bluuebunny/crossref_metadata_2025_split huggingface dataset:
Height and cancer risk in a network of case‐control studies from northern Italy
Authors: La Vecchia Carlo , Negri Eva , Parazzini Fabio , Boyle Peter , D'Avanzo Barbara , Levi Fabio , Gentile Antonella , Franceschi Silvia 
Published: February 2007

AbstractThe relationship between self‐reported height and cancer risk was investigated in an integrated series of case‐control studies including 273 cases of cancer of the oesophagus, 474 of the stomach, 558 of the colon, 352 of the rectum, 227 of the liver, 267 of the pancreas, 110 of the larynx, 2,388 of the breast, 545 of the cervix uteri, 563 of the endometrium, 688 of the ovary, 80 of the prostate, 263 of the bladder, 105 of the kidney, 43 Hodgkin's disease, 152 non‐Hodgkin's lymphomas, 109 multiple myelomas, and a total of 5,574 controls admitted to hospital for acute, non‐neoplastic conditions. No significant positive trend in risk was observed for any of the cancer sites considered, and some suggestion of elevated risks for the upper quintile of height was observed only for prostate (relative risk, RR =1.4), kidney (RR =2.7) and colon (RR =1.2) in males (but not in females). For breast cancer, all the RRs for subsequent quintiles of height were close to unity. Four neoplasms showed significant inverse trends with height: oesophagus (RR =0.7 for highest vs. lowest quintile), cervix (RR =0.4), endometrium (RR =0.7) and ovary (RR =0.6). For oesophagus and cervix the trends could be explained, at least in part, in terms of social class correlates (multivariate RR 0.8 and 0.5, respectively), while for endometrium they could possibly be related to an inverse correlation between height and body mass (multivariate RR 0.9). Thus, our study did not support the hypothesis that nutrition in childhood and adolescence (which in this population is a determinant of adult height) is directly related to the subsequent risk of cancer at several major cancer sites. A number of inverse associations emerged, which may be either spurious and incidental, or suggest that poorer nutrition early in life may be an unfavourable indicator of the subsequent risk of selected neoplasms.
Establishment of an EBV‐positive lymphoblastoid cell line that grows as a lymphoma in nude mice and expresses membrane CD2 molecules
Authors: Roncella S. , Ramarli Dunia , Cooper M. K. , Forni M. , Caretto Patrizia , Rowe M. , Celle Paola Francia Di , Sessarego M. , Foá R. , Forni G. , Burrows P. , Pistoia V. , Ferrarini M. 
Published: February 2007

AbstractWe describe a human lymphoblastoid cell line (LCL), called ZS, that originated spontaneously from the cultures of gamma‐irradiated (50 Gy) peripheral‐blood mononuclear cells of a normal donor. When injected subcutaneously in sublethally irradiated, splenectomized and anti‐asialo‐GM1‐treated nude mice, ZS cells invaded the lymph nodes, that appeared 10 to 50‐fold enlarged in all of the mice tested. Furthermore, ZS cells expressed a typical T‐cell surface structure, the CD2 molecule, detectable by a variety of different anti‐CD2 monoclonal antibodies (MAbs). However, other T‐cell markers were not found, with the possible exception of a truncated messenger of the β chain of the T‐cell receptor and ZS cells could be identified as B cells since they (i) expressed a battery of markers of the resting and activated B cells, (ii) displayed a monoclonal rearrangement of the lgH chain locus and (iii) synthesized lgM K molecules.The Epstein‐Barr virus (EBV) genome was detected in ZS cells in approximately ten copies per cell by DNA hybridization techniques. Furthermore, the cells were positive for EBV nuclear antigens (EBNA). Western blotting analysis of EBV encoded antigens demonstrated clear differences with those present in the B 95.8 virus‐producer cell line, indicating that ZS cells were not infected by EBV in vitro and that they already harbored the virus in vivo. ZS cells formed colonies in vitro with a high cloning efficiency and displayed chromosomal abnormalities in all of the mitoses (karyotype 47, xy, +13,–14, 8p+, 21p+, +m). In spite of these malignant features, ZS cells expressed the full range of EBV latent proteins as usually do “normal” LCSs and did not have any of the chromosomal abnormalities that juxtapose the c‐myc oncogene to one of the genes coding for immunoglobulir molecules.
Effect of ornithine decarboxylase inhibitor on tetragastrin treatment of gastric carcinogenesis induced by N‐methyl‐N'‐nitro‐N‐nitrosoguanidine in wistar rats
Authors: Tatsuta Masaharu , Iishi Hiroyasu , Baba Miyako , Taniguchi Haruo 
Published: February 2007

