bluuebunny/crossref_metadata_2025_split huggingface dataset:
Formaldehyde and cancers of the pharynx, sinus and nasal cavity: II. Residential exposures
Authors: Vaughan Thomas L. , Strader Clifton , Davis Scott , Daling Janet R. 
Published: February 2007

AbstractTo investigate the possible association between residential formaldehyde exposures and risk of cancer of the oro‐ and hypopharynx (OHPC, N = 205), nasopharynx (NPC, N = 27) and sinus and nasal cavity (SNC, N = 53), a population‐based case‐control investigation was carried out in 13 counties of western Washington. Controls (N = 552) were selected by random digit dialing. Subjects' residential histories, including type of dwelling, were determined from a structured telephone interview which also collected smoking, alcohol and demographic information. Multiple logistic regression was used to estimate exposure odds ratios (OR) while adjusting for known risk factors. A strong association was found between a history of having lived in a mobile home and NPC, but not OHPC or SNC. The NPC risk increased with the number of years lived in a mobile home: for those with I to 9 years the OR = 2.1 (95% confidence interval = 0.7–6.6), and for those with 10 or more years, the OR = 5.5 (95% CI = 1.6–19.4). No associations were found between any of the cancers and a history of exposure to new constructions containing particle board and plywood, or to urea‐formaldehyde foam insulation. The association found with living in a mobile home must be interpreted with caution since it is based on a small number of cases, and may be due to factors other than formaldehyde. This report emphasizes the need for additional studies focusing on potential associations between indoor air pollutants and respiratory cancers.
Suppression and re‐expression of transformed phenotype in hybrids of HA‐ras‐1 ‐transformed rat‐1 cells and early‐passage rat embryonic fibroblasts
Authors: Griegel S. , Traub O. , Willecke K. , Schäfer R. 
Published: February 2007

AbstractRat‐1 cells which had been transformed with the activated Ha‐ras‐1 gene from human EJ bladder carcinoma cells were fused with diploid embryonic rat fibroblasts. Four selected cell hybrids expressed the human transforming gene product p21 at levels of 10 to 30% compared to 100% in the transformed parental cells. The hybrid cells, however, exhibited normal morphology, anchorage requirement for proliferation, and largely extended latency periods of tumorigenicity in newborn rats. Tumorigenic hybrid derivatives contained lower numbers of chromosomes than the tetraploid parental hybrids. DNA of the non‐tumorigenic cell hybrids transformed Rat‐1 cells to anchorage‐independent proliferation as expected for the transforming human Ha‐ras gene present in the donor DNA. We conclude that the transforming properties of the activated Ha‐ras gene in Rat‐1 cells can be suppressed at the post‐translational level by the presence of the genome from diploid embryonic rat fibroblasts but additional controls of expression of the transforming gene are likely to exist. Normal cells contain suppressor gene(s) which safeguard these cells against transformation by the product of the transforming Ha‐ras‐1 oncogene.
Plasminogen activators, plasminogen activator inhibitors and procoagulant analyzed in twenty human tumor cell lines
Authors: Cajot Jean‐Franc̨ois , Kruithof Egbert K. O. , Schleuning Wolf‐Dieter , Sordat Bernard , Bachmann Fedor 
Published: February 2007

AbstractWe have analyzed the CM of 20 human tumor cell lines for the presence of PA, PA‐I and PC. Most of the cell lines expressed PA activity as measured by a ra‐dioiodinated fibrin plate assay. The urinary type and tissue‐type PA activities were specifically quantified by means of purified inhibitory antibodies. U‐PA and/ or t‐PA antigen, as measured by radioimmunoassays, were detected in all but 4 of the CM and were generally 10 times more concentrated than PA activity, indicating the presence of specific PA‐Is. Analysis of CM by electrophoresis followed by fibrin‐agarose zymog‐raphy demonstrated the presence not only of free but also of inhibitor‐complexed PA. Affinity purification demonstrated that 8/20 cell lines expressed detectable PA‐I activity. The PA‐I1 and PA‐I2 inhibitors were most frequently observed, while PN was recovered only from CM of the HT 1080 fibrosarcoma cell line. PC activity, as measured by the plasma recalcification time method, was found in 9/20 CM. It was of the thromboplastin tissue factor type since most of its activity was lost when assayed with a Factor VII‐deficient plasma.
Lymphoblastoid cell lines and burkitt‐lymphoma‐derivee cell lines differ in the expression of a second epstein‐barr virus encoded nuclear antigen
Authors: Ernberg Ingemar , Kallin Bengt , Dillner Joakim , Falk Kerstin , Ehlin‐Henriksson Barbro , Hammarskjöld Marie‐Louise , Klein George 
Published: February 2007

