bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reduced occurrence of mdr‐1 amplification in stage‐IV breast‐cancer patients treated with tamoxifen compared with other endocrine treatments
Authors: Lönn Ulf , Lönn Sigrid , Stenkvist Björn 
Published: February 2007

AbstractAmplification of mdr‐1 occurs in breast cancer patients receiving endocrine treatment. We have compared a group of patients receiving tamoxifen and a group receiving second‐line endocrine treatment after failure of tamoxifen treatment. Chronological tumor samples were obtained by fine‐needle biopsies from the same tumor lesion of each patient and PCR was used to detect the appearance of gene amplification. Three of 20 patients receiving tamoxifen developed amplified mdr‐1 whereas 7 of 17 patients receiving second‐line endocrine treatment developed mdr‐1 amplification.
Cigarette smoking, alcohol, tea and coffee consumption and pancreas cancer risk: A case‐control study from opole, Poland
Authors: Zatonski W. A. , Boyle P. , Przewozniak K. , Maisonneuve P. , Drosik K. , Walker A. M. 
Published: February 2007

AbstractA population‐based, case‐control study of pancreas cancer was undertaken in Opole, Poland, within the framework of the SEARCH Programme of the International Agency for Research on Cancer: this is the first aetiological study of pancreas cancer reported from Poland where the reported mortality rate has doubled since 1963. This study of pancreas cancer has provided some further supporting evidence of an association between increased pancreas risk with increasing levels of cigarette smoking. The risk rose with increasing lifetime cigarette consumption with a trend which was weakly significant (p=0.061). Findings regarding lifetime tea and coffee consumption were not consistent with intake of either beverage increasing the risk of this disease. There was a strongly significant trend of decreasing risk with increasing lifetime consumption of tea (p<0.001), which was also apparent when the analysis was restricted to subjects who were interviewed directly. For coffee consumption, which is low in Poland, there was also a negative association apparent in the data which was not statistically significant among the sub‐set of subjects who were directly interviewed. The findings regarding alcoholic beverages were overall null, although the weakly positive trend in risk with spirits consumption (p=0.71) may deserve further investigation in view of the special nature of the source of spirits (vodka) in Poland.
Establishment and characterization of 7 ovarian carcinoma cell lines and one granulosa tumor cell line: Growth features and cytogenetics
Authors: van den Berg‐Bakker Cornelia A. M. , Hagemeijer Anne , Franken‐Postma Elsa M. , Smit Vincent T. H. B. M. , Kuppen Peter J. K. , Claasen Hedda H. Van Ravenswaay , Cornelisse Cees J. , Schrier Peter I. 
Published: February 2007

AbstractThe characteristics of 7 newly established ovarian carcinoma cell lines and one granulosa tumor cell line obtained from tumor samples of 7 patients with varying histology of the primary tumor are reported. The cell lines were isolated from 5 serous carcinomas, a mucinous carcinoma, an endometrioid carcinoma and a granulosa cell tumor. All cell lines were passaged at least 25 times and showed stable growth rates. Colony‐forming efficiency varied on plastic from 2 to 57% and in agar from 0.01 to 9.30%. The DNA index of the granulosa tumor cell line was diploid, while the ovarian carcinoma cell lines were all aneuploid. In 2 cell lines polyploidisation occurred during culturing. A thorough cytogenetic analysis of 7 cell lines revealed that the granulosa tumor cell line has only minor cytogenetic abnormalities (+5, 22q+). In contrast, the epithelial ovarian‐cancer cell lines gave very complex karyotypes with numerous markers and structurally rearranged chromosomes. The chromosomes most often in excess were 15 and 20. Structural rearrangements of chromosomes 1, 3, 7 and 11 were prominent in all ovarian cell lines. In addition, we found changes in chromosomes X, 5, 8 and 13 that have rarely been described before.
Inhibition of N‐linked oligosaccharide processing in tumor cells is associated with enhanced tissue inhibitor of metalloproteinases (TIMP) gene expression
Authors: Korczak Bozena , Dennis James W. 
Published: February 2007

