bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stability of phenotypic and genotypic traits during the establishment of a human neuroblastoma cell line, IGR‐N‐835
Authors: Bettan‐Renaud Laurence , Bayle Chantal , Teyssier Jean‐Raymond , Benard Jean 
Published: February 2007

AbstractA prerequisite for the study of biological characteristics in neuroblastoma is the establishment of cell lines from tumors of patients. For our study a neuroblastoma cell line, IGR‐N‐835, was established from a primary tumor. During in vitro establishment of this line morphological changes were observed. IGR‐N‐835 exhibited both anchored cells and floating clusters. When cultured on bovine endothelial corneal cellular matrix, all tumor cells anchored to the matrix and proliferated, giving a continuous cell line. IGR‐N‐835 was studied in vitro and in vivo. Treatment with retinoic acid resulted in cell growth arrest and morphological differentiation. IGR‐N‐835 was highly tumorigenic in nude mice, exhibited a doubling time of 65 hr and was able to form colonies in methyl‐cellulose with a cloning efficiency of 0.46%. Immunocyto‐chemical studies showed reactivity of this line and its primary passages with CE7 monoclonal antibody (MAb). Cytogenetic analyses revealed stable mode and markers resulting from structural changes in chromosomes 10, 11 and 21 with no homogeneously staining regions or double minute chromosomes. Genomic amplification and overexpression of the N‐myc oncogene exhibited by the patient's tumor remained unchanged in nude mouse xenografts and the IGR‐N‐835 cell line. These phenotypic and genotypic traits were unchanged during establishment of this neuroblastoma line. IGR‐N‐835 could therefore constitute a suitable material for the study of the biology or therapeutics of human neuroblastoma.
Transplantable Marek's disease lymphomas. III. Induction of MHC‐restricted tumor immunity by lymphoblastoid cells in F1 hosts
Authors: Difronzo Nancy L. , Schierman Louis W. 
Published: February 2007

AbstractF1 chickens, which were a cross between birds of the related inbred lines G‐BI and G‐B2, were immunized with in vitro cultured virus‐non‐producer lymphoblastoid cells that were either syngeneic or allogeneic with the challenge tumor cells. The lymphoblastoid cells were derived from Marek's disease herpesvirus (MDV)‐induced transplantable tumors. Previous findings showed that such immunization of G‐BI and G‐B2 chickens prevented early mortality caused by the tumors. Lymphoblastoid cells syngeneic with the tumors were more effective than allogeneic cells, suggesting that an MHC‐restricted immune response was induced, or, alternatively, that immune elimination of allogeneic cells prevented them from initiating strong immunity to MDV‐associated tumor antigens. Immune elimination of the immunizing cells should not occur in F1 birds heterozygous for the 2 different parental MHC haplotypes (B6 and B13). Early mortality among F1chickens immunized with lymphoblastoid cells that were syngeneic with the challenge tumor cells was significantly lower than for non‐immunized control chickens or for birds immunized with lymphoblastoid cells that were allogeneic with the challenge tumor cells. Our results suggest that MDV‐induced tumor antigens may be recognized by the host as altered‐self MHC antigens.
Influence of interferon on adriamycin uptake of cultured tumor cells
Authors: Yoneda Kazunori , Yamamoto Tetsuya , Osaki Tokio 
Published: February 2007

AbstractEffect of human interferon β (IFNβ) or interferon γ (IFNγ) on cellular uptake of adriamycin (ADM) was measured in 3 in vitro‐cultured human tumor cell lines. Pre‐incubation of tumor cells with 100 lU/ml of IFNβ or γ for 6 hr resulted in an increased intracellular ADM concentration, but ADM efflux was not affected by the IFNs. The increase in cellular uptake of ADM was in agreement with both DNA and protein synthesis inhibition. 3H thymidine (3H‐TdR) incorporation was remarkably inhibited by ADM with pre‐treatment of 100 IU/ ml of each IFN, and an additive effect of ADM and IFN on cell growth inhibition could be observed. Similar additive inhibition against tumor‐cell proliferation in nude mice, which received combined treatment (twice/week) of IFNγ (5,000 IU/ mouse) and ADM (5‐20 μg/mouse), was also observed. These results indicate that IFN increases cellular influx of ADM, and antiproliferative activity against tumor cells is enhanced by a combination of IFN and ADM.
Overcoming effect of antibody against rat alpha‐fetoprotein (AFP) on the growth of daunorubicin‐resistant mutant rat ascites hepatoma cell line AH66
Authors: Ohkawa Kiyoshi , Tsukada Yutaka , Abe Toshio , Takada Koji , Hibi Nozomu 
Published: February 2007