AbstractThe effects of combined administration of tetragastrin and the ornithine decarboxylase inhibitor 1,3‐diaminopropane (DAP) on the incidence and number of gastric cancers induced by N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG), and the BUdR labelling indices of the fundic and antral mucosae, were investigated in inbred Wistar rats. Rats were given drinking water containing 2.5 g/l of DAP ad libitum and received alternate‐day injections of 1 mg/kg body weight of tetragastrin in depot form after 25 weeks of oral treatment with MNNG. At week 52, prolonged administration of tetragastrin alone resulted in a significant reduction in the incidence and number of gastric cancers and a significant increase or decrease in the labelling indices of the fundic and antral mucosae, respectively. Concomitant administration of tetragastrin and DAP had no effect on the inhibition by tetragastrin of gastric carcinogenesis. With this treatment, the labelling index was significantly reduced in the fundic mucosa but not in the antral mucosa. These results suggest that ODC inhibitor does not attenuate tetragastrin inhibition of gastric carcinogenesis, and that anti‐trophic action of tetragastrin on antral mucosa may be related to tetragastrin inhibition of gastric carcinogenesis.
Role of CD18 in lymphokine, activated killer (LAK) cell‐mediated lysis of human monocytes: Comparison with other lak targets
Authors: Kay Blanchard D. , Hall Robert E. , Djeu Julie Y. 
Published: February 2007

AbstractThe role of CD 18, identified as the beta chain of the CD 11 family of adhesion glycoproteins, in the lysis of normal autologous monocytes by interleukin‐2‐activated killer (LAK) cells was explored. The addition of several preparations of anti‐CD18 monoclonal antibodies (MAbs) to the incubation mixture of LAK cells and various target cells indicated that lysis of autologous monocytes, K562 erythroleukemia tumor cells, FMEX melanoma tumor cells, and fresh ovarian tumor cells were readily inhibited by all anti‐CD 18 antibodies tested. Kinetic experiments demonstrated that significant inhibition of lysis occurred if RH1‐38 antibody was added up to 2 hr after LAK cells were added to target cells. By the use of selective coating of targets and effector cells with RH1‐38, it was determined that anti‐CD 18 antibody inhibited lysis at the effector cell level but not at the target cell level, although CD18 was detectable on the surface of monocyte targets by FACS analysis and immunoprecipitation. Furthermore, specific binding of LAK cells to all targets tested was not affected by the presence of anti‐CD 18, indicating that lysis of target cells was blocked at a post‐binding event. Finally, of the 3 alpha chains associated with CD18, only antibodies to LFA‐1 (CD 11 a) partially blocked binding of LAK cells to monocytes and tumor cells. It is possible, then, that both CD 11a and CD18 may work in concert to effect the lysis of target cells by LAK cells.
Residual immunity of athymic NCr/sed nude mice and the xenotransplantation of human tumors
Authors: Silobricic Vlatko , Zietman Anthony L. , Ramsay Jonathan R. , Suit Herman D. , Sedlacek Robert S. 
Published: February 2007

AbstractThis study assessed the residual immunity possessed by NCr/Sed (nu/nu) athymic nude mice and examined strategies to reduce it in order to enhance the transplantability of human tumors for experimentation. Adult (8‐week‐old) female mice had fewer T cells (11%) and more B and NK (asialo‐GM1‐positive [ASGM1+]) cells in their spleen than euthymic (nu/+) controls. The number of phenotypically mature T cells increased with age, peaking at 16 weeks. ASGM1+ cells also increased in number over time, although the NK‐activity decreased after 12 weeks. B cells remained relatively constant in number. Athymic NCr/Sed nude mice displayed reactivity against a human squamous carcinoma xenograph (FaDu), in a Winn's test and TD50 assay. Immunity against xenografts (TD50 assay) was significantly lower (by a factor of 2) in 4‐week‐old than in 12‐week‐old nude mice. Similarly, a significant 2‐fold reduction in TD50 was obtained after a single intraperitoneal injection of cyclophosphamide into 8‐week‐old animals. Chronic (>8 weeks) exposure of the nude mice to subcutaneously administered β‐estradiol markedly reduced the number of splenic NK cells and their cytolytic activity, but the TD50 reduction was not statistically significant (p =0.1). Six Gray whole‐body irradiations (WBI) had been shown to produce a highly significant, 3‐fold reduction in the TD50 for FaDu. Flow cytometric analysis of splenic lymphoid cells from whole‐body‐irradiated recipients revealed: (a) marked initial depletion in the absolute numbers of lymphoid cells; (b) marked and long‐lasting depletion of T cells, with slow and minimal recovery only evident between 6 and 12 weeks; (c) rapid, almost complete, depletion of B cells with prompt and partial recovery after 2 weeks; (d) depletion of NK cells and NK activity, with recovery by 10 weeks. No change in the number or phagocytic capacity of resident peritoneal macrophages was seen. These data give further support to a postulated role for residual T cells in the xenoreactivity of NCr/Sed nude mice.
Cytokine‐mediated modulation of HLA‐class II, ICAM‐1, LFA‐3 and tumor‐associated antigen profile of melanoma cells. comparison with anti‐proliferative activity by RIL1‐β, RTNF‐α, RIFN‐γ, RIl4 and their combinations
Authors: Mortarini Roberta , Belli Filiberto , Parmiani Giorgio , Anichini Andrea 
Published: February 2007