AbstractPrevious studies on tumor‐cell glycosylation mutants and drugs which inhibit oligosaccharide processing suggest that expression of sialylated and highly branched complex‐type N‐linked oligosaccharides is required for efficient tumor‐cell metastasis. These observations prompted the present investigation, in order to determine whether loss of sialylated and highly branched complex‐type oligosaccharide in cellular glycoproteins might affect the expression of genes, particularly of genes which can influence the malignant phenotypes. Swainsonine, an inhibitor of Golgi α‐mannosidase II, has previously been shown to inhibit invasion in vitro and reduces solid tumor in vivo. Metastatic sub‐lines of the SPI murine mammary carcinoma cells cultured in the presence of swainsonine for 48 hr showed approximately 3‐fold enhancement of TIMP mRNA levels, while urokinase (uPA) transcripts remained unchanged. To determine whether swainsonine's effect on TIMP mRNA levels was related to inhibition of oligosaccharide processing, we examined somatic glycosylation mutants with processing defects which attenuate metastatic potential. The Golgi UDP‐Gal transport defect in murine MDAY‐D2 lymphoma cells, Chinese hamster ovary cells (CHO) and human MeWo melanoma cells (i.e., D35W25, Lec8, 355 cell lines, respectively) was associated with increased TIMP mRNA levels. A revertant of Lec8 showed a return to the wild‐type levels of TIMP mRNA, consistent with a causal relationship between the glycosylation mutation and TIMP gene expression. Similarly, CHO and MDAY‐D2 mutants defective in GlcNAc‐TV (i.e., Lec4 and KBL‐I respectively), which also reduces metastatic potential, showed increases in TIMP transcript levels. Nuclear run‐on assays showed that transcription of the TIMP gene was increased in cells where N‐linked oligosaccharide processing was inhibited either by swainsonine or by a glycosylation mutation. The results suggest that cell‐specific patterns of glycoprotein glycosylation in human, murine and hamster cell lines affects the transcription of select genes, including TIMP, which may influence the invasive phenotype.
Gp51 of bovine leukemia virus gene expression in hamster cells
Authors: Slávikova Katarína , Zajac Vladimir , Klobuǐká Margita , Aida Yoko , Tevurková Viola 
Published: February 2007

AbstractRecombinant pMMEx‐bovine leukemia virus env gene DNA fragments were produced and expressed in eukaryotic cells. Clone C4, containing an Smal‐Smal fragment of the gene coding for gp51, was co‐transfected with pSVZneo DNA into Chinese hamster cells. About 800 geneticin‐resistant cell clones were isolated and then morphologically and biologically characterized. The presence of gp51 encoding env gene fragments was detected in 17 of them by Southern blotting. The expression of gp51 gene in hamster cells was confirmed by Western blotting of their lysates with monoclonal antibodies (MAbs) directed against different epitopes of gp51 of bovine leukemia virus. The immunoreactivity of the expressed peptides with MAbs directed against neutralizing epitopes of gp51 of bovine leukemia virus was confirmed.
Anti‐tumor activity of ceramides and glycosphingolipids in a murine tumor system
Authors: Maru Morimasa , Haraguchi Muneo , Higashi Hideyoshi , Kato Shiro , Kurimura Takashi , Naiki Masaharu , Wakamiya Nobutaka 
Published: February 2007

AbstractThe anti‐tumor activity of 7 sphingolipids, 2 ceramides and 5 glycosphingolipids against the syngeneic murine ascitic tumors MH 134 and MM 102 in C3H mice was examined. Five of these compounds showed anti‐tumor activity against the tumors, ceramide type‐IV (Cer‐lv) having the highest activity without cytotoxic or cytostatic activity. These results indicate that the fatty acid in ceramide and sugar chains binding to it affect the anti‐tumor activity in vivo. The anti‐tumor activity of Cer‐IV depended on the time of treatment. Mice treated with Cer‐IV one day after tumor implantation showed the highest rate of survival. The cured mice were resistant to rechallenge with the same tumor (MH 134 → MH134, MM102 → MM102) but not with a heterologous tumor (MH 134 → X5563, MM102 → X5563), indicating that the effect of Cer‐IV may be due to in vivo induction of specific immunity. Studies with various antibodies demonstrated that the anti‐tumor effect of Cer‐IV was inhibited by all the antibodies tested (L3T4, Lyt‐2, and Thy‐1.2 T cells, macrophages, and TNFα) in the induction phase (before Cer‐IV administration) and by the antibodies of L3T4 and TNFα in the effector phase (after Cer‐IV administration). Therefore, the anti‐tumor effect of Cer‐IV in this system depended on the host immune response rather than on its direct cytotoxic and/or cytostatic action.
In vivo and in vitro reactivity of rat spleen cells against regressor and progressor colon‐cancer cell variants
Authors: Reisser Danièle , Olsson Nils‐Olivier , Martin François 
Published: February 2007

