bluuebunny/crossref_metadata_2025_split huggingface dataset:
K‐ras mutations (codon 12) are not involved in down‐regulation of mhc class‐i genes in colon carcinomas
Authors: Oliva Maria Rosario , Cabrera Teresa , Esquivias Javier , Perez‐Ayala Millán , Redondo Maximino , Ruiz‐Cabello Francisco , Garrido Federico 
Published: February 2007

AbstractFifty‐eight colorectal carcinomas were studied for HLA class‐l antigen expression and for the presence of point mutations in codons 12 and 61 of the K‐ras gene. Eight carcinomas were completely negative for class I by the APAAP technique. Analyses using the polymerase chain reaction (PCR) method, together with selective hybridization using mutation‐specific synthetic oligonucleotides, demonstrated K‐ras mutations in 14 cases (24.1 %), all of them in codon 12. None of the mutations corresponded to the negative cases for class‐l HLA antigen expression. We did not observe any correlation between K‐ras mutations and the extent of tumor differentiation.
Food temperature and gastric cancer
Authors: La Vecchia Carlo , Negri Eva , D′Avanzo Barbara , Franceschi Silvia 
Published: February 2007

AbstractThe relationship between preference for food temperature and the risk of stomach cancer was analysed using data from a case‐control study conducted in Northern Italy on 563 histologically confirmed incident gastric cancers and 1,501 controls admitted to hospital for acute, non‐neoplastic, non‐digestive tract disorders. A specific question was related to food temperature, subjectively defined as “warm”, “hot” or “very hot”. Compared with subjects indicating preference for “warm” foods, the relative risk (RR) was 1.1 (95% confidence interval, C1, 0.9‐1.4) for “hot” and 1.8 (95% C1 = 1.3‐2.4) for “very hot”. The test for trend in risk was statistically significant, and the results were not appreciably modified by allowance for a number of identified potential distorting factors. The elevated risk, however, appeared to be restricted to the 17% of cases reporting a preference for “very hot” foods. This may be due to an absence of substantial mixlassification between “warm” and “very hot”, but also to the existence of a threshold temperature, below which no appreciable thermal irritation is evident. Thus, although the difficulties and uncertainties on measures of food temperature are substantial, these data suggest that thermal irritation may have a role in gastric carcinogenesis.
Histocompatible miniature boar model: Selection of transformed cell lines of b and t lineages producing retrovirus
Authors: Kaeffer Bertrand , Bottreau Elisabeth , Thanh Luu Phan , Olivier Michel , Salmon Henri 
Published: February 2007

AbstractA lymphoblastoid cell line (BI) was isolated in culture following a brief exposure to 5‐azacytidine from peripheralblood mononuclear cells of a boar previously injected with cells (Shimozuma) producing porcine retrovirus (Tsukuba‐I) and suffering a severe non‐neoplastic syndrome at autopsy. BI cell line and 5 of its sublines were propagated for more than 100 generations, retaining doubling times comprised between 16.8 and 27.5 hr and growing readily in agarose or agar (plating efficiency: 5 to 50%). Karyotype analyses showed that 4 sublines were nearly diploid, except for cells of L14, which displayed a monosomy affecting chromosome 18 pair. Two sublines (L35 and L45) were considered as being of T‐cell lineage, since MSA antigen was observed on the surface of approximately 30% of cells. Three sublines (L23, L14 and L52) were considered of B‐cell lineage, since membrane immunoglobulins were observed on the cell surface. In addition, sublines L23 and L52 were actively secreting immunoglobulin of μ isotype. Retrovirus particles were evidenced in gradient purified preparation of 200‐fold‐concentrated cell culture supernatants of the BI cell line, L14, L35 and L52 sublines, using both a reverse transcriptase activity assay and electron microscopic observation. These cell lines can be used to select for porcine retrovirus variants with transforming potential for lymphocytes of B and T lineages.
Effect of tetragastrin on azaserine‐induced carcinogenesis in rat pancreas
Authors: Tatsuta Masaharu , Iishi Hiroyasu , Baba Miyako , Nakaizumi Akihiko 
Published: February 2007

AbstractThe effect of tetragastrin on pancreatic tumors induced by azaserine was investigated in Wistar rats. Rats were given 25 weekly injections of 10 mg/kg body weight of azaserine and I mg/kg body weight of tetragastrin as a suspension in olive oil every other day. Carcinogen‐induced pancreatic lesions were examined by histochemical techniques, and were classified as ATPase‐positive or ATPase‐negative. In week 62, quantitative histological analysis showed that prolonged administration of tetragastrin had little or no influence on the number and size of the carcinogen‐induced pancreatic lesions, although it caused significantly increased cell proliferation, indicated by a greater labelling index of the pancreatic acinar cells.
Enhancement of anchorage‐independent growth of a human adrenal carcinoma cell line by endogenously produced basic fibroblast growth factor
Authors: Corin Shari J. , Chen Lucian C. , Hamburger Anne W. 
Published: February 2007