AbstractA daunorubicin (DNR)‐resistant variant (AH66DR) of al‐pha‐fetoprotein (AFP)‐producing rat ascites hepatoma AH66 was established. AH66DR was 169 times more resistant to DNR than AH66. A growth‐inhibitory effect due to the decrease in sugar uptake following treatment of the cell lines with specific antibody against highly purified rat AFP was also observed. Pre‐incubation of both lines with antibody prior to the measurement of 2‐deoxy‐D‐glucose (2dG) uptake resulted in a 45‐55% decrease in 2dG uptake compared to control cells with a 2‐fold reduction of Vmax value while the Km remained unchanged. Upon pre‐incubating AH66DR with antibody, an increased intracellular level of DNR concentration with reduction of efflux rate was observed. A significantly superior cytotoxic effect against AH66DR, which reached almost the same level as the cytotoxic effect of DNR against AH66, was found, as compared to various other controls when tumor cells were cultured with a mixture of antibody and DNR. Our in vitro results suggest that the DNR‐resistance of the AFP‐producing tumor cells may be overcome if the cells are treated with specific antibody.
Oestrogen potentiates topoisomerase‐II‐mediated cytotoxicity in an activated subpopulation of human breast cancer cells: Implications for cytotoxic drug resistance in solid tumours
Authors: Epstein R. J. , Smith P. J. , Watson J. V. , Waters C. , Bleehen N. M. 
Published: February 2007

AbstractPrimary resistance to chemotherapeutic agents is a major problem in the management of advanced cancer. By using oestrogen to modulate the topoisomerase II content of T‐47D human breast cancer cells, we show here that cell subpopu‐lations resistant to the topoisomerase‐ll‐interactive drug VP16 (etoposide) can be identified and quantified using single‐cell analytical techniques. Immunohistochemical studies reveal topoisomerase II to be present in approximately 10% of control cells compared with 30% of oestrogen‐stimulated cells, and this difference is reflected in the proportions of cells exhibiting VP16‐induced cell‐cycle delay. This moderate increase in overall cell sensitivity is accompanied by massive enhancement of clonogenic cell kill, suggesting that oestrogen enhances VP16 cytotoxicity by recruiting a clonogenic cell subpopulation characterized by increased topoisomerase II content. Flow cytometry confirms that the increase in topoisomerase II is localized to an activated G1‐phase cell subset. We conclude that (i) single‐cell analysis of cellular topoisomerase II content is predictive of VP16 chemosensitivity; (ii) the existence of resistant tumour‐cell subpopulations does not necessarily indicate the presence of phenotypically divergent subclones; and (iii) rational strategies for eliminating tumour resistance may be based on biological manipulation of specific cytotoxic drug targets.
Site‐associated expression of endogenous tumor lectins
Authors: Glaves Dorothy , Gabius Hans‐Joachim , Weiss Leonard 
Published: February 2007

AbstractThe expression of endogenous lectins was compared in mouse Lewis lung carcinomas growing in the kidney or sub‐cutaneously. A panel of carbohydrates coupled to a biotiny‐lated carrier molecule (bovine serum albumin), biotinylated desialylated glycoproteins and sulfated polysaccharides were used in histochemical assays to detect the presence and distribution of carbohydrate receptors. Heterogeneous staining patterns were observed with most carbohydrates in sections of tumor tissue from both anatomic sites, and staining intensities also varied within each section. At least 2 populations of cells were identified at each site, of which one had receptors for all carbohydrates, while the other had no receptors for melibiose, sialic acid, or α‐glucosides (maltose and glucose). There were quantitative differences in expression of endogenous lectins by tumors growing s.c. or in the kidney; 3LL cells growing in the kidney bound 6 out of 10 carbohydrates to a greater extent than 3LL cells in s.c. tumors. Conversely, 3LL cells in s.c. tumors bound heparin and asialofetuin to greater extents than cancer cells in kidney tumors. Biochemical analyses of detergent extracts of tissues subjected to affinity chromatography and subsequent SDS‐PAGE revealed quantitative and also qualitative differences in lectins between tumors growing in the 2 anatomic sites.
Detection by in situ hybridization of messenger RNAs of collagen types I and IV in murine mammary cancer
Authors: Clavel Christine , Doco Martine , Lallemand Aude , Laurent Maryvonne , Birembaut Philippe 
Published: February 2007

