects on the malignant phenotype and expression of tumor‐specific and H‐2 antigens
Authors: Wivel Nelson A. , Pitha Paula M. 
Published: February 2007

AbstractA virus‐free methycholanthrene‐induced sarcoma (Meth‐A) in BALB/c mice was grown in culture and treated with purified mouse interferon (α and β mixture) prior to testing for oncogenicity in the host animal. Use of interferon in vitro caused growth inhibition, but not cytotoxic effects; such effects were fully reversible upon interferon removal from the system. There was a significant decrease in tumor incidence in mice challenged with interferon‐treated cells, but this could be overcome by sufficiently increasing the number of cells in the inoculating dose. By transplanting these BALB/c sarcoma cells into Sprague‐Dawley nude mice, the effects of interferon could be negated. Since these mice have an unaltered activity of NK cells, the results suggest that NK cells do not play a major role in rejection of the Meth‐A tumor, but that the reduction in tumor incidence is dependent on the presence of functional T cells. Interferon caused a detectable reduction in the expression of the tumor‐specific transplantation antigen (TSTA) associated with Meth‐A cells, but increased the expression of H‐2 antigens. It has recently been shown that H‐2 antigens play a role in host recognition of the TSTA of methylcholanthrene‐induced sarcomas. It is suggested that the increased expression of H‐2 antigens on interferon‐treated Meth‐A cells could lead to an increased frequency of recognition by T‐cells.
Acquisition of sensitivity to exogenous fibronectin by friend leukemia cells correlates with reduction of their tumorigenic potential
Authors: Benedetto A. , Amici C. , Djaczenko W. , Zaniratti S. , Elia G. 
Published: February 2007

AbstractStrongly adhesive, highly flattened clones (FF clones) can be selected from Friend leukemia cells (FLC) cultivated on top of monolayers of human embryonic fibro‐blasts (HEF). The flattened phenotype of FF clones is stable during cell replication either in soft agar or in vivo. With the number of passages of FLC on HEF the fibronectin (FN) sensitivity of FF clones increases with a proportional reduction of their tumorigenicity. The FN‐sensitivity was defined as the ability of a certain dose of FN to flatten 50% of cells of a given FF clone. Tumorigenicity was defined as the number of FF cells able to give palpable tumors, in 50% of inoculated mice. Exogenous FN does not modify the duplication time of FF clones but strongly influences their growth behavior. In the presence of FN, the growth rate of FF cells is controlled by the size of the growth area available. Highly FN‐sensitive FF cells grown on FN‐coated substrata die at confluency while FF cells not adherent to substrata escape cell death and grow in suspension. We conclude that the high intrinsic FN‐sensitivity of FF cells and FN availability at the site of tumor inoculation could be responsible for the reduced tumorigenicity of highly flattened FF clones.