bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tar yields of cigarettes and the risk of oesophageal cancer
Authors: La Vecchia Carlo , Liati Paola , Decarli Adriano , Negrello Ivano , Franceschi Silvia 
Published: February 2007

AbstractThe relationship between cigarettes with varying tar yields and the risk of oesophageal cancer was evaluated using data from a hospital‐based case‐control study conducted in Northern Italy on 129 histologically confirmed cases and 426 controls with acute, non‐ neoplastic or digestive diseases unrelated to tobacco or alcohol consumption. Compared with never‐smokers, the relative risks of developing cancer of the oesophagus were 2.9 for subjects who smoked mainly middle‐ or low‐tar (< 22 mg) cigarettes and 8.9 for those smoking high‐tar cigarettes (⩾ 22 mg).The difference between the two categories was evident among ever‐smokers and only current smokers, was not explained by adjustment for the major covariates of interest (social class, alcohol consumption and dietary indicators), and persisted when allowance was made for duration of smoking and number of cigarettes smoked per day by means of multiple regression analysis. The present findings suggest that the relation between tar deliveries of cigarettes and risk may be even more marked for oesophageal than for lung cancer. Further, they have important public health implications, in consideration of the current relatively high tar yields of Italian cigarettes, particularly in a few areas of north‐eastern Italy where death certification rates from cancer of the oesophagus are among the highest in Europe. Nonetheless, in this study, smokers of prevalently low‐ to mid‐tar cigarettes still did experience a significantly higher oesophageal cancer risk than life‐long non‐smokers.
Failure to induce cervical cancer in mice by long‐term frequent vaginal exposure to live or inactivated herpes simplex viruses
Authors: Meignier Bernard , Norrild Bodil , Thuning Claire , Warren Joel , Frenkel Niza , Nahmias Andre J. , Rapp Fred , Roizman Bernard 
Published: February 2007

AbstractC57 mice aged 8–10 weeks in groups of 50 each received vaginal cotton pellets soaked in lysates of HEp‐ 2 cells, either mock‐infected or infected with herpes simplex virus I, herpes simplex virus 2, and highly attenuated recombinant viruses 5 times a week for 89 to 114 weeks. An untreated group was also included. The mock‐infected and some of the infected cell lysates were exposed to ultraviolet light at a dose sufficient to inactivate virus. Smears of exfoliated vaginal cells collected once a month and histopathologic sections of genital organs removed at autopsy were coded and examined blind for the presence of abnormal cells indicative of malignant changes and cervical cancer, respectively. Sera collected before termination of the study were tested blind for the presence of antibody to infected cell lysates and to purified herpes simplex virus glycoprotein B. The results were as follows: (i) Over 74% of 826 mice examined at autopsy contained tumors at non‐genital sites. The tumors were randomly distributed among the various groups, (ii) Gross genital abnormalities were less common in untreated animals than in mice receiving vaginal implants, (iii) The fraction of mice which developed cervical cancer diagnosed by histopathologic examination was small (7.2%) and not significantly different among various groups, (iv) There was no correlation between the presence of abnormal exfoliated cells indicative of early invasive or invasive cancer lesions and the histopathologically proven diagnosis of micro‐invasive or invasive cervical cancer, (v) The incidence and levels of antibody were highest in animals exposed to live virus; some mice exposed to inactivated virus also developed weak or moderately high antibody levels. The presence of antibodies did not correlate with the presence of histopathologically proven cervical cancer. The results do not support the ability of herpes simplex viruses to cause genital neoplasia in mice.
Analyses of transplanted murine tumors for HSV DNA sequences
Authors: Yehiely Fruma , Thuning Claire , Meignier Bernard , Norrild Bodil , Warren Joel , Nahmias Andre J. , Rapp Fred , Roizman Bernard , Frenkel Niza 
Published: February 2007

AbstractMeignier et al. (1986) report the results of exposure of C57BL/6NCr mice to vaginal plugs containing live or inactivated herpes simplex virus 1 or 2 (HSV‐1 or HSV‐2) or recombinant viruses 5 times a week for up to 114 weeks. Genital organs showing abnormalities were transplanted into nude mice. Of 33 transplants, 13 produced subcutaneous tumors in nude mice and 12 were subsequently transplanted into C57BL/6NCr mice. We report that the DNA extracted from coded tumor tissues of nude mice and from normal viscera of the same rodents did not hybridize with HSV‐1 and HSV‐2 DNA probes representing the viral genomic regions shown previously to be capable of morphologically transforming cells in culture. The sensitivity of the assays was such that we could detect 0.5 copies of the HSV sequences of complexity equal to or greater than 1 Kbp per cell DNA equivalent. To control for the sensitivity of the assays in the actual hybridizations, the tumor‐cell DNA was also hybridized with a β‐globin mouse DNA probe. A striking feature of these control hybridizations was the detection of β‐globin polymorphism in some nude mouse tumors. The β‐ globin polymorphism allowed us to conclude that the analyzed tissues contained significant amounts of the tumor cells occurring in the C57BL/6NCr mice.
cAMP metabolism in B16 melanoma clones during the formation of experimental and spontaneous metastases
Authors: Lester Bruce R. , Greig Russell G. , Buscarino Charles , Sheppard Jack R. , Corwin Steven P. , Poste George 
Published: February 2007