AbstractTen breast carcinomas developing in C3H/Bi female mice were studied by an in situ hybridization technique using cDNA probes encoding α‐I chains of collagens of types I and IV. The results obtained are compared to histochemical data on antibodies to collagens of types I and IV and ultrastructural observations on these tumors. Immunohistochemistry has revealed the presence of type‐IV collagen in basement membranes lining intraductal and well‐differentiated cancer nests. Type‐I collagen was detected in the stroma surrounding these cells. There was no cellular labelling when these antisera were used. In situ hybridization has shown that type‐IV collagen mRNA is detected in non‐invasive intraductal and welldifferentiated tumor cells and in endothelial cells in the stroma. Good correlation between detection of type‐IV collagen lining these cells and evidence of mRNA by in situ hybridization was thus observed. Invasive cancer cells did not express hybridization grains with the type‐IV collagen probe. Type‐I collagen mRNA was visualized in stromal cells, probably fibroblasts and myofibroblasts as shown by electron microscopy. The most active cells were localized close to noninvasive areas. Our data indicate persistent in‐vivo biosynthesis of type‐IV collagen by some cancer cells that produce their own limitative environment; they suggest that type‐IV collagen is not produced by invasive tumor cells and that stromal cells lining the non‐invasive regions have a peculiar behavior.
Replication of latent Epstein‐Barr virus genomes in normal and malignant lymphoid cells
Authors: Adams Alice , Pozos Tamara C. , Purvey Helen V. 
Published: February 2007

AbstractDNA replication of 2 human lymphoid cell lines (U296 and Raji), latently infected with the Epstein‐Barr virus, has been compared using a density transfer approach. Typical of nonmalignant lymphoblastoid cells, U296 cells divided once in brornodeoxyuridine‐supplemented medium to form hybrid but not heavy‐density host DNA. Replication of the intracellular Epstein‐Barr virus DNA was selectively inhibited in these ceils with only 15% of the viral genomes duplicating once to form hybrid‐density viral DNA. However, some heavy‐density viral DNA was formed in the U296 cells and DNA synthesis can thus initiate again on newly duplicated viral genomes in cells that have traversed only a single S phase. These results contrast strongly with observations concerning the Burkitt‐lymphoma‐derived cell line. Lymphoma cells are not growth‐inhibited and most of the latent Epstein‐Barr virus genomes of the Raji line replicated once, and only once, in successive S phases. While the majority of the 50 Epstein‐Barr virus genomes of both the Raji and U296 cell lines are maintained as extra‐chromosomal DNA plasmids, the control of their duplication is distinctly different in the respective malignant and non‐malignant host cells.
Cytogenetic abnormalities in human ependymomas
Authors: Stratton M. R. , Darling J. , Lantos P. L. , Cooper C. S. , Reeves B. R. 
Published: February 2007

AbstractThe karyotypes of 4 human ependymomas have been determined. In one ependymoma, translocations involving chromosomes 9, 17 and 22 were observed together with the loss of the normal chromosome 17. A second ependymoma had many chromosomal alterations that included a translocation between chromosomes 1 and 2 and re‐arrangements involving chromosome 17. No major consistent alterations were detected in the remaining 2 cases. Our karyotypes do not resemble the few previously published karyotypes of ependymomas, but had features, such as the alterations involving chromosome 17, that were similar to those of other brain tumours in children.
Functional interactions of IL2 and TNF in the differentiation of LGL into lak effectors
Authors: Blay Jean Yves , Bertoglio Jacques , Fradelizi Didier , Chouaib Salem 
Published: February 2007

AbstractWe have previously reported on the synergistic effect of IL2 and TNF on the differentiation of LGL into LAK effectors. In the present study, we have further investigated the molecular basis of this synergistic mechanism and examined the role of TNF in the induction of LAK activity. We show that the generation of optimal LAK activity by low doses of IL‐2 in the presence of TNF involves the induction of high‐affinity IL2 receptors on LGL and occurs without promoting significant proliferation, suggesting a functional activation rather than a proliferative expansion of LAK precursors. Using blocking studies with anti‐Tac and with an anti‐IL2 (IHII), which specifically inhibits the binding of IL2 to the p75 IL2 receptor component, we also show that both the p55 and the p75 are involved in the increase in TNF binding sites on LGL and the subsequent acquisition of LAK activity. We also demonstrate that the failure of low doses of IL2 to induce LAK activity is related to their incapacity to induce TNF production. Moreover, when specific antibodies against TNF were added to the culture, the differentiation of LGL into LAK effectors by optimal concentrations of IL2 in our system (2.5–5.0 ng/ml) was partially inhibited. This suggests that TNF may be a physiologic mediator in the sequential activation stages of LGL into LAK effectors.
A case‐control investigation of cancer of the oral tongue and the floor of the mouth in Southern India
Authors: Sankaranarayanan R. , Duffy Stephen W. , Day Nicholas E. , Nair M. Krishnan , Padmakumary G. 
Published: February 2007

