bluuebunny/crossref_metadata_2025_split huggingface dataset:
Changes in the expression of idiotype antigen on murine B‐cell lymphoma after hyperthermia alone and in combination with interferon and tumour necrosis factor
Authors: Davies Catharina De L. , Basham Teresa Y. , Anderson Robin L. , Hahn George M. 
Published: February 2007

AbstractThe effect of interferon (IFN) and tumour necrosis factor (TNF), either alone or combined with hyperthermia, on cell proliferation and expression of idiotype antigen on a murine B‐cell lymphoma has been studied. Incubation with same doses of IFN‐α and IFN‐γ reduced cell proliferation to the same extent. Hyperthermia potentiated the antiproliferative activity of IFN‐α and IFN‐γ. Pretreatment with IFN‐γ induced a synergistic response with heat, while IFN‐α and heat had an additive effect. Tumour necrosis factor (TNF) alone did not affect cell proliferation, nor did TNF modify the heat‐induced delay in cell growth.The quantitative expression of surface idiotype antigen was studied by flow cytometry using an anti‐idiotype monoclonal antibody (MAb). Heat reduced the expression of idiotype antigen approximately 50%. The duration of the reduction depended on the heat‐dose. Recovery of antigen expression correlated with recovery of cell growth, and 2–5 days after the treatment antigen expression returned to the normal level for untreated cells.IFN‐γ and TNF increased antigen expression (30–50%) which lasted for 4–6 days after treatment. When cells were incubated with IFN‐γ or TNF for 2 days prior to hyperthermia, the increase in antigen expression was observed immediately after heating, but by the following day, antigen expression was similar to that after heat treatment alone. Expression of idiotype antigen recovered within 2–5 days to the same values as after heat treatment alone. IFN‐α alone or combined with hyperthermia did not have any significant effect on antigen expression.
Mapping of linear epitopes of human papillomavirus type 16: The L1 and L2 open reading frames
Authors: Dillner Joakim , Dillner Lena , Utter Göran , Eklund Carina , Rotola Antonella , Costa Silvano , Diluca Dario 
Published: February 2007

AbstractCertain types of human papillomavirus (HPV), notably HPV type 16, are associated with flat or inverted proliferative lesions of the cervix uteri that can progress to malignancy. As a first step towards the serological study of the epidemiology of HPV, we have synthesized the entire amino acid sequences of the 2 major viral capsid proteins of HPV type 16, L1 and L2, as a set of 66 synthetic 20‐residue peptides with an overlap of 5 amino acids. The peptides were tested for reactivity with IgA, IgG and IgM antibodies in the sera of 30 patients with HPV‐16‐carrying cervical neoplasms. Both IgG and IgM antibody responses were detected, but most of the reactivity found was of the IgA class. The most immunoreactive peptides were futher analyzed for reactivity with sera from 22 patients with parotid gland tumors and with sera from 38 healthy individuals. The L2‐encoded protein contained only one major linear epitope, which was not specific for HPV‐16‐carrying neoplasms. In contrast, the L1‐encoded protein contained several epitopes that were regularly immunoreactive with antibodies present in the sera of patients with HPV‐16‐carrying cervical neoplasms, but only rarely so in the sera of patients with other tumors or of healthy individuals.
Suramin inhibits proliferation of rat glioma cells and alters N‐cam cell surface expression
Authors: Fantini Jacques , Guo Xiao‐Jun , Marvaldi Jacques , Rougon Geneviève 
Published: February 2007