AbstractThe ability of B16 melanoma clones to form tumor colonies in the lung after i.v. injection (experimental metastases) correlates positively with their capacity to respond to activators of cyclic adenosine 3‐, 5‐ monophosphate (cAMP) metabolism (such as melano‐ cyte‐stimulating hormone and forskolin). To investigate whether this relationship is causal, the cAMP responses of 4 B16 melanoma clones of differing colonizing potential have been examined in freshly established stock cell cultures, in pulmonary colonies in vivo and in cultures established from these lesions. In all cases, the cAMP responsiveness of the excised colonies (and cultures derived from them) mimicked the responsiveness of the cultures from which they arose. B16 clones exhibiting low cAMP responsiveness gave rise to few experimental metastases all of which were poorly responsive to activators of cAMP metabolism. Similarly, clones with high cAMP responsiveness formed multiple lung colonies which displayed a marked sensitivity to agents that stimulated cAMP production. Parallel experiments on the spontaneous metastatic behavior of the same clones revealed that the cAMP responsiveness of cells in the primary (intra‐ footpad) tumor and spontaneous metastatic lesions in the lung faithfully reflected the response profile of the original tumor‐cell inoculum but no correlation was found between cAMP responsiveness and the capacity to form spontaneous metastases. These data suggest that cAMP‐dependent events may influence the survival, arrest and organ colony formation by cells injected directly into the circulation but appear to be of little or no importance in determining the early event(s) involved in the evolution of spontaneous metastases prior to the entry of cells into the circulation.
Density distributions of human squamous carcinoma cells: Influence of growth conditions, proliferative status and DNA content
Authors: Ng C. E. , Keng P. C. , Sutherland R. M. 
Published: February 2007

AbstractHuman squamous carcinoma cells (A43I, CaSki) were grown in vitro as multicellular spheroids or as exponential and plateau‐phase monolayer cultures. Single‐cell suspensions were obtained by disaggregating the spheroids and monolayer cultures with trypsin‐EDTA. Their buoyant density distributions were then compared by centrifuging the suspensions for 30 min at about 800 gave and 4°C in linear, continuous Percoll gradients. We found differences in buoyant density related to the growth condition (i.e. cells grown as spheroids or plateau‐phase cultures were more dense than those from exponential cultures) and to the cell‐line (i.e. CaSki cells were more dense than the A43I cells). Cells isolated from the inner layers of the spheroids appeared to be less dense than those from the outer layers. In addition, quiescent cells separated from the A431 spheroids by centrifugal elutriation, a technique based on cell size, were more dispersed in buoyant density than the corresponding proliferating cells recovered from the same spheroids. Flow cytometric analysis with mithramycin was performed to measure the DNA content of the cells. We found that the CaSki cells contained relatively more DNA than the A431 cells whereas, for the same cell line, growth as monolayer cultures or as multicellular spheroids did not influence their relative DNA content. We conclude that the growth conditions, the proliferative status of the cells and possibly their relative DNA content may influence the density distribution of these cells.
Interactions with host macrophages and ability of human melanoma cell lines to grow in nude mice
Authors: Benomar Abdeljalil , Gerlier Denis , Doré Jean‐Franc̨ois 
Published: February 2007

