bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lung cancer and passive smoking
Authors: Trichopoulos Dimitrios , Kalandidi Anna , Sparros Loukas , Macmahon Brian 
Published: February 2007

AbstractFifty‐one women with lung cancer and 163 other hospital patients were interviewed regarding the smoking habits of themselves and their husbands. Forty of the lung cancer cases and 149 of the other patients were non‐smokers. Among the non‐smoking women there was a statistically significant difference between the cancer cases and the other patients with respect to their husbands' smoking habits. Estimates of the relative risk of lung cancer associated with having a husband who smokes were 2.4 for a smoker of less than one pack and 3.4 for women whose husbands smoked more than one pack of cigarettes per day. The limitations of the data are examined; it is evident that further investigation of this issue is warranted.
Chromosome pattern, growth in agar and tumorigenicity in nude mice of four human bladder carcinoma cell lines
Authors: Hastings R. J. , Franks L. M. 
Published: February 2007

AbstractFour human bladder carcinoma cell lines have been characterized by G‐banding, and the chromosomal patterns correlated to growth in agar and tumorigenicity in nude mice. Each cell line was shown to be chromosomally unique and although numerical and structural anomalies were present, none were common to all four cell lines. However, one or more copies of a structurally altered chromosome 8 were present in all four cell lines and may be associated with tumorigenicity in nude mice. A combination of three marker chromosomes was found in the more anaplastic cell lines, but not in the two well‐differentiated tumour cell lines. Growth in agar may be associated with the presence of the three marker chromosomes but was not correlated with tumorigenicity in nude mice.
Inhibitory effect of cholera toxin on human natural cell‐mediated cytotoxicity and its augmentation by interferon
Authors: Fuse Akira , Sato Takeyuki , Kuwata Tsuguo 
Published: February 2007

AbstractCholera toxin inhibits human natural cell‐mediated cytotoxicity in a dose‐ and time‐dependent manner. Pretreatment of lymphocytes with 10 ng/ml of cholera toxin for 2 h almost completely inhibited cytolysis. Interferon augmented human natural cell‐mediated cytolysis, but when lymphocytes were pretreated with cholera toxin before interferon treatment, no enhancement of cytolysis occurred. Cholera toxin could inhibit the enhancement of cytolysis by interferon even when lymphocytes were treated with cholera toxin after 2 h interferon treatment. Cholera toxin subunit B which binds cell surface ganglioside galactosyl‐N‐acetylgalactosaminyl ‐ [N‐ acetylneuraminyl]‐galactosylglucosyl ‐ ceramide (GMI) without activating adenyl cyclase had no effect either on natural cytolysis or on the enhancement of natural cytolysis by interferon, suggesting that mere binding of cholera toxin to the cellular receptor was not enough to inhibit natural cell‐mediated cytolysis. Cyclic adenosine 3′,5′‐monophosphate (cAMP) levels increased in cholera toxin‐treated lymphocytes and the time course of cAMP accumulation was similar to that of cytotoxicity inhibition. Exogenous dibutyryl‐cAMP (db‐cAMP) and theophylline inhibited cytolysis, while exogenous dibutyryl cyclic guanosine 3′,5′‐phosphate (db‐cGMP) enhanced cytolysis slightly, suggesting that the process of inhibition of human natural cell‐mediated cytolysis was at least partly modulated by intracellular cyclic nucleotides.
Characterization of the effects of asparaginase from escherichia coli and a glutaminase‐free asparaginase from vibrio succinogenes on specific cell‐mediated cytotoxicity
Authors: Durden Donald L. , Distasio John A. 
Published: February 2007