AbstractSuramin, a drug used in the treatment of trypanosomiasis and onchocerciasis inhibits growth‐factor‐induced mitogenesis. We have investigated the effect of suramin on the growth rate and the morphology of C6 glioma cells cultured in the presence of serum or in a serum‐free defined medium. Exponentially growing cells were seeded in multi‐dish plates (5 × 104 cells/2 cm2 well) in DMEM supplemented with 5% fetal calf serum and were continuously exposed to 1 μg/ml to 1,000 μg/ml suramin. Growth rate (determined 9 days after seeding) was reduced by 5%, 33%, 56% and 97%, respectively for suramin concentrations of 1, 10, 100 and 1000 μg/ml. Similar results were obtained in serum‐free defined medium (DMEM/F12, 1:1, v:v, EGF 5 ng/ml, transferrin 5 μg/ml, selenium 10 ng/ml). Moreover, the concentration of suramin in the culture medium remained constant, demonstrating that the drug was not actively metabolized by the cells. Suramin also induced marked changes in cell morphology: the usual bipolar shape of C6 cells evolved toward a more differentiated appearance, with numerous cellular processes allowing a wide number of cell‐cell contacts. In parallel, we monitored expression of an adhesion molecule (N‐CAM) at both the mRNA and protein levels. Indirect immunofluorescence technique showed an important increase in cell surface N‐CAM expression, starting from a dose of 10 μg/ml suramin, whereas total cellular content of N‐CAM protein as well as its mRNA levels were unaffected. We also observed that the levels of expression of actin and N‐CAM mRNAs decreased by a factor of two in cells maintained in defined medium. However, the relative ratio of N‐CAM mRNA over actin mRNA was virtually unchanged following suramin treatment. Taken together, our results suggest that suramin (i) exerts a blocking effect of autocrine growth factors, (ii) interferes with the turn‐over mechanisms of N‐CAM expressed at the cell surface, either by impairing its endocytosis and/or the process of release of the N‐CAM 120 isoform.
Deregulated c‐myc expression in epstein‐barr‐virus‐immortalized b‐cells induces altered growth properties and surface phenotype but not tumorigenicity
Authors: Hotchin Neil A. , Allday Martin J. , Crawford Dorothy H. 
Published: February 2007

AbstractEndemic Burkitt's lymphoma (eBL) is characterized by the presence of Epstein‐Barr virus (EBV) and a chromosomal translocation which results in deregulation and constitutive expression of the c‐myc proto‐oncogene. In order to examine the role played by activation of c‐myc in determining the eBL phenotype, we have introduced into EBV‐immortalized lymphoblastoid cells (LCL) plasmids which permit constitutive expression of c‐myc. The resulting cells show a reduced serum dependence, reduced homotypic cell aggregation, and changes in surface characteristics. In particular, levels of the cell adhesion molecule, LFA‐1, are greatly reduced. However, the cells continue to express all the EBV latent antigens associated with the LCL phenotype and they remain nontumorigenic. These results suggest that, whilst constitutive expression of c‐myc may contribute to the malignant phenotype, it is insufficient to induce tumorigenicity.
Neoplastic transformation of a human kidney epithelial cell line transfected with V‐HA‐ras oncogene
Authors: Haugen Aage , Ryberg David , Hansteen Inger‐Lise , Amstad Paul 
Published: February 2007

AbstractWe have recently shown that normal human kidney epithelial (NHKE) cells were immortalized by treatment with Ni(II) alone. In the present study the immortalized human kidney cell line (IHKE) was transfected with a plasmid construct containing the v‐Ha‐ras oncogene (pZipras). After transfection, the cell lines formed tumors in athymic nude mice, whereas the ZipNeoSV(X)‐transfected IHKE control cultures formed no tumors. Tumor cell lines (THKE) were established from the tumors in nude mice. These cells appear to be of human epithelial origin and express high levels of Ha‐ras transcript. Karyotypic analysis was performed. The cell lines were tritetra‐ or pentaploid. A consistent finding in the IHKE, IHKZE and THKE cells was increased numbers of chromosomes 17 and 7p+. Some marker chromosomes were identical in the IHKE and THKE cell lines, underlining their common origin and their possible importance in the carcinogenic process. This shows that the combined action of a chemical carcinogen [i.e., Ni(II)] and v‐Ha‐ras oncogene resulted in fully transformed human kidney epithelial cells, consistent with a stepwise progression of human epithelial cell transformation.
Tumor progression by dna flow cytometry in human colorectal cancer
Authors: Giaretti Walter , Santi Leonardo 
Published: February 2007

AbstractWe wished to better understand the role of aneuploidy during the progression of human colorectal cancer. Fresh or frozen multiple samples from 221 human colorectal adenomas, 93 carcinomas, and corresponding control mucosa were investigated using high‐resolution DNA flow cytometry. A total number of 164 DNA abnormal clones were observed and characterized by a quantitative index of DNA aneuploidy (DI). In precancerous lesions the vast majority of DNA abnormal clones (almost 3/4 in adenomas with mild to moderate dysplasia) was hypo‐ and hyper‐diploid with DI values from 0.8 to 1.2 (near‐diploidy). In moderately to poorly differentiated carcinomas the vast majority of abnormal clones was near‐triploid and hypotetraploid with DI values from 1.4 to 1.8 (near hypertriploidy) and only 12% were near‐diploid. Adenomas with foci of carcinomas, a group of special interest since they represent a link in colorectal tumor progression, had median triploid DNA content. In addition to an increase in DI values, the carcinomas had a clear increase in the proportion of cells actively synthesizing DNA (S‐phase fraction). These results are interpreted as evidence for a ploidyevolution model according to which near‐diploid clones in adenomas at early stages of dysplasia would derive from abnormal mitotic cells that divide their DNA unequally between two daughter cells. Tetraploidization of these near‐diploid cells and successive DNA loss would then lead in later stages of tumor progression to near‐hypertriploid clones characterized by a balance of chromosomes bearing growth‐promoting and growth‐suppressing genes confering a selective proliferative advantage.
Heterogeneity of immunoglobulin gene rearrangements in B‐cell lymphomas
Authors: Kneba M. , Bergholz M. , Bolz I. , Hulpke M. , Bätge R. , Schauer A. , Krieger G. 
Published: February 2007