AbstractNine different human melanomas and 16 clones, isolated from 2 of them, were characterized for susceptibility to rIL1‐β, rIL4‐, rTNF‐α‐ and rIFN‐γ‐mediated effects on proliferation and surface expression of class‐II HLA (DR and DP), ICAM‐1 and LFA‐3 molecules and of 3 tumor‐associated antigens (recognized by MAb 763.74T, 149.53 and R24). In spite of marked inter‐ and intra‐tumor heterogeneity for susceptibility to the effects of each cytokine, the most frequent upregulation was induced on the HLA class‐II antigens by rIFN‐γ and on adhesion molecules by rIFN‐γ, rTNF‐α and rlL1‐β, while tumor‐associated antigens were often down‐modulated by rIFN‐γ. Tumor heterogeneity was also evident on tumorcell proliferation with an apparent hierarchy in the frequency and extent of inhibitory effects: rIFN‐γ >rTNF‐α >rIL1‐β =rIL4. Combinations of 2 cytokines resulted in rare and limited changes in the antigenic profile in comparison to the effects seen with single factors, while the combination of rTNF‐α and rIFN‐γ resulted in significant synergistic antiproliferative effects on most tumor cells and clones. Taken together, these results indicate that single cytokines can profoundly affect the antigenic profile of melanoma cells, while strong tumor‐growth inhibition is often achieved by combinations of 2 cytokines acting in synergism.
Regulation of C‐FGR proto‐oncogene expression in epstein‐barr virus infected B‐cell lines
Authors: Patel Mukesh , Leevers Sally J. , Brickell Paul M. 
Published: February 2007

AbstractWe and others have previously shown that in vitro conversion of Epstein‐Barr virus (EBV)‐negative Burkitt lymphoma (BL) cell lines with the immortalizing B95‐8 strain of EBV results in a marked elevation in levels of c‐fgr proto‐oncogene mRNA. We now show, using a nuclear run‐off assay, that this induction results from an increase in the rate of transcription of the c‐fgr gene. We also show that BL cell lines freshly converted with the non‐immortalizing HR‐I strain of EBV do not accumulate higher levels of c‐fgr mRNA, suggesting that EBNA‐2 and/or LMP, the genes which are deleted in the HR‐I strain, may be involved in the pathway which leads to changes in c‐fgr gene expression. In order to assess the generality of a role for the c‐fgr gene in the response of B‐lymphocytes to EBV‐infection, which is controversial, we have analysed c‐fgr expression in 6 freshly immortalized cell lines established by EBV (B95‐8) infection of B‐lymphocytes from the peripheral blood of normal adults and of adults with rheumatoid arthritis, from cord blood, and from foetal liver. All 6 cell lines expressed c‐fgr mRNA at elevated levels compared to EBV‐negative BL cell lines.
Enhanced suppression of human myeloid leukemic cell lines by combinations of IL‐6, LIF, GM‐CSF and G‐CSF
Authors: Maekawa Taira , Metcalf Donald , Gearing David P. 
Published: February 2007

AbstractThe interactions of purified recombinant human leukemia inhibitory factor (LIF), interleukin‐6 (IL‐6), granulocyte colony stimulating factor (G‐CSF), and granulocyte‐macrophage CSF (GM‐CSF) on the clonogenicity of HL60 cells and U937 cells were studied in vitro. 11‐6 alone strongly suppressed colony formation by U937 cells with induction of differentiation and loss of clonogenicity. GM‐CSF interacted synergistically with IL‐6 to further reduce colony number and suppress the growth of clonogenic cells formed by HL60 and U937 cells. LIF synergized with IL‐6 to reduce colony number and enhance the suppression of the clonogenic U937 cells. The results suggest that these 4 glycoproteins, acting alone or in combination, may be able to suppress human leukemia cells of appropriate type and be of value in the clinical management of myeloid leukemia.
Age at first and second births and breast cancer risk in biparous women
Authors: Negri E. , La Vecchia C. , Duffy S. W. , Bruzzi P. , Parazzini F. , Day N. E. 
Published: February 2007