AbstractPrevious reports demonstrated that progressor and regressor tumor‐cell variants isolated from the same colon carcinoma chemically induced in a BD‐IX rat differed in their capacity to induce an immune response. The present study was aimed at analyzing the characteristics of the responses to the regressor REGb and progressor PROb clones. Spleen cells from rats bearing early REGb tumors neutralized PROb cell tumorigenicity in a Winn‐type local transfer assay, but responded occasionally to REGb and PROb cells in vitro. However, spleen cells from rats immunized by several injections of REGb and PROb cells strongly proliferated when cultured with PROb or REGb cells. This response was selective for the cell lines generated from the individual tumor at the origin of PROb and REGb lines, was dependent on CD4+ spleen cells, and was partially inhibited by an antibody against major histocompatibility complex class‐II molecules. Although PROb cells shared tumor‐rejection antigen(s) with REGb cells, splenocytes from PROb tumor‐bearing rats did not neutralize PROb‐cell tumorigenicity in vivo, nor did they proliferate when cultured with PROb or REGb cells in vitro. The unresponsiveness of spleen cells from PROb tumor‐bearing rats was not due to the presence of immune suppressive cells, and a defect of antigen‐presenting cells was shown to be unlikely. This unresponsiveness was limited to a lymphocyte subpopulation, since spleen cells from tumor‐bearing rats responded normally to stimulation by PHA or allogeneic lymphocytes. These results strongly suggest that unresponsiveness of spleen cells from tumor‐bearing rats is due to a tumor‐specific anergy of the lymphocyte clones able to respond to tumorassociated antigens.
Binding activities of cis‐platin‐damage‐recognition proteins in human tumour cell lines
Authors: McLaughlin Karen , Coren Grant , Masters John , Brown Robert 
Published: February 2007

AbstractProteins can be detected by South‐western analyses of human tumour‐cell extracts binding to double‐stranded oligonucleotide DNA treated in vitro with the chemotherapeutic drug cis‐diamminedichloroplatinum (11) (CDDP), but not to untreated DNA. The relative molecular masses of proteins binding to the CDDP‐treated double‐stranded oligonucleotide are 25, 48 and 97 kDa. The binding activity of 2 of the CDDP‐damage‐recognition proteins, of relative molecular mass 48 and 97 kDa, is greater in a CDDP‐resistant human ovarian tumour cell line than in the parental sensitive line. South‐western analysis of panel of human bladder cell lines and CDDP‐sensitive testicular cell lines show consistent patterns of CDDP‐damage‐recognition proteins within each cell type, however with differences between the 2 cell types. Binding of the proteins to CDDP‐damaged DNA and the altered binding activity detected in tumour cell lines suggests that alteration in damage‐recognition proteins could play a role in tumour response to CDDP.
Granulocyte‐macrophage colony‐stimulating factor stimulates the metastatic properties of lewis lung carcinoma cells through a protein kinase a signal‐transduction pathway
Authors: Young M. Rita I. , Lozano Yvonne , Djordjevic Andelka , Devata Sandeep , Matthews John , Young Melvin E. , Wright Mark A. 
Published: February 2007

AbstractExpression of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) by metastatic Lewis lung carcinoma cells (LLC‐ LN7) was previously shown to contribute to the maintenance of phenotypic characteristics associated with an increased capacity to metastasize. In the present study, pre‐incubation of LLC‐LN7 cells with neutralizing anti‐GM‐CSF antibodies diminished the capacity of the tumor cells to form experimental metastases after i.v. inoculation, while pre‐incubation with recombinant GM‐CSF (rGM‐CSF) increased formation of metastases. In the presence of rGM‐CSF, the LLC‐LN7 cells exhibited an increased capacity to migrate, invade through a reconstituted basement membrane, and adhere to lung tissue. Studies to identify the signal transduction pathway through which GM‐CSF enhanced the in vitro metastatic properties of the LLC‐LN7 tumor cells implicated protein kinase A (PKA). Signaling through PKA was suggested by the demonstration that the stimulation of tumor‐cell motility by GM‐CSF was blocked in the presence of the adenylate cyclase inhibitor nicotinic acid, or the PKA inhibitors A3 or KT5720. In addition, the role of PKA as a signaling mechanism for GM‐CSF was assessed by using REV‐LN7 cells, which are LLC‐LN7 cells that have been stably tranrfected with an expression vector encoding a mutant PKA RIα. subunit and which, in turn, express a cAMP‐resistant PKA. Adherence and invasion by the PKA‐defective REV‐LN7 cells were not stimulated by rGM‐CSF, contrasting with the stimulation observed for wild‐type LLC‐LN7 cells. These data suggest that rGM‐CSF can further enhance the in vitro metastatic characteristics of LLC‐LN7 tumor cells and that this is dependent on signal transduction through PKA.
Generation of cytotoxic antibodies to the B16 murine melanoma using a formalinized vaccine
Authors: Shrayer David , Kouttab Nicolas , Maizel Abby , Wanebo Harold , Hearing Vincent J. , Gersten Douglas M. 
Published: February 2007