AbstractWe have examined 69 B‐cell non‐Hodgkin's lymphomas (NHL) for rearrangements of the immunoglobulin (Ig) or T‐cell antigen receptor (TCR) genes. The lymphomas were assigned to the categories of the Kiel classification and their B‐cell nature was confirmed by immunostaining. Only 2 cases (with CLL) displayed clonal Tβ‐chain TCR gene rearrangements together with rearranged heavy‐ and light‐chain Ig genes. The remaining 67 lymphomas had a germline β‐chain TCR‐gene configuration. Three different patterns of Ig gene rearrangements were identified; (A) presence of both heavy‐ and light‐chain rearrangements (H+L+); (B) rearrangement of heavy‐chain gene only (H+L−); (C) heavy‐ and light‐chain genes in germline configuration (H−L−). All the 45 low‐grade NHLs and the 4 immunoblastic lymphomas exhibited pattern A and all had their kappa gene rearranged or deleted. Of 24 low‐grade lymphomas tested, 13 (54%) had an additional rearrangement of the lambda light‐chain gene. In contrast, the 19 high‐grade centroblastic (cb) B‐NHLs had distinct patterns of Ig‐gene rearrangement: 12 with pattern A, 4 with B and 2 with C. In this group only 2 of 17 (12%) cases analyzed had evidence of lambda light‐chain rearrangement whereas 12 of 18 (67%) had a kappa gene rearrangement or deletion. In one case expressing sIgM/lambda and with heavy chain Igrearrangement, no DNA was available for Ig light‐chain analysis.
Prevalence of cervical dysplasia and HPV infection according to sexual behavior
Authors: Azocar Jose , Abad S. M. J. , Acosta Humberto , Hernandez Rosa , Gallegos M. , Pifano E. , Blanch Ricardo , Kramar Andrew 
Published: February 2007

AbstractA total of 165 uterine cervix smears from Venezuelan women were examined by cytological techniques to identify malignant and pre‐malignant cervical changes, as well as to identify Human Papilloma Virus (HPV) DNA types 6, 11, 16, 18, 31, 33 and 35. Of these smears, 119 were from nonmonogamous women who participated in a cervical carcinoma screening program. In this group, HPV‐DNA was detected by hybridization in 42 samples (35%) and cervical intraepithelial neoplasia (CIN) in 13 (11%). Forty‐six monogamous aboriginal women were similarly studied and no evidence of abnormal cytology or HPV‐DNA of the types studied here was found in any of them. In the non‐monogamous group, age at first sexual intercourse and index of parity were not associated with cervical HPV infection and/or CIN. The rates of HPV infection, however, were significantly different between the two populations, confirming that sexual behavior involving multiple partners is associated with HPV infection.
The capsule surrounding primary liver tumors: Wherefrom its prognostic significance?
Authors: Grigioni W. F. , D'Errico A. , Biagini G. , Mazziotti A. , Bolondi L. , Liotta L. A. , Mancini A. M. , Garbisa S. 
Published: February 2007

AbstractPrimary liver neoplasms in cirrhotic and non‐cirrhotic patients were studied by electron microscopy and immunohistochemical methods for extracellular matrix (ECM) antigens. A capsule of variable thickness was present in many expanding hepatocellular carcinomas, while it was absent in those of small size, and either fragmented or absent in the infiltrating ones. In the capsules of early onset, fibronectin was the most frequent stromal glycoprotein. In the completely formed capsular structures, fibronectin, type‐V collagen and laminin were the most common macromolecules seen. No differences were evident in the pattern of ECM macromolecules in the capsules surrounding hepatocellular carcinomas compared with those found in benign lesions, such as hepatocellular adenomas or focal nodular hyperplasia. The possibility is discussed that the capsule could be a result of the following sequence: tissue with expansive (not infiltrative) growth–mechanical compression–ischemic necrosis of surrounding tissues–repair process with ECM deposition.
The distribution of non‐burkitt, non‐Hodgkin's lymphomas in Uganda in relation to malarial endemicity
Authors: Schmauz R. , Mugerwa J. W. , Wright D. H. 
Published: February 2007