AbstractWe have previously observed that a human adrenal carcinoma cell line (SW‐13) produces autocrine growth factors that enhance the ability of these cells to clone in soft agar. We now show that a basic FGF‐like protein is found in SW‐13 lysates and stimulates SW‐13 colony growth. Basic FGF (bFGF) was identified in SW‐13 lysates by both its chromato graphic behavior on heparin‐Sepharose and its reactivity with an antibody specific for bFGF. Incubation of lysates with an tibodies specific for bFGF abolished their ability to support anchorage‐independent growth. Northern analysis demon strated that the cells produced multiple bFGF mRNA tran scripts. SW‐13 cells also expressed bFGF cell‐surface recep tors. These data suggest that SW‐13 cells produce and re spond to a factor structurally and functionally related to bFGF. Such findings support recent evidence indicating that FGF secreted by human tumor cell lines plays a role in the maintenance of the transformed phenotype.
Modulation of the antigenic phenotype of early‐passage human melanoma cells derived from multiple autologous metastases by recombinant human leukocyte, fibroblast and immune interferon
Authors: Giacomini Patrizio , Fraioli Rocco , Nistico Paola , Tecce Raffaele , Nicotra Maria Rita , Filippo Franco Di , Fisher Paul B. , Natali Pier Giorgio 
Published: February 2007

AbstractWe have investigated the relationship between in vitro cultivation of autologous melanoma metastases derived from different patients and their levels of expression of class‐l and‐11 major histocompatibility complex (MHC) antigens and melanoma‐associated antigens (MAAS). Cell cultures were established from 23 individual metastatic melanoma lesions from 10 patients and were tested early after isolation (between 3rd and 10th passages) for both constitutive expression and modulation by recombinant human leukocyte (IFN‐α), fibroblast (IFN‐β) or immune (IFN‐γ) interferon of MHC antigens and MAA. All of the melanoma cell lines displayed altered antigen expression following IFN treatment. While in vitro cultures derived from different individuals varied in both constitutive and IFN‐modified antigenic expression. cultures of autologous metatases derived from the same patient were very similar. In addition, differences in antigenic profile were apparent when early‐passage in vitro cultures were compared with the same melanoma lesion, not established in culture, from which they were derived. The unique de novo and IFN‐modified antigenic phenotype of cultures derived from different patients indicates that the antigenic phenotype displayed by melanoma cultures grown in vitro is genetically determined. The differences found between in vitro cultures and their corresponding in vivo lesions, as well as the antigenic heterogeneity displayed by multiple autologous melanoma lesions in vivo, suggest that the in vivo antigenic phenotype may be determined, at least in part, at an epigenetic level.
A two‐site enzyme‐linked immunosorbent assay for cytokeratin 8
Authors: Sundström B. , Stigbrand T. 
Published: February 2007

AbstractA monoclonal enzyme‐linked immunosorbent assay (ELISA) was developed for the determination in biological fluids of cytokeratin 8, a potential marker for malignant diseases. Two monoclonal antibodies (MAbs), TS 3 and TS 4, with different epitope specificity, were selected from 4 cytokeratin‐8 reactive antibodies. TS 3 was used for coating and TS 4 as HRP‐conjugate, respectively. Antibodies were selected with the aim of optimizing the discriminatory capacity between cytokeratin 8 levels in sera from healthy persons and from patients with malignant diseases. In sera from healthy individuals the mean value was determined to be 3.1 ± 2.3 ng/ml with an upper cut‐off level of 7.8 ng/ml (+ 2 SD) using purified cytokeratin 8 as standard. Sera from patients with colon cancer and pancreatic cancer were found to have significantly elevated levels, showing a 4‐ to more than 10‐fold increase compared with the normal level. In patients with ovarian cancer no significant elevation was seen. Cytokeratin 8 monitoring may be of value for patients with colon and pancreatic cancer.
Histologic variation among experimental tumors of common origin: Relationships to viral p21 expression and to tumor‐derived extracellular matrix
Authors: Auersperg Nelly , Wong Andre , Maclaren Ian A. 
Published: February 2007