AbstractAsparaginases isolated from Escherichia coli and Erwinia carotovora are effective in the treatment of acute lymphoblastic leukemia in man. During treatment with either of these enzymes, patients frequently experience pronounced toxicity, including liver and pancreatic dysfunction and immunosuppression. The capabilities of these enzymes to hydrolyze L‐glutamine, an important amino acid in mammalian intermediary metabolism, have led investigators to suggest that the glutaminase activity may be responsible for the observed toxicities. Unlike other asparaginases, an enzyme isolated in our laboratory from Vibrio succinogenes, has been shown to be a potent antilymphoma agent and to be highly specific for L‐asparagine. Our previous work has established that the glutaminase‐free asparaginase from V. succinogenes does not suppress the in vivo humoral or cell‐mediated immune responses of mice to sheep red blood cells, whereas the E. coli enzyme abolishes these responses. In this study, we describe the mechanisms by which E. coli asparaginase suppresses specific antibody‐dependent cell‐mediated cytotoxicity. An analysis of the kinetics of appearance of the specific cell‐mediated cytotoxic response of spleen cells after immunization with sheep red blood cells revealed that it paralleled the IgG plaque‐forming cell response. In addition, 18‐h culture supernatants from immune spleen cells conferred upon non‐immune cells the ability to specifically lyse sheep red blood cells. Pretreatment of immune supernatants with protein A‐Sepharose 4B absorbed out the soluble arming factor. An analysis of E. coli asparaginase‐induced suppression of specific antibody‐dependent cell‐mediated cytotoxicity revealed that a decreased synthesis of specific IgG was responsible for the observed reduction in cytotoxic reactivity. When culture supernatants from spleen cells of immunized animals not treated with asparaginase were added to spleen cells from E. coli asparaginase‐treated mice, however, there was an increased cytotoxic response. This suggested that there was an increase in the number or ratio of effector cells for the specific antibody‐dependent cell‐mediated cytotoxic response in spleens of enzyme‐treated animals. Through the characterization of the immunosuppressive effects of two asparaginases—one having the catalytic capability to hydrolyze L‐glutamine and the other lacking this catalytic activity—we now have evidence that the immunosuppressive effects of E. coli asparaginase on specific antibody‐dependent cell‐mediated cytotoxicity cannot be the result of asparagine depletion alone. Our data demonstrate that the glutaminase‐free asparaginase from V. succinogenes is not immunosuppressive and suggest that an asparaginase with high substrate specificity for L‐asparagine may be a safer treatment for leukemia patients.
Hormones, chemicals and proviral gene expression as contributing factors during mammary carcinogenesis in C3H/StWi mice
Authors: Smith Gilbert H. , Teramoto A. , Medina Daniel 
Published: February 2007

AbstractC3H/StWi mice spontaneously lost their exogenous MMTV (MMTV‐S) in 1958 and became a low mammary cancer subline. They do not ordinarily express their endogenous MMTV provirus as virions. Virigin C3H/StWi females were exposed to chemical carcinogens, 7‐12 dimethyl(α)benzanthracene (2,6 mg) and urethane (200 mg) in the presence or absence of chronic hormonal stimulation of the mammary gland by pituitary isografts. By 10 months of age, mammary tumors developed in 40% of the females given DMBA, and in 59% of those given DMBA and carrying pituitary isografts. With urethane treatment alone, 14% of the mice developed mammary cancer during a 12‐months period; however, 74% of the mice bore mammary tumors when pituitary isografts were present. None of the females given pituitary isografts alone developed mammary cancer during the experimental period. Mammary tumors from each group were evaluated by radioimmune competition assay, immunoperoxidase and electron microscopy to determine the extent of endogenous MMTV gene expression. In addition, the mammary glands of some of the non‐tumor‐bearing mice were studied by whole mount and by histology to determine the type, extent, and number of mammary dysplasias present in each group. In general, there was no correlation between tumor incidence and the presence of mammary tumor virus antigens. Of 32 mammary tumors tested in all groups, 10 were positive at low levels for MMTV antigens. In the positive tumors, the internal MMTV gag gene antigen, p28, was prevalent. Immunoperoxidase studies on these same tumors gave quantitatively similar results. It is apparent from these observations that chemical carcinogenesis of mouse mammary glands does not require or even favor the complete expression of endogenous MMTV genes. In this study, hormonal stimulation of the glands during and after exposure to the carcinogen increases the rate of tumorigenesis, but does not seem to favor MMTV gene expression. We conclude that C3H/StWi mice are susceptible to DMBA and urethane induction of mammary cancer and to an extent this process is positively influenced by the presence of hormonal stimulation. Our results support the view that a qualitative or quantitative shift in the expression of MMTV proviral sequences does not occur during tumor development.
Experimental studies of tumor radioimmunodetection using antibody mixtures against carcinoembryonic antigen (CEA) and colon‐specific antigen‐p (CSAp)
Authors: Gaffar Shaik A. , Pant Keshab D. , Shochat Dan , Bennett Sidney J. , Goldenberg David M. 
Published: February 2007