AbstractBiopsies of malignant lymphomas collected from all districts of Uganda, filed in the Kampala Cancer Registry for the 8‐year period 1966–1973, were reviewed. This review confirmed a relatively low frequency of follicle‐centre‐cell lymphomas with a follicular growth pattern and the geographical co‐distribution between malaria and Burkitt's lymphoma (BL). It also showed a similar, though less marked, association between non‐Burkitt, non‐Hodgkin's lymphoma (NBNHL) and malarial endemicity, and a correlation in the regional incidence between BL and NBNHL in both comparisons, these associations were strong for high‐grade lymphomas and weak for low‐grade neoplasms. BL and other NHL may therefore share, to a varying degree, some common pathogenesis. The excess in frequency of NBNHL of high‐grade malignancy in malarial endemic areas appears to be in contrast to Western countries where most non‐Hodgkin's lymphomas are of low‐grade malignancy.
DNA adducts in different tissues of smokers and non‐smokers
Authors: Cuzick Jack , Routledge Michael N. , Jenkins David , Garner R. Colin 
Published: February 2007

AbstractPurified DNA from human lung, liver, bladder, pancreas, breast and cervix has been analysed for DNA adducts using the nuclease P1 modification of the 32P post‐labelling technique. Tissues were obtained at autopsy from 13 men and 6 women. Relatives were asked to provide information on smoking history for deceased subjects. All tissues examined except the breast had detectable adducts. In lung, bladder and pancreatic tissue a characteristic pattern of adducts was seen which has previously been reported as typical of cigarette‐smoke‐induced damage. Smokers and former smokers tended to have higher adduct levels than non‐smokers in the tissues examined but this was only significant for the lung. There appeared to be considerable variation in adduct levels among smokers which could not be accounted for by duration or daily consumption level. Certain smokers had high adduct levels in all tissues examined, whilst in others high levels were only seen in some tissues. All cervical samples examined had detectable adducts. These results confirm the finding that cigarette smoking is associated with DNA damage in the lung and suggest that similar damage may be related to tobacco‐induced neoplasms of other tissues.
Morphologic analysis of human lymphokine‐activated killer (LAK) cells
Authors: Groscurth P. , Diener S. , Stahel R. , Jost L. , Kägi D. , Hengartner H. 
Published: February 2007

AbstractLymphokine‐activated killer (LAK) cells obtained from normal donors at various days of in vitro cultivation have been studied by several methods including scanning (SEM) and transmission (TEM) electron microscopy, immuno‐electron microscopy, in situ hybridization and flow cytometric DNA measurements. In addition, the cytotoxic activity of LAK cells against several tumor cells was examined by 51Cr‐release assay and by SEM and TEM. The LAK cells displayed a uniform ultrastructural appearance concerning surface structure and morphology of organelles. They contained typical lysosomal granules which by immuno‐electron microscopy showed a specific localization of perforin 1 (P1). The presence of P1 and granzymeA mRNA in the cytoplasm was confirmed by in situ hybridization using specific antisense probes. Frequency and increase of specific mRNA‐containing cells was similar for both genes. Single LAK cells were further characterized by peculiar nuclear inclusion bodies (IB) which were presumably formed by trapped profiles of endoplasmic reticulum. Flow cytometric analysis revealed normal DNA content of LAK cells even after prolonged cultivation indicating that the IB were not associated with aneuploidy of the effector cells. The LAK cells were highly effective in lysing K562 and DAUDI cells as shown by 51Cr‐release assay. They caused characteristic morphologic alterations of target cells similar to those found in cytotoxic T‐lymphocyte (CTL) and NK‐cell‐mediated cytolysis. SEM and TEM studies on specimens prepared by routine procedures or by cryopreparation showed that the tumor cell membrane was the initial target for the LAK cell attack whereas other cell compartments were damaged only in advanced stages of cytolysis. Summarizing our study demonstrates that LAK cells have a characteristic ultrastructure which in some aspects differs from that of CTL and NK cells, and that LAK cells appear to destroy tumor cells by mechanisms similar to those of other cytotoxic effector cells.
Characterization of an embryonal rhabdomyosarcoma cell line showing amplification and over‐expression of the N‐myc oncogene
Authors: Hayashi Yasuhide , Sugimoto Tohru , Horii Yoshihiro , Hosoi Hajime , Inazawa Johji , Kemshead John T. , Inaba Toshiya , Hanada Ryoji , Yamamoto Keiko , Gown Allen M. , Sawada Tadashi 
Published: February 2007