AbstractThe role of age at first and at second birth on subsequent breast cancer risk was analyzed using pooled data from 2 hospital‐based case‐control studies conducted in Italy, for a total of 1,200 biparous cases and 987 controls. Compared with women who gave birth for the first time below age 20, the relative risks were above unity for those with later first birth, even after allowance for age at second birth, although the trend was inconsistent across subsequent strata. A similar direct trend in risk was observed in relation to age at second birth: compared with less than 25 years and after allowance for age at first birth, the point estimates were 1.2, 1.4 and 1.4 for 25–29, 30–34 and ≥35 (p for linear trend = 0.04). The results for age at first and at second birth were similar in the 2 studies pooled in this analysis. A significant interaction with age was observed in relation to age at first and at second birth. In younger women (below age 50) a strong and direct association with age at first birth was found, while no apparent protection was conveyed by earlier second birth. Among older women (aged 50 or over), there was no apparent relationship with age at first birth after allowance for age at second, but the role of age at second birth was independent and statistically significant. Thus, our study confirms an independent and significant role of age at second birth in biparous women, after allowance for age at first birth, and indicates that, after reciprocal allowance, the role of first and second birth was not apparently different. The relative risks for both variables were quantitatively moderate, and may be influenced by age or other temporal variables.
Cancer mortality among japanese residents of the city of säo paulo, Brazil
Authors: Tsugane Shoichiro , Gotlieb Sabina L. D. , Laurenti Ruy , de Souza Jose M. P. , Watanabe Shaw 
Published: February 2007

AbstractDeath certificates of Japanese residents of the city of Säo Paulo, Brazil from 1979 to 1981 were analyzed for cancer deaths by means of the standardized mortality ratio (SMR) and the standardized proportional mortality ratio (SPMR). Compared with residents of Japan, a significantly higher SMR value was obtained from Japan‐born residents of Säo Paulo for prostate cancer, whereas lower values were obtained for cancer of the liver and gall‐bladder in both sexes, of the esophagus and rectum in males, and of the lung in females. SMR values were higher for cancer of the stomach in both sexes but lower for those of the esophagus and prostate in males and of the gall‐bladder and breast in females, when compared with the general population of Säo Paulo. Among Japan‐ and Brazil‐born residents, stomach cancer in women revealed a significant stepwise decrease by generation when SPMR was used as an indicator. The high proportion of stomach cancer in males, however, was as high among the Brazil‐born generation as in Japan. The SPMR of liver cancer decreased to the low level of the general population of Säo Paulo, even among the first generation. These changes in cancer patterns are discussed in relation to those among Japanese residents in the United States.
Body mass index and risk of breast cancer. A prospective study of 23,826 norwegian women
Authors: Vatten Lars J. , Kvinnsland Stener 
Published: February 2007

AbstractThe association between body mass index (BMI) and the incidence rate of breast cancer has been examined in 236 cases of breast cancer that developed among 23,826 Norwegian women during 11 to 14 years of follow‐up. At the time of height and weight measurement they were 35 to 51 years of age, and at the end of follow‐up their age was between 46 and 63 years. There was an overall age‐adjusted incidence rate ratio (IRR) of 0.52 (95% confidence limits, 0.34 and 0.77) for women in the highest quartile of BMI compared to women in the lowest quartile, which was confined to an effect observed among women who were diagnosed at age 50 or earlier (IRR = 0.36). The association with BMI displayed an inverse dose‐related trend (X2 for trend = 14.22, p < 0.001). The negative trend was particularly pronounced among non‐smoking women (X2 = 14.63), and no clear trend associated with BMI was observed among women who smoked 10 or more cigarettes per day (X1 = 0.41), indicating an interaction between BMI and cigarette smoking (X2 interaction = 3.86, p = 0.05). We thus suggest that there is a negative association between body mass index and risk of breast cancer among premenopausal women.
Lymphocytic infiltration and cytotoxicity under hypoxic conditions in the EMT6 mouse mammary tumor
Authors: Loeffler David A. , Keng Peter C. , Baggs Raymond B. , Lord Edith M. 
Published: February 2007