AbstractExperiments with the GW‐39 human colonic carcinoma growing in hamsters showed that injection of radioactive antibody to a colorectal‐specific, tumor‐associated antigen, CSAp, results in better tumor radiolocalization than was seen previously with radioantibodies to carcinoembryonic antigen (CEA). However, a mixture of both radioactive antibodies resulted in potentiation of CEA‐tumor radioimmunodetection without affecting CSAp‐tumor radiolocalization. Hence, multi‐marker antibody mixtures may be the method of choice in cancer radioimmunodetection.
Selective antiviral activity of human interferons on primate oncogenic and neurotropic herpesviruses
Authors: Daniel Muthiah D. , Tamulevich Ruth , Bekesi J. George , King Norval W. , Falk Lawrence A. , Silva Daniel , Holland James F. 
Published: February 2007

AbstractHuman lymphoblastic, leukocytic and fibroblastic interferons were found to have marked antiviral activity on the replication of Herpes virus saimiri and Herpes virus ateles when used at a concentration of 500 IU/ml or greater but only minimal activity against two neurotropic viruses, viz. Herpes‐virus platyrrhine and herpes simplex virus. All three interferons were equally effective as antiviral agents against the oncogenic herpesviruses. Pretreatment of cells with interferons before virus infection was not required as it failed to enhance or retard the antiviral action of interferon, particularly in the case of the oncogenic herpesviruses. The m.o.i. of virus ranging from 100 to 0.0002 did not alter the effectiveness of the antiviral ability of interferon which was maintained at these virus concentrations. Interferon was equally effective in suppressing the replication of the two oncogenic viruses at low and high m.o.i. (20 to 0.00002). Interferon was able to suppress the advancement of virus‐induced cell cytopathic effect of HVS‐ and HVA‐infected cell monolayers. This event could be repeated continuously over a period of several months by addition and withdrawal of interferon. Virus‐infected cell monolayers exhibiting advance (75%) of cell cytopathology could be treated with 10,000 IU/ml interferon to attain cell confluency. These treated cells subsequently could be subcultivated (if maintained on 2000 IU/ml interferon) for over 14 months and 20 subpassages with an absence of virus, viral antigens or virus particles. These same cells, if maintained in the absence of interferon during each subpassage level, will produce virus; however, from the 14th subpassaged cell cultures virus appears to have been repressed or lost in the absence of interferon, suggesting that long‐term application of interferon may have a therapeutic effect in ‘eliminating’ virus infection. Owl monkey kidney cells infected with HVS or HVA at a m.o.i. of > 1 (2 and 20) or m.o.i. < 1 (to induce a multicycle infection) were successfully treated with interferon.
Lymphoproliferative responses to autologous tumor extracts as prognostic indicators in patients with resected breast cancer
Authors: Cannon G. B. , Dean J. H. , Herberman B. , Keels M. , Alford C. 
Published: February 2007

AbstractPatients with operable breast cancer were tested postoperatively to assess lymphoproliferative responses. Patients with lymphocytes capable of recognizing and proliferating in response to autologous tumor extracts had a significantly longer disease‐free interval than those with a low response to their autologous extract. In this group of patients, immunological responses to autologous tumors predicted subsequent clinical course better than pathological evaluation based on tumor presence in axillary lymph nodes. Low or negative reactivity to autologous tumor often was not accompanied by a general, impaired ability to respond in LP assays. In fact, patients with low autologous tumor response and normal MLC were at a particularly high risk for recurrence.
EBV infection of mitogen‐stimulated human B lymphocytes
Authors: Einhorn Lena , Klein Eva 
Published: February 2007