AbstractA parent rhabdomyosarcoma cell line designated SCMC‐RM2 was established from bone‐marrow tumor cells taken from an 11‐year‐old girl with an embryonal rhabdomyosarcoma. Subsequently a cloned SCMC‐RM2‐1 cell line was isolated from a parent line. These cell lines grew as adherent monolayers in liquid culture with a doubling time of 50 and 52 hr, respectively. In addition, colonies were established in soft agar, which grew in a dose‐dependent fashion with a cloning efficiency of 0.7 and 0.8%, respectively. Chromosomal analysis showed these cell lines had neither double minutes nor homogeneously staining regions. Chromosome number ranged from 61 to 93, translocation; t(9;13)(p22;q14) was identified, and no alteration of chromosome 2 was observed. Surface membrane antigen profile of parent and cloned lines by using a panel of 24 monoclonal antibodies (MAbs) excluded the possibility of these being neuroblastoma cell lines. In addition, MAbs to the cytoplasmic protein desmin, myoglobin, muscle actin (α and γ) and α‐sarcomeric actin reacted with these cell lines, SCMC‐RM2 and SCMC‐RM2‐1 being thus identified as rhabdomyosarcoma. Southern blot analyses revealed 8‐ and 7‐fold amplification of the N‐myc gene in SCMC‐RM2 and SCMC‐RM2‐1 as compared with the promyelocytic cell line HL60. Over‐expression of the N‐myc mRNA was noted over control cell lines.
Differentiation‐inducing and growth‐inhibitory activities of erythroid differentiation factor (EDF/activin A) toward mouse erythroleukemic cells in vivo
Authors: Shiozaki Makoto , Shioya Shigeru , Izawa Masaaki , Eto Yuzuru , Shibai Hiroshiro 
Published: February 2007

AbstractThe in vivo differentiation‐inducing activity of a purified human erythroid differentiation factor (EDF) toward mouse erythroleukemic cells (MEL cells) was examined. BDF1 mice with diffusion chambers implanted in the peritoneal cavity were treated with continuous i.p. administration of EDF. MEL cells within a diffusion chamber differentiated into hemoglobin‐positive cells when treated with EDF, the percentage of the positive cells being 32.3 ± 28.3 on day 5 as compared to 0.2 ± 0.3 in the controls. The anti‐tumor activity of EDF was also examined in a nude mouse MEL solid tumor model. Daily intra‐tumor treatment with EDF for 10 days resulted in 73% suppression of tumor growth on day 25. A histological study revealed that EDF‐treated solid tumor cells became hemoglobin‐positive, indicating the anti‐tumor activity of EDF through induction of differentiation in vivo. EDF could induce in vitro the differentiation of human erythroleukemic cell lines K562 and HEL, as well as the murine cell line. These results indicate the possibility of differentiation therapy for erythroleukemia using EDF.
Enhanced expression of the proto‐oncogenes fos and raf in the rhabdomyosarcoma cell line BA‐HAN‐1C after differentiation induction with retinoic acid and N‐methylformamide
Authors: Gabbert N. E. , Gerharz C.‐ D. , Ramp U. , Hoffmann J. , Oster O. , Oesch F. , Doehmer J. 
Published: February 2007

AbstractBA‐HAN‐1C is a clonal rat rhabdomyosarcoma cell line consisting of proliferating mononuclear tumor cells, some of which spontaneously fuse to form terminally differentiated post‐mitotic myotubes. Exposure of BA‐HAN‐1C cells to retinoic acid (RA) or N‐methylformamide (NMF) resulted in a significant inhibition of proliferation (p < 0.001) and in cellular differentiation, as evidenced by a significant increase in the creatine kinase (CK) activity (p < 0.05) and the number of terminally differentiated post‐mitotic myotubes (p < 0.001). Furthermore, between 5% (NMF) and 30% (RA) of the mononuclear tumor cells exhibited ultrastructural features of rhabdomyogenic differentiation, not observed in their mononuclear counterparts under standard growth conditions. Although BA‐HAN‐1C cells responded to both inducers of differentiation, differences in time course and magnitude of both increase of differentiation and growth inhibition were observed. These effects of RA and NMF were preceded by a marked enhancement of c‐raf expression which became evident 6 and 12 hr after exposure to RA and NMF, respectively, and which persisted throughout the observation period of 5 days. Furthermore, a transient expression of c‐fos could be observed 15 and 30 min after exposure to RA. Our results suggest that c‐raf expression might be implicated in the differentiation process of BA‐HAN‐1C tumor cells.