AbstractThe interactions of nude mouse macrophages with five human melanoma cell lines, characterized by their resistance to mouse NK activity and varying in their ability to grow s.c. in nude mice, were investigated. These lines were equally susceptible in vitro to both cytostatic and tumoricidal activities of activated peritoneal macrophages collected from nude mice inoculated 3 days previously with Brucella abortus B19R strains, I.p. injection of a poorly tumorigenic melanoma cell line (PTCL) in nude mice was followed by the local appearance of macrophages able to kill these cells in a 48‐hr 3H‐thymidine cytotoxicity assay. The level of tumoricidal macrophages was maximum for the first week and then slowly declined to disappear by the 4th week following PTCL inoculation. The use of an HTCL instead of a PTCL also induced macrophages able to kill HTCL cells, but the cytotoxicity level was lower and the activity disappeared more rapidly. In cross‐experiments using PTCL‐activated macrophages as effectors on HTCL targets, these cells were found to be less sensitive than PTCL cells when macrophages were taken at weeks 2 and 3 following PTCL inoculation. To investigate whether tumoricidal macrophages activated In vivo with human melanoma cells could also act in vivo, we inoculated these s.c. into nude mice, simultaneously with live HTCL cells. Peritoneal cells rich in melanoma‐activated macro‐phages prevented HTCL growth in most recipients, whereas spleen cells from the same donor mice did not modify the tumor take. These data indicate that xenogeneic tumors could activate nude mouse macrophages in vivo and suggest that the ability of human tumors to grow in nude mice could be related to their capacity to activate host macrophages locally and to the susceptibility of human tumor cells to the tumoricidal activity of activated macrophages.
Epstein‐barr virus‐related herpesvirus from a rhesus monkey (Macaca Mulatta) with malignant lymphoma
Authors: Rangan S. R. S. , Martin Louis N. , Bozelka Brian E. , Wang Nancy , Gormus Bobby J. 
Published: February 2007

AbstractA herpesvirus (RhEBV) was isolated from a lympho‐blastoid cell line (LCL) that became established from a malignant lymphoma in a rhesus monkey. The predominant cell marker in the LCL was that of B lymphocytes. RhEBV‐induced viral capsid (VCA) and nuclear antigens (NA) in the LCL were serologically related to similar antigens known to be induced by human Epstein‐Barr virus (EBV). RhEBV was of non‐human primate origin and was clearly differentiated from EBV in the anti‐complement immunofluorescence reaction using human and non‐human primate sera with antibodies to the NA induced by the respective viruses. While human sera reacted with NA induced by both EBV and RhEBV, monkey sera failed to recognize the NA induced by EBV. RhEBV‐induced NA was present in nearly all the cells of a suspension prepared from the tumor tissue mass, but not in the monolayer fibroblasts derived from the tumor tissue or in the blood and lymph‐node lymphocytes of clinically healthy animals. RhEBV induced in vitro transformation and establishment of LCLs from peripheral blood lymphocytes of normal rhesus and cynomolgus monkeys but not from those of 6 other non‐human primate species tested. The LCLs, with predominant B‐lymphocyte markers, established after treatment with RhEBV, all had evidence of the virus infection since nearly all cells in the culture expressed the virus‐induced NA.
Characterization of melanoma‐associated surface antigens involved in the adhesion and motility of human melanoma cells
Authors: de Vries Jan E. , Keizer Gerrit D. , Te Velde Anje A. , Voordouw Arie , Ruiter Dirk , Rümke Philip , Spits Hergen , Figdor Carl G. 
Published: February 2007

AbstractThe functional properties of the melanoma‐associated antigens detected by monoclonal antibodies (MAbs) AMF‐6 and AMF‐7 were investigated. These MAbs were selected previously because of their capacity to block the anti‐melanoma reactivity of cytotoxic T‐lymphocyte clones AMF‐6 and AMF‐7 detect a melanoma‐associated proteoglycan (MW > 450–250 kDa) and a molecular complex, which under reducing conditions consists of 4 compounds of 120, 95, 29 and 25 kDa respectively. AMF‐6 reacted strongly with all 30 cultured melanomas and all 41 melanomas in frozen tissue sections. Significant cross‐reactivity was only observed with nevi and perineurium, whereas normal skin melanocytes were negative. AMF‐7 reacted with all 25 cultured melanomas and all 34 melanomas in frozen sections. AMF‐7 cross‐reacted with a proportion of nevi and endothelial cells from small vessels. The antigen detected by AMF‐6 and AMF‐7 could not be modulated by retinoic acid or recombinant 7‐IFN, which induced or enhanced the expression of HLA‐DR, HLA‐DQ and Class‐I MHC antigens. In addition, the antigens were not readily modulated when cells were incubated in excess amounts of AMF‐6 and AMF‐7. Interestingly, the antigen detected by AMF‐7 was strongly associated with the adhesion and cytoplasmic spreading of melanoma cells to plastic surfaces and monolayers of vascular endothelial cells. AMF‐6 did not block the adhesion of melanoma cells but delayed cytoplasmic spreading. Both AMF‐6 and AMF‐7 blocked fibronectin‐induced chemotaxic motility and chemokinesis of melanoma cells. In addition to their membrane localization, the antigens detected by AMF‐6 and AMF‐7 were also abundant in extracellular adhesion plaques deposited by cultured melanoma cells.Our results indicate that the high‐MW melanomaassociated proteoglycan and the antigen detected by AMF‐7 are associated with adhesion and/or cytoplasmic spreading and motility of human melanoma cells, suggesting that these antigens are associated with the (hematogenic) dissemination of human melanoma. This is supported by the finding that AMF‐7 stained primary tumors heterogeneously, whereas metastases were homogeneously stained.
Monoclonal antibody G 250 recognizes a determinant present in renal‐cell carcinoma and absent from normal kidney
Authors: Oosterwdk E. , Ruiter D. J. , Hoedemaeker Ph. J. , Pauwels E. K. J. , Jonas U. , Zwartendijk I. , Warnaar S. O. 
Published: February 2007