AbstractA case‐control study of cancer of the oral tongue and floor of mouth was conducted in Kerala, Southern India, on 228 cases and 453 hospital‐based controls, matched for age, sex and religion. We studied pan(betel)‐tobacco‐chewing, bidi (local type of cigarette)‐and‐cigarette‐smoking, alcohol‐drinking and snuff use, for their associations with risk, in males. Among females, only pan‐tobacco‐chewing was analyzed, as very few females indulged in the other habits. In males, a significantly increased risk was observed in association with pan‐tobacco‐chewing, bidi‐smoking, bidi‐plus‐cigarette‐smoking (but not cigarette‐smoking alone) and alcohol‐drinking (p < 0.001 in all cases), although the effect of alcohol was no longer significant when adjusted for the other significant predisposing factors. Among females, pan‐tobacco‐chewing had a similar predisposing effect to that observed in males (p < 0.001). In males an adjusted relative risk of 6.14 was associated with chewing 10 or more pan‐tobacco quids per day (relative to those who never chewed). The corresponding relative risk in females was 9.27. In males, an adjusted relative risk of 7.46 was observed for those smoking 20 or more bidis per day (relative to never‐smokers).
Risk of bladder cancer by source and type of tobacco exposure: A case‐control study
Authors: Burch J. D. , Rohan T. E. , Howe G. R. , Risch H. A. , Hill G. B. , Steele R. , Miller A. B. 
Published: February 2007

AbstractThe association between tobacco use and risk of bladder cancer was investigated in a population‐based case‐control study conducted in Alberta and south‐central Ontario, Canada, between 1979 and 1982. In all, 826 histologically‐confirmed cancer cases and 792 randomly selected controls, individually matched to cases for age, sex, and area of residence, were recruited into the study. Compared to those who had never smoked cigarettes, males and females who had ever smoked cigarettes had a statistically highly significant 2‐fold increase in risk of bladder cancer; for ex‐smokers, the risk was intermediate between that for current smokers and never‐smokers. There was a dose‐dependent increase in risk of bladder cancer with total lifetime cigarette consumption, of similar magnitude for males and females. In males, risk increased with self‐reported degree of inhalation in ex‐smokers and in current smokers (statistically significant trend), while in females there was no association in current smokers, and a statistically significant inverse association in ex‐smokers. Overall, risks of bladder cancer associated with lifetime consumption of plain and filter cigarettes were similar, and there was little evidence to suggest that switching from plain to filter cigarettes was beneficial. Neither passive smoking nor other forms of tobacco consumption (pipes, cigars, chewing tobacco, or snuff) were associated with altered risk of bladder cancer. The population attributable risk for cigarette smoking was about 47% in males and about 33% in females.
Expression of c‐sis and other cellular proto‐oncogenes in human sarcoma cell lines and biopsies
Authors: Fahrer Claus , Brachmann Rainer , von der Helm Klaus 
Published: February 2007

AbstractSix biopsies (4 of human fibrosarcomas, I of a B‐cell lymphoma and I of a normal lymph node from a melanoma patient) and 6 cell lines (derived from 5 different human osteosarcomas and from I rhabdomyosarcoma), together with control cells, were examined for the expression of c‐sis, c‐fosand c‐myc. The expression of c‐sis/PDGF‐B‐related proteins was also examined in cultured cells (not in biopsies). In situ hybridization studies further showed that the occurrence and level of expression of c‐sis mRNA and c‐sis/PDGF‐B‐related proteins were significant in the tumor cells. Expression of c‐fos and c‐myc mRNA did not correlate with c‐sis expression. Southern blot analysis of c‐sis, c‐fos and c‐myc of 20 DNAs of cell lines derived from human sarcoma or biopsies showed an identical pattern for BamHI and EcoRI restriction fragments of c‐sis(except for I fibrosarcoma biopsy), implicating no gene rearrangement as a cause of enhanced proto‐oncogene expression. The nucleotide sequence of c‐sis is highly homologous to that of the viral v‐sis oncogene which is capable of transforming infected cells. We conclude that enhanced expression of c‐sis in the sarcomas we have examined is involved in the initiation and/or maintenance of the cell transformed state.
Differential response to 1,3‐bis (2‐chloroethyl)‐1‐nitrosourea in drug‐resistant and ‐sensitive 9L rat brain tumor cells pretreated with α‐difluoromethylornithine and 6‐thioguanine
Authors: Hunter Karl J. , Deen Dennis F. , Marton Laurence J. 
Published: February 2007