AbstractTwenty‐seven Epstein‐Barr virus (EBV)‐transformed lymphoblastoid cell lines and 27 EBV‐carrying Bur‐kitt‐lymphoma‐derived lines were analyzed for expression of the second EBV‐encoded nuclear antigen (EBNA‐2) by immunoblotting and anticomple‐ment immunofluorescence with EBNA‐2‐specific sera. While all lymphoblastoid cell lines expressed EBNA‐2, only 10 of the 27 BL lines were EBNA‐2‐positive. Comparison of the EBNA‐2 coding Bam HI W‐Y‐ and H‐fragments of EBV‐DNA in the different cell lines by restriction enzyme analysis suggests that EBNA‐2 negativity is due either to sequence diversity or to a deletion in the BamHI WYH region.
Oligoclonal tumours
Authors: Woodruff M. F. A. , Ansell J. D. , Hodson B. A. , Potts R. B. 
Published: February 2007

AbstractTumours are commonly classified as monoclonal or polyclonal. The question of how many clones are present in a polyclonal tumour is seldom asked; it is important, however, because the answer may show whether or not clones arise and develop independently, and whether the number of clones in tumours of a particular kind tends to increase or decrease with time. We have used two procedures to assess the clon‐ality of chemically‐induced murine fibrosarcomas, one based on the heterozygosity of the tumour hosts for an X‐linked marker, the other on the expression of tumour‐associated transplantation antigens (TATA) by the tumours. As we have reported previously, many of these tumours are pleoclonal. Evidence now presented suggests that the clones do not develop independently and that many of the tumours are biclonal.
Cysteine proteinases produced by cultured rabbit V2 carcinoma cells and rabbit skin fibroblasts
Authors: Baici Antonio , Knöpfel Margrit 
Published: February 2007

AbstractRabbit V2 carcinoma cells and normal rabbit skin fibroblasts produced cysteine proteinases with properties similar to those of purified rabbit liver cathepsin B. Both cell types secreted into the culture medium enzymes with an apparent Mr of 43,000, which reacted with synthetic substrates commonly used for cathepsin B. After limited proteolysis with pepsin or treatment at pH 3, the Mr = 43,000 species could be converted into forms with Mr = 34,000 and an increased specific activity. In the intracellular pool of both V2 carcinoma cells and fibroblasts, a cysteine proteinase with the same Mr of cathepsin B (27,000) was found. Despite the similarity in molecular size, substrate specificity and sensitivity to inhibitors, the tumor and fibroblast enzymes were not identical in their stability at pH ≧ 7 and were produced by the 2 cell types in considerably different amounts. In terms of enzyme units and normalized to an equal cell number, the ratios of fibroblast enzyme/tumor enzyme were as follows: secreted 130–150; intracellular, 150–180. The pH stability of the cysteine proteinases was determined quantitatively by measuring the half‐life of enzyme activity. At pH 8.0 and 25°C the secreted tumor cysteine proteinase had a half‐life of at least 5 hr, whereas the secreted fibroblast enzyme and liver cathepsin B had half‐lives of 8.8 min and 4.4 min, respectively.
Anti‐tumor effects of interferon in mice injected with interferon‐sensitive and interferon‐resistant friend leukemia cells. V. Comparisons with the action of tumor necrosis factor
Authors: Gresser I. , Belardelli F. , Tavernier J. , Fiers W. , Podo F. , Federico M. , Carpinelli G. , Duvillard P. , Prade M. , Maury C. , Bandit M.‐T. , Maunoury M.‐T. 
Published: February 2007

AbstractA number of similarities and dissimilarities in the anti‐tumor effects of TNF and interferon α/β have been observed in DBA/2 mice injected with Friend erythroleukemia cells (FLC). Mouse TNF exerted marked anti‐tumor effects in mice injected either s.c. or i.p. with FLC lines 3C 18 or 3 γR8 resistant in vitro to the cytotoxic effects of TNF. Likewise, mouse interferon α/β had anti‐tumor activity in mice injected with these FLC, resistant to the action of interferon α/β or γ in vitro. The results of histopathologic examination and 31P nuclear magnetic resonance analyses of 3C18 FLC s.c. tumors injected with TNF resembled the results previously obtained for 3C18 FLC tumors injected with interferon α/β, although the effects of TNF occurred more rapidly. Injection of mice with antibody to mouse interferon α/β or γ did not abrogate the anti‐tumor effects of TNF in mice injected i.p. with FLC. Our results suggest that in this experimental system the anti‐tumor effects of TNF, like interferon α/β, do not result from a direct effect on the tumor cells themselves but are host‐mediated.
Pharmacokinetics of methotrexate and its 7‐OH metabolite in cancer patients treated with different high‐methotrexate dosage regimens
Authors: Ei‐Yazigi Adnan , Amer Magid , Al‐Saleh Iman , Martin Cazemiro 
Published: February 2007