AbstractInfiltration of lymphocytes, neutrophils and macrophages was evaluated in hypoxic and well‐oxygenated areas of the EMT6 mouse mammary adenocarcinoma, by in vivo staining with the fluorescent dye Hoechst 33342 followed by cell sorting on the basis of fluorescence intensity. Tumors were grouped by days post‐injection (days 11–14, 15–17 and 20–27). As lymphocytes are the only host cell population in this tumor model to possess lytic activity against EMT6 tumor cells, the ability of sensitized T lymphocytes to lyse syngeneic EMT6 cells was examined under conditions of varying oxygen concentrations. Infiltrating lymphocytes were detected to the same extent in cell fractions from both areas in all tumors. In contrast, neutrophils were found in significantly higher percentages in the hypoxic population than in the well‐oxygenated cell fraction of all but the largest tumors. Macrophages were present in significantly higher percentages in the well‐oxygenated fraction than in the hypoxic fraction of day‐11 to ‐14 tumors. Extreme radiobiological hypoxia (0% O2) resulted in a significant decrease in T‐cell‐mediated lysis of EMT6 tumor cells, compared to lysis in room air (20% O2), but lysis was not impaired under conditions of mild radiobiological hypoxia (1% O2). Our study indicates that host‐cell infiltration into areas of differing oxygenation may be quantitated via in situ Hoechst staining followed by cell sorting; in the EMT6 tumor, lymphocytes appear to infiltrate hypoxic areas to the same extent as well‐oxygenated areas, and T‐lymphocyte killing of syngeneic tumor cells is significantly reduced, although still present, under these hypoxic conditions.
Inhibitory effects of 9‐(2‐Phosphonylmethoxyethyl)adenine and 3′‐azido‐2′,3′‐dideoxythymidine on tumor development in mice inoculated intracerebrally with moloney murine sarcoma virus
Authors: Balzarini Jan , Sobis Halina , Naesens Lieve , Vandeputte Michel , De Clercq Erik 
Published: February 2007

Abstract9‐(2‐Phosphonylmethoxyethyl)adenine (PMEA), a potent inhibitor of human immunodeficiency virus (HIV), caused a dose‐dependent suppression of tumor formation, and mortality associated therewith, in 6‐day‐old NMRI mice inoculated intracerebrally with Moloney murine sarcoma virus (MSV). Even at a dose as low as I mg/kg/day, PMEA effected a significant delay in tumor formation. When evaluated in parallel with PMEA, 3′‐azido‐2′,3′‐dideoxythymidine (AZT) conferred a comparable tumor‐inhibitory effect at a 5‐ to 10‐fold higher dose than PMEA. Prolonged treatment of MSV‐infected mice with PMEA resulted in long‐term survivors without apparent signs of tumor development. In view of the propensity of HIV to spread to the central nervous system (CNS), the marked activity shown by PMEA against experimental retrovirus infection of the brain in mice points to its potential in the treatment of AIDS and other retrovirus infections of the CNS.
Epstein‐barr virus internalization and infectivity are blocked by selective protein kinase C inhibitors
Authors: Cirone Mara , Angeloni Antonio , Barile Giuseppe , Zompetta Claudia , Venanzoni Marco , Torrisi Maria Rosaria , Frati Luigi , Faggioni Alberto 
Published: February 2007

AbstractSelective protein kinase C inhibitors can either block or significantly reduce Epstein‐Barr virus infectivity: inhibition of transformation and decreased 3H‐thymidine (3H‐TdR) incorporation in human B lymphocytes infected with B95‐8 EBV, as well as a significant reduction in the induction of early antigens in Raji cells superinfected by P3HRI EBV was achieved by pre‐treating the cells with the inhibitors. The inhibitors do not act by blocking binding of the virus to its cellular receptor CR 2, but rather are effective in the viral internalization process. Our results suggest that protein kinase C may be involved in the process of viral entry into cells.
Increased levels of 5‐fluorouracil‐induced dna lesions in bloom's syndrome
Authors: Lönn Ulf , Lönn Sigrid , Nylen Urban , Winblad Gerard 
Published: February 2007

AbstractIn Bloom's syndrome (BS) the regulation of uracil‐DNA glycosylase, an enzyme involved in the repair of DNA containing 5‐FU, is altered. 5‐FU induces higher levels of DNA fragmentation in BS cells than in non‐BS cells. The increase in DNA fragmentation is connected to the cytotoxic mechanism where 5‐FU is incorporated into DNA. When 5‐FU induces DNA fragmentation by a mechanism not involving the incorporation of drug into DNA, the levels of DNA fragmentation in BS and non‐BS cells remain similar.