AbstractThis report describes a monoclonal antibody designated G 250, subclass IgGI, that recognizes an antigen preferentially expressed on cell membranes of renalcell carcinoma cells (RCC) and not expressed in normal proximal tubular epithelium. G 250 antibody reacted with 46 of 47 primary RCC, with 7 of 8 RCC metastases and with a few other malignant tumors. The staining pattern of G 250 differs from that of other RCC‐related antibodies described. Preliminary experiments show that this antibody can be used to visualize RCC xenografts in nude mice by immunoscintigraphy.
Synergism of recombinant human interferon gamma with liposome‐encapsulated muramyl tripeptide in activation of the tumoricidal properties of human monocytes
Authors: Sone Saburo , Tandon Priti , Utsugi Teruhiro , Ogawara Mitsumasa , Shimizu Eiji , Nii Akihiko , Ogura Takeshi 
Published: February 2007

AbstractFreshly isolated human peripheral blood monocytes from healthy volunteers are not cytotoxic to allogeneic A375 melanoma cells, but they were rendered tumoricidal by incubation in vitro with either liposomes containing 5 μg/μtmol phospholipid of muramyl tripeptide phosphatidylethanolamine (liposome‐MTP‐PE; optimal dose, 500 nmol/ml) or recombinant human interferon gamma (rIFN‐γ; optimal dose, 100 U/ml). A combination of sub‐threshold concentrations of liposome‐MTP‐PE (50 nmol/ml) and rIFN‐γ (1 or 10 U/ml) also induced significant tumor‐cell killing, indicating that the effects of rIFN‐γ and liposome‐MTP‐PE in monocyte activation are synergistic. In contrast to rIFN‐γ, recombinant INF‐α and IFN‐β had additive effects with liposome‐MTP‐PE in human monocyte activation. Since recombinant human IFN‐γ has a synergistic effect with liposome‐MTP‐PE in monocyte activation, unlike IFN‐α or IFN‐β, and liposome‐MTP‐PE as well as rIFN‐γ is available at standardized concentrations, this combination could be of clinical value in the treatment of disseminated malignant disease.
Somatic rearrangement of the c‐myc oncogene in primary human diffuse large‐cell lymphoma
Authors: Chenevix‐Trench Georgia , Behm Frederick G. , Westin Eric H. 
Published: February 2007

AbstractChromosome translocations involving 8q24, the band to which c‐myc has been mapped (Dalla‐Favera et al., 1982), are a uniform finding in Burkitt's lymphoma (Bernheim et al., 1981). However, in only a minority of the tumors is the rearrangement of the c‐myc locus sufficiently close to the gene to be detected with currently available probes (Dalla‐Favera et al., 1983). Approximately 25% of diffuse large‐cell lymphomas have also been reported to have translocations involving 8q24 (Mitelman, 1985), but there have been no reports of c‐myc rearrangements in this form of non‐Hodgkin's lymphoma. We have examined the structure of the c‐myc locus in primary tumor tissue of 10 cases of diffuse large‐cell lymphoma. In one patient, Southern blot analysis revealed additional c‐myc fragments in the tumor DMA but not in the germ‐line DNA. Southern blot analysis using probes from both the heavy‐and light‐chain immunoglobin loci showed that the myc rearrangement was unlikely to involve the immunoglobulin loci in this patient.
Reversible inhibition of lymphokine‐activated killer cell activity by lipoxygenase‐pathway inhibitors
Authors: Sibbitt Wilmer L. , Imir Turgut , Bankhurst Arthur D. 
Published: February 2007