AbstractPretreatment of 9L cells with either α‐difluoromethylorni‐thine (DFMO), which depletes intracellular levels of poly‐amines, or 6‐thioguanine (6TG), which substitutes for guanine in DNA, potentiates the cytotoxic effects of 1,3‐bis (2‐chloroethyl)‐1‐nitrosourea (BCNU). We examined the effects of these 2 agents in combination on the cytotoxicity of BCNU in sensitive (9L) and resistant (BTRC‐19) rat brain tumor cell lines. 9L cells were incubated with 0.2 μM 6TG for 72 hr; during the last 48 hr, I mM DFMO was added to cell cultures. The cytotoxicity of BCNU in pretreated cells was increased in an additive manner compared with the effects of each agent alone. Results of experiments in which the BCNU‐resistant BTRC‐19 cell line was treated similarly showed that only 6TG enhanced BCNU cytotoxicity. Flow cytometry studies showed that these effects are not related to cell‐cycle processes.
Effect of IFN‐γ treatment and in vivo passage of murine tumor cell lines on their sensitivity to lymphokine‐activated killef (LAK) cell lysis in vitro; association with H‐2 expression on the target cells
Authors: Tsai Li , Öhlén Claes , Ljunggren Hans‐Gustaf , Kärre Klas , Hansson Mona , Kiessling Rolf 
Published: February 2007

AbstractInterferon‐gamma (IFN‐γ) treatment or in vivo passage of the murine YAC‐I lymphoma resulted in reduced sensitivity to in vitro lysis by syngeneic murine spleen cells cultured in rlL‐2 (LAK‐cells). IFN‐γ treatment also rendered the murine BI6 melanoma less sensitive to lysis by syngeneic LAK cells, whereas in vivo passage did not alter LAK sensitivity. The reduction in sensitivity to lysis correlated with enhanced expression of cell surface H‐2 on the target cells. The possible role of H‐2 was studied with a β2‐microglobulin‐deficient, and thus H‐2‐deficient, variant of the YAC‐I lymphoma. This variant line remained H‐2 negative even after IFN‐γ treatment or in vivo passage, and was highly sensitive to LAK‐cell‐mediated lysis, even after IFN‐γ treatment or in vivo passage. The present results are discussed in relation to IFN‐γ and in vivo induced modulation of MHC class‐l molecules on target cells and the possible consequences for interaction with activated as well as “natural” effector cells.
NK sensitivity and lung clearance of MHC‐class‐I‐deficient cells within a heterogeneous fibrosarcoma
Authors: Algarra Ignacio , Ohlén Claes , Perez Matias , Ljunggren Hans‐Gustaf , Klein George , Garrido Federico , Karre Klas 
Published: February 2007

AbstractThe present study examines clonal variations in NK sensitivity in a methylcholanthrene‐induced fibrosarcoma. Previous studies of clones from this tumor have shown considerable heterogeneity in H‐2 expression, and an association between deleted or low levels of class‐l products and increased tumorigenicity after subcutaneous implantation in immunocompetent syngeneic mice. Here, fibrosarcoma clones with no or low expression of MHC‐class‐l products were found to be sensitive to NK‐mediated lysis, while clones with high levels of MHC‐class‐l expression were relatively resistant. One H‐2+ (G2) and one H‐2− (B9) clone were chosen for more detailed studies. Cold‐target competition assays and conjugate cytotoxicity assays in agarose showed that splenic effector cells bound equally well to the H‐2+ and H‐2− tumor clone, although only the latter was sensitive to NK cell lysis. Treatment with 50 U/ml of rlFN‐γ for 48 hr increased the levels of H‐2 expression and made both clones more resistant to NK‐mediated lysis. In vivo studies with radiolabeled tumor cells showed that cells from the H‐2+ clone survived better than cells from the H‐2− clone in the pulmonary capillary bed after i.v. inoculation. This difference disappeared in mice treated with anti‐asialo GM, serum, known to deplete NKcell activity.