AbstractTransformed lines, obtained by infection of adult rat adrenocortical fibroblast‐like cells with Kirsten murine sarcoma virus, produce s. c. tumors which range histologically from fibrosarcomas to carcinomas to undifferentiated neoplasms. This study was undertaken to determine whether the histology was a stable characteristic of individual lines and whether it was related to oncogene expression and to differentiation in culture. Three lines were infected at passage 1 and tumor histology, differentiation markers and expression of the transforming protein v‐p21 were evaluated periodically over a 1‐year period. The original stromal characteristics of the target cells (metachromatic extracellular matrix (ECM), a high rate of collagen production and collagen incorporation into ECM, and a fibroblastic morphology) diminished with transformation. In contrast, parenchymal differentiation markers (lipid, steroidogenic enzymes) were enhanced and constitutively expressed in all lines. The two lines in which ECM production was most reduced formed carcinomas in vivo, while the third line showed a smaller shift in these characteristics and formed sarcomas. Thus, histopathology seemed to be influenced by tumor‐derived ECM but unrelated to the expression of steroidogenic properties. The tumors became less differentiated with time, but retained distinct line‐specific phenotypes. Throughout the study, v‐p21 remained overexpressed in all lines to a similar degree, but the subcellular localization of v‐p21 differed between fibroblastic and epithelial cells, suggesting a possible correlation with differentiation.
Quantity and saturation degree of dietary fats as modulators of oxidative stress and chemically‐induced liver tumours in rats
Authors: Hietanen E. , Bartsch H. , Bereziat J.‐C. , Ahotupa M. , Camus A.‐M. , Cabral J. R. P. , Laitinen M. 
Published: February 2007

AbstractMale rats were fed, from weaning onwards, either 2, 12.5 or 25% sunflower seed oil (polyunsaturated fatty acids, PSA) or lard (saturated fatty acids, SFA) and from the age of 15 weeks subgroups were given N‐nitrosodimethylamine (NDMA) for 30 weeks. Blood levels of lipids were assayed and during the study exhaled ethane was measured as an index of in vivo lipid peroxidation (LPO). At the age of 50 weeks, rats were killed and livers were analysed for tumours. PSA diets decreased plasma cholesterol and triglyceride concentrations vs. respective SFA diet; NDMA administration did not affect plasma cholesterol but enhanced triglyceride concentration. NDMA markedly enhanced LPO. An increase in dietary fat content from 2 to 25% enhanced ethane exhalation, more in rats fed PSA than the SFA diet. In the 25% PSA group, indomethacin in the diet strongly inhibited LPO. Prevalence of liver haemangiosarcomas increased from 42% to 80% (p < 0.05) in NDMA‐treated animals when PSA increased from 2 to 25%; in the group having a 25% PSA diet containing indomethacin, the NDMA‐induced tumour incidence was reduced to 64%. In NDMA‐treated rats fed SFA diets the prevalence of haemangiosarcoma increased from 43% (2% fat) to 67% (25% fat). The data show that NDMA modifies plasma lipids and increases LPO. The quantity and saturation degree of fats altered the frequency of chemically‐induced tumours and modified LPO. As an index of free radical reactions, LPO may have an important role in carcinogenesis. Dietary fat thus appears to promote carcinogenesis through mechanisms that involve LPO.
A comparative study on the effect of tumor promoters on poly ADP‐ribosylation in A431 cells
Authors: Singh Neeta 
Published: February 2007

AbstractPoly ADP‐ribosylation is a post‐translational modification of chromatin proteins catalyzed by the enzyme poly‐ADPR transferase (poly‐ADPRT) and affects the structure as well as the functional properties of chromatin. It is of particular relevance in carcinogenesis, as it represents an epigenetic mechanism for modulation of gene expression. In the present study, A431 cells were exposed to tumor promoters phorbol 12‐myristate‐ 13‐acetate (PMA), benzoyl peroxide (BP), mezerein and 6‐keto‐lithocholic acid (KA), and their effect on poly‐ADP‐ribosylation was studied. All these tumor promoters increased the activity of poly‐ADPRT in these cells‐PMA 2.3‐fold, BP and mezerein 2.2‐fold each and KA 1.3‐fold. The enzyme inhibitor 3‐amino benzamide (3AB) partially prevented the stimulation of poly‐ADPRT by these promoters. There was a concomitant decrease in NAD levels, the substrate for poly‐ADPRT. The decrease was 44% for PMA, 46% for BP, 21% for KA and 34% for mezerein. The induction of poly‐ADP‐ribose synthesis by PMA and BP appears to be mediated at least in part by active oxygen species, as they induced an increase in superoxide anions and anti‐oxidants prevented the increase of poly‐ADPRT activity to varying extents.
T‐cell subsets, IFN‐γ production and efferent specificity in anti‐parental tumor immunity induced by mouse sensitization with xenogenized variant cells
Authors: Bianchi R. , Fioretti M. C. , Romani L. , Grohmann U. , Cenci E. , Puccetti P. 
Published: February 2007