AbstractNatural killer (NK) cells and lymphokine‐activated killer (LAK) cells are anomalous cytotoxic cells which are potentially important in host defense against cancer. Several studies have demonstrated that natural killer (NK) cell activity can be suppressed by chemical inhibitors of the lipoxygenase pathway through inhibition of the production of leukotriene B4 (LTB4). The present study investigated the effects of the lipoxygenase inhibitors BW755C and nordihydroguaiaretic acid (NDGA) on NK and LAK cell activity. NK cell function of fresh peripheral blood mononuclear cells (PBMC) was determined via a standard chromium release assay employing K562 as the tumor target. The LAK cell activity of PBMC which had been stimulated with 10 IU of interleukin‐2 for 72 hr was determined against the NK‐resistant cell line Oaudi. Both BW755C and NDGA inhibited NK and LAK cell function at a variety of concentrations. Indomethacin, a prostaglandin synthesis inhibitor, did not bring about an appreciable diminution in NK or LAK cell activity. Inhibition of NK and LAK cell activities by BW755C and NDGA could be reversed by washing the effector cell suspensions prior to the cytotoxic assay or by adding LTB4(10−11–10−8 M) directly to the effectortarget suspensions. These data indicate that certain arachidonic acid oxidation products of the lipoxygenase pathway are essential for the function of LAK cells.
Epstein‐barr virus‐related ultrastructural modifications of plasma membrane during B‐cell transformation
Authors: Arancia G. , Ragona G. , Rocchi G. , Donelli G. 
Published: February 2007

AbstractUltrastructural modifications are described in the plasma membrane of in vitro established human B cells. By the freeze‐fracture technique, intramembrane particles (IMPs) are quantified in B lymphocytes following Epstein‐Barr virus (EBV) transformation in vitro, and in B‐lymphoma (Burkitt‐type) cells, either positive or negative for EBV genome. Analysis shows an overall increase in IMP density as compared to normal controls. Differences are observed between the protoplasmic and exoplasmic faces of fractured membranes as well as among in vitro transformed and clearly neoplastic cells. Results indicate that conformational changes in IMP distribution parallel neoplastic evolution of transformed cells.
Generation of mouse natural killer (NK) cell activity: Effect of interleukin‐2 (IL‐2) and interferon (IFN) on the in vivo development of natural killer cells from bone marrow (BM) progenitor cells
Authors: Riccardi Carlo , Giampietri Antonio , Migliorati Graziella , Cannarile Lorenza , D'Adamio Luciano , Herberman Ronald B. 
Published: February 2007

AbstractThe possible effect of IL‐2, α, β‐IFN and poly I:C (an IFN inducer) administration on the generation of NK cells of LI and BM‐reconstituted animals was investigated. B6D2F, mice were LI (9.5 Gy) by total‐body irradiation and reconstituted by i.v. injection of different doses (ranging from 106 to 2 × 107) of syngeneic BM, after which the levels of splenic NK activity were evaluated on days 4, 7, 9, 12 and 14 after LI and BM graft. After a marked decline on day 4 (no detectable NK activity at any effector to target ratio tested), NK activity gradually returned, reaching the levels of untreated controls on day 9. Groups of LI and BM‐reconstituted mice were also treated i.p. with mouse or human recombinant IL‐2 from day 0 through day 3 (15–50 U/day/mouse) after BM transplantation. It appears that an earlier reconstitution of NK activity occurs in IL‐2‐treated animals as compared to medium‐injected controls. LI and BM‐reconstituted animals were also treated i.p. with α, β‐IFN (104 U/mouse) or Poly I:C (1 mg/kg/mouse) from day 0 through day 3, and the splenic NK activity was evaluated at 4, 7, 9, 12 and 14 days after LI and BM graft. Our data indicate that in vivo administration of IFN or Poly I:C was able to cause an earlier maturation of NK activity as measured on days 7 and 9 after LI. In contrast, when the NK activity of IFN‐treated animals was compared with that of controls 14 days after LI and BM graft, a significant inhibition was found due to the induction of suppressor cells. Pre‐treatment of donor BM with Poly I:C or IFN was also able to induce a more rapid reconstitution of NK activity of recipient mice. The NK activity reconstitution paralleled the increase in the number of splenic LGL. A synergistic effect was obtained when LI mice were transplanted with Poly I:C‐pre‐treated BM and then treated with IL‐2. The effector cell in the IFN and IL‐2 treated chimeras is a typical NK cell: asialo GM‐1+, Thy 1±, Lyt 1−, Lyt 2−and reactive only against NK‐susceptible targets. These data suggest that IL‐2 as well as IFN may represent maturational signals in the in vivo physiological regulation of growth and differentiation of BM NK stem‐cells.