AbstractThe pharmacokinetics of methotrexate (MX) and 7‐OH methotrexate (MXOH) was studied in 18 cancer patients treated with 6‐hr intravenous (i.v.) infusion of 100 mg/kg (S), 80 mg/kg preceded by 30 mg/kg i.v. loading dose (C). Simultaneous analysis of MX and MXOH was performed by high‐performance liquid chromatography. The data for MX conformed to a 2‐compartment model with overall mean ± SD for beta k12, k21, and k13 of 0.225 ± 0.196, 1.33 ± 1.44, 0.954 ± 1.06, and 0.994 ± 1.28 hr−1, repectively. The total body clearance, Vc, and V‐beta were 0.123 ± 0.037 1/hr.kg, 0.15 ± 0.122 l/kg, and 0.965 ± 0.87 l/kg, respectively. No significant differences (p > 0.05) in these parameters, attributable to the difference in regimens, were observed. With regimens A, B and C, the maximum observed concentrations of MXOH occurred at 9.2, 11.5, and 9.2 hr and the mean ± SD values of these concentrations were 15.02 ± 14.91 ± 9.95 μm, respectively. With regimens A and C, maximum obserced concentration of MX equal to 231 ± 67.1 and 204 ± 69.5 μm, occurred at 0.5 and 6 hr, respectively. Only with regimen B was a steady‐state MX concnetration of 179 μm, achieved throughout infusion; this regimen is therefore highly advantageours for high‐dose MX treatment.
Diet and breast cancer: A case‐control study in Greece
Authors: Katsouyanni K. , Trichopoulos D. , Boyle P. , Xirouchaki E. , Trichopoulou A. , Lisseos B. , Vasilaros S. , Macmahon B. 
Published: February 2007

AbstractA case‐control study of the role of diet in the etiology of breast cancer was conducted in Athens, Greece. There are reasons to believe that the diet of the Greek population is characterized by greater heterogeneity than that in most countries where such studies have been undertaken. The case series consisted of 120 consecutive patients with histologically confirmed breast cancer admitted to either of two teaching hospitals over a 12‐month period. The controls were 120 patients admitted to a teaching hospital for trauma and orthopedic conditions during the same period. Dietary histories concerning the frequency of consumption of 120 foods and drinks were obtained by interview. Cases reported significantly less frequent consumption of vegetables as a group and, within that group, specifically of cucumber, lettuce and raw carrot. After adjustment for potential external confounding variables and for confounding between food categories, the odds ratio for persons in the highest quintile of vegetable consumers, relative to those in the lowest quintile, was 0.09 with 95% confidence limits 0.03–0.30. That is to say, the lowest quintile of vegetable consumers had about 10 times the breast cancer risk of the highest quintile. For a score based on consumption of only the 3 specified salad items the odds ratio over the extreme quartiles was 0.12 (0.05–0.32). There was no association with consumption of fats and oils, alcohol or coffee, and no significant association with any other major food category (including alcohol and coffee) after adjustment for confounding variables.
Evaluation of a mass screening program for stomach cancer with a case‐control study design
Authors: Oshima Akira , Hirata Noriko , Ubukata Takashi , Umeda Katstuhiko , Fujimoto Isaburo 
Published: February 2007