AbstractB lymphocytes from human blood were treated with the mitogen Protein A (Staph. aureus), which induces DNA synthesis in, as well as differentiation of, the B lymphocytes. The cells were subsequently exposed to Epstein‐Barr virus (EBV). EBV‐infected and mitogen‐stimulated cells were detected simultaneously, by using a combination of immunofluorescence (for EBNA) and autoradiography (for DNA‐synthesis). In the initial phase (1‐2 days) after addition of the mitogen, stimulated cells were as susceptible to infection as resting cells. Thereafter, their susceptibility decreased. This suggests that, although initiation of DNA‐synthesis does not seem to limit sensitivity to the viral infection, differentiation of the B cells might do so. The intensity and pattern of EBNA‐staining in prestimulated cells differed from that of the controls.
Naturally occurring humoral immunity to endogenous xenotropic and amphotropic type‐C virus in the mouse
Authors: Kende Meir , Veronese Fulvia , Hill Dick W. , Dinowitz Marshall , Kelloff Gary J. 
Published: February 2007

AbstractNatural humoral cytotoxic antibodies from 13‐ and 18‐month‐old BALB/c mice showed a virus‐specific complement‐dependent activity against target cells productively infected with xenotropic, amphotropic or ecotropic type‐C viruses. The cytotoxic activity was lowest against ecotropic virus‐shedding cells. Serum obtained from mice less than 12 months old had no such reactivity. The cytotoxic reactivity was found to reside solely in the immunoglobulin M fraction which yielded reactivity comparable to the unfractionated sera concerning both titer and relative reactivities to the target cells infected with different type‐C viruses. In hyperimmune mouse serum cytotoxic reactivity resided in IgG and IgM fractions. Examination of serum from individual, normal 18‐month‐old BALB/c mice revealed that 80–90% of them were cytotoxic against virus non‐producer mink target cells expressing gp70 or gaggene product. Absorption of sera from 18‐month‐old normal BALB/c mice with cells shedding Class II or Class III xenotropic virus, amphotropic virus, Rauscher‐MuLV, or Class I murine leukemia virus indicate a closer amphotropic‐FMR viral subtype specificity of the natural cytotoxic immune response as compared to the amphotropic‐xenotropic or amphotropic‐ecotropic specificity. The incidence and the level of measured humoral cytotoxic activity was sustained in the tumor‐bearing animal up to 28 months of age as compared to the background established in the 18‐month‐old animal. However, in the non‐tumor‐bearing animal, the incidence and level of cytotoxic reactivity declined rather rapidly with aging. The sustained cytotoxic reactivity of the serum from old tumored mice might be involved in the progression of the tumor.
Rapid hepatoma induction in rats by dipentylnitrosamine and its modification by other carcinogens
Authors: Davis William E. , Jones David C. L. , Rosen Victor J. , Sasmore Daniel P. 
Published: February 2007

AbstractDipentylnitrosamine (DPN), administered in the diet at a concentration of 2,000 ppm to Fischer‐344 rats, produced hepatomas in 27% of both males and females within 8 weeks. Bile‐duct carcinomas were also produced. All animals also showed liver nodular hyperplasia and bile‐duct cell proliferation. Feeding DPN at 1,500 ppm produced hepatomas or bile‐duct carcinomas in 7% of the males and varying degrees of nodular hyperplasia and duct cell proliferation after 8 weeks of feeding. The total cumulative dose after feeding 2,000 ppm DPN was of the order of 7,700 mg/kg body weight in males and 8,200 mg/kg in females. There was a 28% weight decrement in animals fed 2,000 ppm DPN when compared to controls but no mortality. DPN carcinogenicity was enhanced when DPN was combined with a liver carcinogen, cycasin (fed as cycad nut flour, equivalent to 160 ppm cycasin). No effect on DPN carcinogenicity was found in rats fed DPN and lasiocarpine, another known liver carcinogen with antimitotic activity. Neither was there any effect on DPN carcinogenicity in rats fed DPN and N‐butyl‐N‐(4‐hydroxybutyl) nitrosamine or N‐methyl‐N′‐nitro‐N‐nitrosoguanidine. In contrast, the trisodium salt of nitrilotriacetic acid reduced the hepatocarcinogenic action of DPN. The enhancement of DPN carcinogenicity with cycasin is compatible with the hypothesis that DPN‐induced liver cell populations (hyperplastic nodules) can resist the cytotoxic effect of cycasin and differentiate rapidly toward hepatomas, while other areas of the liver are suppressed.
Prognostic value of chromosomal findings in the blast phase of Ph1‐positive chronic myeloid leukaemia (CML)
Authors: Oláh ÉVa , Rák Kálmán 
Published: February 2007