AbstractIn addition to previous evidence for a role of L3T4+ T cells in the protective anti‐parental tumor immunity induced by xenogenized variant cells of a murine lymphoma (L5I78Y/DTIC), we have investigated the possible participation in this effect of L5I78Y tumor‐specific lymphocytes of the Lyt‐2+ T cell subset. Spleen cells from L5178Y/DTIC tumor‐immunized mice produced high levels of IFN‐γ in vitro in response to parental antigens, and this activity was only abolished by treating the responder population with anti‐Thy‐1.2 antibody or a combination of anti‐L3T4 and anti‐Lyt‐2.2 monoclonal antibodies (MAbs) plus complement. Positively selected L3T4+ and Lyt‐2+ cells also produced IFN‐γ in vitro, provided accessory cells (plastic‐adherent and Thy‐I− Ia− splenocytes, respectively) were added to the lymphocyte‐tumor cell co‐cultures. The production of IFN‐γ by purified L3T4+ and Lyt‐2+ cells was inhibited by addition of the respective anti‐class‐II and anti‐class‐I H‐2 antibody to the cultures. Administration of anti‐IFN‐γ MAb in vivo significantly impaired the resistance of L5178Y/DTIC‐immune mice to challenge with parental cells, as manifested by survival criteria and increased tumor‐cell proliferation in the spleens of antibody‐treated mice. Although anti‐parental tumor protection in vivo and T‐cell activation in vitro for IFN‐γ production were strictly antigen‐specific, bystander tumor inhibition was observed when antigenically irrelevant cells were inoculated with the L5178Y lymphoma. These results suggest that both L3T4+ and Lyt‐2+ T cells play a role in the protective anti‐parental tumor immunity induced by xenogenized cells, and that their activity may involve IFN‐γ‐mediated stimulation of non‐specific tumoricidal mechanisms.
Mechanisms of macrophage‐mediated tumor cell killing: A comparative analysis of the roles of reactive nitrogen intermediates and tumor necrosis factor
Authors: Keller R. , Keist R. , Wechsler A. , Leist T. P. , Van Der Meide P. H. 
Published: February 2007

AbstractThe roles of tumor necrosis factor (TNFα) and reactive nitrogen intermediates (RNI) as effectors of macrophagemediated tumor cell killing were investigated in a variety of tumor cell lines. Three TNFα‐sensitive tumor targets were also susceptible to resting bone‐marrow‐derived mononuclear phagocytes (BMMP). This macrophage lytic activity was markedly diminished or even abolished by anti‐TNFα, indicating that TNFα is the major effector of macrophagemediated killing of these targets. The other 21 tumor cell lines examined were resistant to TNFα but, in their large majority, were more or less susceptible to killing by interferon γ (IFNγ)‐ and Corynebacterium parvum (CP)‐activated BMMP. Among the various analogues of L‐arginine used to assess the role of L‐arginine‐derived RNI as mediators of macrophage tumoricidal activity, NG‐monomethyl‐L‐arginine (NMMA) was most efficient in suppressing RNI secretion by activated macrophages. In some macrophage tumor‐cell combinations, NMMA inhibited both the generation of RNI and the expression of tumoricidal activity in a dose‐dependent manner, suggesting a central role for RNI as effectors. In other combinations, NMMA in concentrations that abolished secretion of RNI either affected tumor‐cell killing only after its induction by IFNγ, or not at all. The findings not only support the thesis that macrophages possess various means of coping with tumor cells but also suggest that the mechanism becoming operative is determined predominantly by the pathway of macrophage activation and the properties of the tumor‐cell type.
Modulation of multidrug resistance by verapamil or mdr1 anti‐sense oligodeoxynucleotide does not change the high susceptibility to lymphokine‐activated killers in mdr‐resistant human carcinoma (LoVo) line
Authors: Rivoltini Licia , Colombo Mario P. , Supino Rosanna , Ballinari Dario , Tsuruo Takashi , Parmiani Giorgio 
Published: February 2007