AbstractIn order to evaluate the effectiveness of a mass screening program for stomach cancer, a case‐control study was conducted in Nose town in Osaka, Japan. The case series consisted of all deaths from stomach cancer during the period 1969–1981 (54 in males and 37 in females). For each case, 3 controls of the same sex and from the same precinct as the case, and born within 5 years of the case birth‐year, were selected at random from Nose town residents alive at the date of death of the relevant case. We then investigated whether each case and corresponding controls had ever had screening tests before the date of diagnosis of the case. From the matched analysis of the distribution of screening in case‐control combination, the odds ratio of screened vs. unscreened among those who died from stomach cancer compared to those who did not was calculated as 0.595 (90% confidence interval: 0.338–1.045) among males and 0.382 (0.185–0.785) among females. When the screening tests conducted within 12 months of diagnosis were ignored on the presumption that they were symptom‐related, the odds ratio was calculated as 0.519 (0.297–0.905) among males and 0.486 (0.239–0.986) among females. These data strongly suggest that the mass screening program is effective in reducing stomach cancer mortality.
Plant‐derived diterpene esters enhance HTLV‐I‐induced colony formation of lymphocytes in co‐culture
Authors: Matsuda Shuichi , Nakao Yoshinobu , Ohigashi Hajime , Koshimizu Koichi , Ito Yohei 
Published: February 2007

AbstractThe addition to culture dishes of 10–50 ng/ml of the essential diterpene ester of Sapium sebiferum, 12‐O‐hexadecanoylphorbol‐13‐acetate (HPA), increased colony formation of normal peripheral blood lymphocytes co‐cultured with γ‐irradiated HTLV‐1‐producing HUT102 cells. The cells in the stimulated colonies showed an approximately 3‐fold increase in the expression of interleukin‐2 (IL‐2) receptors and a 1.5‐to 2.0‐fold increase in human T‐lymphotropic virus type‐I (HTLV‐I) p19‐positive cells. This biological potency was analogous to that induced by the most potent tumor promoter 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) and stronger than that of 12‐O‐hexade‐canoyl‐16‐hydroxyphorbol‐13‐acetate (HHPA) isolated from Aleurites fordii.
Establishment of a murine leukemia L1210‐specific T‐cell clone displaying novel in vivo anti‐tumor activity
Authors: Nagase Fumihiko , Ueda Kaoru , Nakashima Izumi , Kawashima Kohei , Isobe Ken‐Ichi , Nagura Ei‐Ichi , Yamada Kazumasa , Yokochi Takashi , Hasegawa Yoshinori , Yoshida Tomoaki , Ando Ko‐Ichi 
Published: February 2007

AbstractThe murine leukemia L1210‐specific cytotoxic T‐cell clone K7 was established by repeated antigenic stimulation of spleen cells of L1210‐immune CD2F, mice in long‐term culture. K7 possessed L1210‐specific cytolytic activity detectable by the 51Cr‐release test, but lost its cytolytic activity about 100 days after initiation of culture (designated as clone K7L). Clone K7L retained its L1210‐specific tumor‐growth‐inhibitory activity independently of culture supplementation with IL‐2. K7L possessed the cell‐surface antigenic phenotype of cytotoxic T cells, Thy‐1+, Lyt‐1+, Lyt‐2+. This clone K7L displayed surprisingly strong activity in specifically inhibiting In vivo tumor growth of L1210 by day 5 in the peritoneal cavity of CD2F1 mice when injected together with 105 tumor cells (more than 90% inhibition at E/T = 5), and prolonged survival times of most of the mice for more than 60 days, whereas control mice inoculated with L1210 alone died on day 9–17. This unique in vivo anti‐tumor activity was not correlated to the In vitro cytolytic activity. Nevertheless, bystander inhibitory effect on the growth of third‐party tumor cells (P388) was not seen in mice injected with a mixture of L1210 and P388 together with K7L, suggesting that K7L inhibited L1210 growth by direct cell‐to‐cell interaction. Host cells such as X‐irradiation (800R)‐sensitive lymphocytes and Carrageenan‐sensitive macrophages were not involved in the early growth inhibition of L1210 by K7L.
The differentiated form of nasopharyngeal carcinoma contains epstein‐barr virus DNA
Authors: Raab‐Traub Nancy , Flynn Kathy , Pagano Joseph , Pearson Gary , Huang Andrew , Levine Paul , Lanier Anne 
Published: February 2007

AbstractImmunologic studies of Epstein‐Barr virus (EBV) have implicated EBV in undifferentiated and partially differentiated, non‐keratinizing nasopharyngeal carcinoma (NPC). Patients with the well‐differentiated, keratinizing form of NPC have EBV serologic patterns similar to those of control populations. In addition, viral DNA has not been detected in the differentiated tumors using viral cRNA probes to DNA immobilized on filters. In this study we have tested for EBV DNA using recombinant DNA probes to Southern blots of DNA from 33 NPC specimens. The 24 undifferentiated and 4 partially differentiated specimens generally contained a relatively high number of EBV genome equivalents, while the 5 well‐differentiated NPC all contained detectable EBV, but at low copy number. The viral DNA from one of the well‐differentiated specimens was cloned into a cosmid vector. Five recombinant clones representing the fused viral termini were obtained, indicating the presence of episomal, intracellular DNA in the tumor. These findings indicate that all histologic subsets of NPC contain EBV DNA.
Circulating tumour‐associated antigen detected by the monoclonal antibody HMFG2 in human epithelial ovarian cancer
Authors: Ward B. G. , Cruickshank D. J. 
Published: February 2007