AbstractThe goal of our experiments was to determine the extent to which the humoral response to a melanoma vaccine elicits the production of cytotoxic antibodies in tumor‐challenged mice. Mice were immunized with a vaccine produced from formalinized extracellular antigens (FECA) derived from B 16 F 10 melanomas. The production of antibodies that recognized the vaccine preparation was determined by ELISA, as was their cross‐reactivity with the B700 melanoma,antigen. The antibodies were shown to be anti‐proliferative by inhibition of tritiated thymidine incorporation into the DNA of cultured target cells and cytotoxic by assays for complement‐mediated and antibodydependent cellular cytotoxicity. Flow cytometric analyses indicated that‐60% of the target cells specifically bound antibody from the immune sera. These results confirm that B700 is a significant antigenic component of the FECA vaccine, and provide encouragement for this approach to developing useful melanoma vaccines.
Enhancement by isoproterenol of hepatocarcinogenesis induced by n‐nitrosomorpholine in sprague‐dawley rats
Authors: Uehara Hiroyuki , Nakaizumi Akihiko , Baba Miyako , Iishi Hiroyasu , Tatsuta Masaharu 
Published: February 2007

AbstractThe effect of isoproterenol on hepatocarcinogenesis induced by N‐nitrosomorpholine (NNM) was investigated in male Sprague‐Dawley rats. Rats were given drinking water containing NNM for 8 weeks and S.C. injections of isoproterenol or vehicle every other day for 13 weeks. Pre‐neoplastic and neoplastic lesions staining positive for γ‐glutamyl transpeptidase (GGT) or the placental type of glutathione‐S‐transferase (GST‐P) were examined histochemically at week 13. Prolonged administration of isoproterenol resulted in a significant increase in the number of GGT‐positive, but not GST‐P‐positive, lesions. The incidence, number and size of hepatocellular carcinomas were also significantly greater in rats treated with isoproterenol than in controls. Administration of isoproterenol significantly increased the intracellular cAMP and the labeling indices of pre‐neoplastic lesions and adjacent liver. These findings indicate that isoproterenol enhances hepatocarcinogenesis and that this may be related to its enhancing effect, mediated by cAMP, on cell proliferation in neoplastic lesions and surrounding hepatocytes.
Food‐group consumption and colon cancer in the adelaide case‐control study. I. Vegetables and fruit
Authors: Steinmetz Kristi A. , Potter John D. 
Published: February 2007

AbstractPrevious epidemiologic studies have shown an inverse association between vegetable and fruit consumption and risk of colon cancer. Vegetables and fruit contain a large number of potentially anti‐carcinogenic substances, thus lending biological plausibility to this association. We conducted a case‐control study in Australia, comparing 220 persons with histologically confirmed incident adenocarcinoma of the colon with 438 age‐ and gender‐matched controls. Cases were identified via the South Australian Cancer Registry (1979‐80); controls were randomly selected from the electoral roll. All participants completed 14I‐item food‐frequency questionnaire and were interviewed regarding demographic and other information. Consumption of 15 vegetable and fruit groups was investigated. Odds ratios (OR) for quartiles of consumption were derived using conditional logistic regression. All analyses were conducted separately for females and males. For females, greater intakes of onions and legumes were associated with decreased risk, with protein‐adjusted OR of 0.48 and 0.53 respectively. Greater intakes of raw fruit and cabbage were associated with protein‐adjusted OR of 0.76 and 0.71 respectively. For males, greater intakes of onions, green leafy vegetables, legumes, carrots and cabbage were associated with protein‐adjusted OR in the range of 0.72 to 0.77. Consumption of potatoes was positively associated with risk in both genders. All 95% confidence intervals included I.O. Analyses stratified by colon‐cancer sub‐site showed no strong and consistent differences between sub‐sites for the vegetable and fruit associations. Results for meat, poultry, seafood, dairy foods and eggs are presented in a companion report.
Food‐group consumption and colon cancer in the adelaide case‐control study. II. Meat, poultry, seafood, dairy foods and eggs
Authors: Steinmetz Kristi A. , Potter John D. 
Published: February 2007