AbstractTwenty‐three patients in various cytological subgroups of blast phase of Ph1‐positive chronic myeloid leukaemia were investigated cytogenetically. The correlation between prognosis and the cytological and cytogenetic features of blast cells was studied. The best prognosis was found in the myeloid group, followed by the lymphoid, myelomonocytic, megakaryoblastic and finally the promyelocytic groups, in this order. As regards the prognostic significance of the cytogenetic finding, the survival seemed to be the longest among patients with mosaic karyotypes i.e. when further aberrations occurred in some Ph1‐positive cells. The course of the disease was the most favourable in the presence of i(17q), especially in patients whose cells had i(17q) as the only aberration. The most severe course of the disease could be found in patients with +8 and/or two Ph1. The results demonstrate the usefulness of chromosome investigations in distinguishing the different cytogenetic subgroups in terminal stages of CML, which also differ prognostically from each other.
Difference in viral binding between two epstein‐barr virus substrains to a spectrum of receptor‐positive target cells
Authors: Wells Alan , Koide Norio , Klein George 
Published: February 2007

AbstractRadio‐labelled Epstein‐Barr virus (EBV) was utilized in a direct binding assay to detect the presence of EBV receptors. The sensitivity of this method was affirmed by the detection of EBV‐receptors on three EBV‐carrying cell lines that have previously been reported as receptor negative. Two laboratory substrains of EBV, derived from the cell lines B95‐8 and P3HR‐1 (designated B and P virus respectively), were tested in the binding assay. The main receptor prototype adsorbed both viral strains without apparent distinction. In contrast, two lines, a Swedish EBV‐negative B‐cell lymphoma (U698) and a virus non‐producer subline of the receptor‐negative P3HR‐1 line, adsorbed P virus selectively but failed to adsorb B virus.
Deficiency of natural killer cell activity in patients with chronic lymphocytic leukemia
Authors: Ziegler Hans‐W.(Löms) , Kay Neil E. , Zarling Joyce M. 
Published: February 2007

AbstractNatural killer (NK)6 cell activity of peripheral blood lymphocytes against human leukemia cell lines was measured in patients with chronic B‐cell lymphocytic leukemia (CLL) and age‐ and sex‐matched controls. In order to remove the leukemia cells that interfere with the in vitro assay we (1) isolated lymphocytes that form rosettes with sheep red blood cells (SRBC) or (2) lysed the CLL cells with a monoclonal anti‐B cell antibody and complement. NK activity in either lymphocyte preparation from nine of 10 patients with advanced disease was not detectable and, when calculated in terms of lytic units per ml of blood, was at least seven times lower than in controls; only one of these patients exhibited activity within the control range. Two patients with early disease had measurable, but low, NK‐cell activity. Prolongation of the NK cell assay from 6 to 18h gave rise to significant killing in the CLL patients lacking NK cell activity in the 6‐h assay; however, the activity still was six times lower than in controls. Treatment of leukemia cell‐depleted lymphocytes from CLL patients with human fibroblast interferon or the interferon inducer poly I:C enhanced NK‐cell activity in the two early stage patients but this treatment was ineffective in three later stage patients. The percentage of cells with characteristics of NK cells, i.e. those with receptors for SRBC and Fc‐portion of IgG, was four times higher in CLL patients and the percentage of lymphocytes binding to NK‐sensitive target cells was equal to that in controls despite the fact that, in the majority of patients, lysis of the target cells by the lymphocytes does not ensue. The NK deficiency may be responsible for the increased incidence of secondary malignancies in CLL patients.
Host range and oncogenicity studies of the murine myeloma MOPC‐315 type‐C retrovirus
Authors: Gazit Arnona , Guthmann Daphna , Yaniv Abraham 
Published: February 2007

AbstractThe biological features of an endogenous type‐C RNA tumor virus released by the murine plasmacytoma MOPC‐315 were determined. The virus was found to be pure ecotropic and, according to its capability to infect both NIH/3T3 and BALB/3T3 cells, it was established as an NB tropic virus. This tropism became more pronounced as a consequence of multiple passages in BALB/3T3 cells. In view of the ability of myeloma viruses to efficiently infect BALB/c cells, their possible role in myeloma induction is considered.