AbstractA radioimmunometric sandwich assay for the tumour‐associated antigen defined by the monoclonal antibody (MAb) HMFG2, has been used to measure serum levels of the antigen in 76 healthy controls, 38 ovarian carcinoma patients pre‐operatively, 98 patients 2 to 6 weeks after surgery and 36 patients at relapse or in complete remission at 12 months. HMFG2 antigen levels were elevated in 33% of stage‐I and 62% of II‐IV patients pre‐operatively; they reflected bulk of disease post‐surgically and were signficantly higher in patients in relapse than in those who were in complete remission. HMFG2 antigen levels predicted the clinical course of disease in the majority of patients.
Analysis of the inhibition of tumour metastasis by sulphated polysaccharides
Authors: Coombe Deirdre R. , Parish Christopher R. , Ramshaw Ian A. , Snowden John M. 
Published: February 2007

AbstractLung metastases resulting from the intravenous (i.v.) injection of cells from the rat mammary adenocarcinoma 13762 MAT were significantly reduced by a variety of sulphated polysaccharides, the most effective being heparin, fucoidan and Carrageenan lambda. Although all the inhibitory polysaccharides were anticoagulants, it is unlikely that anticoagulation is the total explanation of their antimetastatic effect because: (1) heparin preparations from 2 different suppliers, although exhibiting comparable anticoagulant activities, differed 10‐fold in their antimetastatic capability; (ii) certain sulphated polysaccharides consistently gave a 30% difference in the number of metastatic lesions, yet exhibited identical anticoagulant activity; and (iii) the entrapment of 13762 MAT cells in the lung was not impaired by heparin or fucoidan. It was more probable that the sulphated polysaccharides were interfering with the passaging of tumour cells across the capillary wall as heparin significantly inhibited metastasis when injected up to 3 hr after lodgement, and heparin and fucoidan caused a gradual loss of tumour cells from the lung which only became apparent greater than 1 hr following cell lodgement. The data did not eliminate the possibility that tumour cell adhesion to the endothelium occurred via sulphated polysaccharide recognition. A negative correlation existed between the sulphated polysaccharides that bound to the surface of the tumour cells and those that inhibited metastasis.
Purified colony stimulating factors (G‐CSF and GM‐CSF) induce differentiation in human HL60 leukemic cells with suppression of clonogenicity
Authors: Begley C. Glenn , Metcalf Donald , Nicola Nicos A. 
Published: February 2007

AbstractPurified recombinant human granulocyte‐macrophage colony‐stimulating factor (rHGM‐CSF) and purified native murine granulocyte‐CSF (G‐CSF) both induced differentiation in HL60 cells as evidenced by expression of granulocyte and macrophage membrane antigens, although this was not accompanied by morphological evidence of differentiation. Both types of CSF suppressed clonogenic HL60 cells with evidence of complete clonal extinction. The suppression of clonogenic HL60 cells was preceded in some experiments by CSF‐stimulated proliferation of HL60 cells, and this was most evident in cultures containing low concentrations of fetal calf serum (FCS).
Surveillance, latency and the two levels of MCA‐induced tumor immunogenicity
Authors: Prehn Richmond T. , Bartlett Gerald L. 
Published: February 2007

AbstractAmong 154 different, MCA‐induced mouse sarcomas, the immunogenicities of those tumors that had had the shortest original latencies in their autochthonous hosts were of an intermediate level with relatively little scatter. This fact is not predicted by the theory of immunological surveillance, but does fit the predictions of the immunological facilitation theory of oncogenesis. The frequency distribution of the tumor immunogenicities showed 2 peaks; the cluster of higher immunogenicity had a shorter latency than did the cluster of lower immunogenicity. The data for tumors initiated within in vivo diffusion chambers also showed 2 immunogenicity clusters, suggesting that the discrete clusters were not caused by host immunity. However, immunity apparently reduced the mean latency of the more immunogenic cluster and/or lengthened the mean latency of the less immunogenic, a result also inconsistent with the theory of immunological surveillance.