AbstractWe conducted a case‐control study in Australia, comparing 220 persons with histologically confirmed incident adenocarcinoma of the colon with 438 age‐ and gender‐matched controls. Cases were identified via the South Australian Cancer Registry (1979‐80); controls were randomly selected from the electoral roll. All participants completed a 14I‐item food‐frequency questionnaire and were interviewed regarding demographic and other information. Consumption of 8 groups of foods from animal sources was investigated. Odds ratios (OR) for quartiles of consumption were obtained using conditional logistic regression. All analyses were conducted separately for females and males. The most striking finding was a positive association for egg consumption in females, with an unadjusted OR of 2.4 (1.1‐5.3) for consumption in the uppermost quartile. The uppermost septile of egg consumption was associated with an unadjusted OR of 6.3 (1.5‐26.1) and a dose‐response pattern was suggested. Intakes of red meat, liver, seafood, and dairy foods were also weakly positively associated with risk in females. In males, intakes of red meat and poultry were weakly positively associated with risk with unadjusted ORs of 1.5 (0.8‐2.8) and 1.4 (0.7‐2.6) respectively. The ratio of intake of red meat to poultry and seafood was also positively associated with risk in males, with an unadjusted OR of 1.4 (0.8‐2.6). Interpretation of analyses stratified by colon cancer subsite was limited by the low number of subjects in each sub‐site stratum, yet the results were somewhat supportive of a stronger risk associated with animal foods in the proximal than in the distal colon. The results for egg consumption suggest a role for cholesterol in the etiology of colon cancer, particularly in proximal cancer for females. Results for vegetable and fruit consumption are presented in a companion report.
Cancer risk in farmers: Results from a multi‐site case‐control study in north‐eastern italy
Authors: Franceschi Silvia , Barbone Fabio , Bidoli Ettore , Guarneri Salvatore , Serraino Diego , Talamini Renato , La Vecchia Carlo 
Published: February 2007

AbstractThe relationship between farming and cancer risk was investigated in an integrated series of case‐control studies conducted from 1985 to 1991 in the Friuli Venezia Giulia region, north‐east Italy. Patients with cancer of the oral cavity and pharynx, larynx, oesophagus, colon and rectum, pancreas, breast, thyroid gland, kidney and urinary tract, bladder, prostate, soft‐tissue sarcomas, Hodgkin's diseases, non‐Hodgkin's lymphomas and multiple myelomas, and controls admitted to hospital for acute, non‐neoplastic conditions, were interviewed. For males, a significantly elevated relative risk was seen for oral cavity and pharynx. Farming, however, was associated with a significant protection against cancer of the colon and rectum and bladder. In females, only one significant association emerged, for multiple myeloma. A few significant interactions between cancer risk and year of birth (i.e., before 1930 or 1930 and after) were observed. The risk of cancer of the larynx was significantly elevated in younger male farmers but not in older ones. Our multi‐site case‐control study confirms that farmers have, for some cancer sites, a distinctive pattern. Excesses of cancer of the oral cavity and pharynx in farmers are characteristic of the present study area and, possibly, of similar European rural populations who have in common high levels of alcohol consumption and, at least in the past, unbalanced diets.
Epstein‐barr virus carriage by nasopharyngeal carcinoma in situ
Authors: Yeung W. M. , Zong Y. S. , Chiu C. T. , Chan K. H. , Sham Jonathan S. T. , Choy Damon T. K. , Ng M. H. 
Published: February 2007

AbstractWe studied the distribution of the EBV genome in tumour biopsies obtained from 42 patients with poorly differentiated or undifferentiated nasopharyngeal carcinoma (NPC) and 3 patients with well‐differentiated NPC. Six carcinoma in situ (CIS) foci were seen in 5 tumour specimens. By in‐situ hybridization, multiple copies of the EBV genome were detected in some of the tumour cells in 3 CIS lesions involving the full thickness of the mucosal epithelium, but without microinvasion, while the viral genome was present in the majority of the tumour cells contained in another 3 CIS lesions with microinvasion. In agreement with previous findings, poorly differentiated and undifferentiated carcinomas regularly carried the viral genome, the number of copies of which was similar to that seen in CIS, while some, but not all, of the tumour cells of the welldifferentiated histological type carried the virus. The viral genome was otherwise rarely detected in other areas of the mucosal epithelium and, where present, the viral carriage was confined to a few epithelial cells, in which the viral genome contents were markedly lower than in tumour cells. These results suggest that EBV may first become associated with NPC at an early stage of the disease shortly after the tumour has been initiated.