AbstractTwo sublines were derived from the colon adenocarcinoma line LoVo, the first one was sensitive (LoVo/H) and the second one was made resistant to doxorubicin (LoVo/Dx). When tested for susceptibility to lysis by different types of immune effectors, LoVo/Dx appeared more sensitive than LoVo/H to the killing of CD3+CDS+CD16−, CD3− CD16+‐enriched lymphokine activated killers (LAK) or activated macrophages. In order to check whether this effect was due to different expression of glycoprotein PI70 between the two LoVo sublines (30% vs. 90% of positive cells), a pharmacological and genetic modulation of PI70 was carried out in LoVo cells. Treatment of LoVo/Dx with the calcium channel blocker verpamil (VRP), strongly impaired PI70 function as evaluated by reduced Dx resistance, without affecting the lysability of LoVo/Dx cells by LAKs. Moreover, the significant inhibition of PI70 expression resulting from the treatment of LoVo/Dx with mdrl antisense olideoxynucleotide also failed to change the high lysability of LoVo/Dx by LAKs. These results, therefore, indicate that molecules other than PI70 are involved in the increased lysis of LoVo/Dx subline by immune effectors and that downregulation of the PI70 expression or function will not reduce the potential effectiveness of cancer chemo‐immunotherapy.
MHC class‐I antigen deficiency, malignancy and susceptibility of P815 mastocytoma to NK and macrophage killing
Authors: Bertschmann May , Käsermann Donald , Keller Robert 
Published: February 2007

AbstractA subline of the murine P815 mastocytoma passaged for a long period of time in histoincompatible hosts was found to be deficient in surface MHC class‐I antigens by serological and biochemical methods. In agreement with the lack of restriction elements, this variant cell line was no longer susceptible to killing by cytotoxic T cells stimulated by and directed against the parental tumor cell line in syngeneic DBA‐2 hosts. We did not observe the appearance of susceptibility to NK killing concomitantly with H‐2 loss. We thus could not confirm the hypothesis of a regulatory function of H‐2 structures in NK recognition/killing. Both cell lines were also resistant to lysis by mouse macrophages. The parental cell line was sensitive to rat macrophage killing, whereas the variant line had lost such sensitivity. In spite of resistance in vitro to various defense mechanisms, the variant H‐2 loss tumor cell line was less tumorigenic in syngeneic hosts and exhibited a lower metastatic capacity than the parental cell line. We propose that in the H‐2 loss subline, survival of cells in vivo is impeded since positive signals mediated by H‐2 structures are missing, which are necessary for cell‐cell contact and survival.
Expression of PDGF β‐receptors in human meningioma cells
Authors: Wang Jia‐Lun , Nistér Monica , Hermansson Monica , Westermark Bengt , Pontén Jan 
Published: February 2007

AbstractMeningioma is a generally benign tumor derived from arachnoid tissue. We have investigated the presence of functionally active PDGF‐receptors on human meningioma cells in culture. Tumor samples were obtained from 3 surgically removed benign meningiomas and normal arachnoid tissue from an autopsy case. Binding studies were performed by using 125I‐labelled recombinant PDGF‐AA and PDGF‐BB. Only 125I‐PDGF‐BB showed specific binding to all tumor‐cell cultures after incubation of cells for 2 hr at 4°C. Effects of PDGF‐AA and PDGF‐BB on DNA synthesis were measured as 3H‐thymidine incorporation during 48 hr of labelling cells maintained in Eagle's minimum essential medium 0.5% fetal calf serum. PDGF‐BB but not PDGF‐AA stimulated DNA synthesis in all 3 tumor‐cell cultures. Total cellular RNA was analyzed by Northern blotting and hybridization with a 32P‐labelled human PDGF β‐receptor probe, and PDGF β‐receptor mRNA was found in both tumor and arachnoid cell cultures. Furthermore, PDGF β‐receptor mRNA was shown to be present in 2 meningioma biopsies and immunohistochemical staining revealed that PDGF β‐receptors are present in meningioma and arachnoid tissues in vivo. It appears that a possible way of maintaining human meningioma cell growth in vivo is through activation of PDGF β‐receptors.
Dietary factors and breast‐cancer risk in Denmark
Authors: Ewertz Marianne , Gill Caroline 
Published: February 2007

AbstractThe influence of dietary factors, in particular the intake of fat and beta‐carotene, on breast‐cancer risk was evaluated in a case‐control study including 1,486 breast cancer cases diagnosed over a 1 year period in Denmark. The control group was an age‐stratified random sample of 1,336 women from the general population. Data on usual diet prior to the breast cancer diagnosis were collected by self‐administered questionnaires of the semi‐quantitative food frequency type. A highly significant trend (p < 0.001) of increasing risk was observed with increasing fat intake, the RR for the highest quartile being 1.45 (95% Cl 1.17‐1.80) compared with the lowest. However, information was not available to allow adjustment for the possible confounding effect of energy intake. The risk of breast cancer was not associated with consumption of vegetables rich in beta‐carotene, multi‐vitamin tablets or other dietary supplements, coffee, tea, sugar or artificial sweeteners.