bluuebunny/crossref_metadata_2025_split huggingface dataset:
CA 494—a new tumor marker for the diagnosis of pancreatic cancer
Authors: Friess Helmut , Büchler Markus , Auerbach Bernhard , Weber Alexander , Malfertheiner Peter , Hammer Kai , Madry Norbert , Greiner Sabine , Bosslet Klaus , Beger Hans G. 
Published: February 2007

AbstractIn 59 patients with ductal pancreatic cancer the monoclonal antibody (MAb) BW 494, which detects the CA 494 glycoprotein antigen, was analyzed in comparison with the reference tumor markers CA 19‐9 and CEA. Eighty‐one patients with non‐pancreatic malignancies of the gastraintestinal (GI) tract, 95 with chronic pancreatitis, 124 with benign non‐pancreatic GI diseases, 30 with diabetes mellitus (type I or type II) and I14 healthy blood donors served as controls. The sensitivity of pancreatic cancer was 90%, 44% and 90% for CA 19‐9, CEA and CA 494, respectively. In chronic pancreatitis, as the most important control population for pancreatic cancer, the specificity was 85%, 72% and 94% for CA 19‐9, CEA and CA 494, respectively.
Loss of RB protein expression in primary bladder cancer correlates with loss of heterozygosity at the RB locus and tumor progression
Authors: Xu Hong‐Ji , Cairns Paul , Hu Shi‐Xue , Knowles Margaret A. , Benedict William F. 
Published: February 2007

AbstractRB‐protein status as determined by immunohistochemical analysis was compared with loss of heterozygosity (LOH) at the RB locus in 68 primary transitional‐cell carcinomas of the bladder. Absence of RB‐protein expression was found in 15 of 17 tumors in which LOH at the RB locus was identified, whereas 31 of 36 tumors from informative patients which showed no LOH had a normal RB‐protein pattern ( p < 0.001). Altered RB‐protein expression was also more frequently seen in muscle‐invasive and high‐grade tumors ( p < 0.003 and <0.005, respectively). Our results indicate that LOH at the RB locus is highly correlated with loss of RB‐protein expression in primary bladder carcinomas and further strengthens the notion that loss of RB function may be associated with more aggressive bladder tumors.
Inhibition by dehydroepiandrosterone of butylated hydroxyanisole (BHA) promotion of rat‐bladder carcinogenesis and enhancement of BHA‐induced forestomach hyperplasia
Authors: Shibata Masa‐Aki , Shirai Tomoyuki , Asakawa Emiko , Hirose Masao , Fukushima Shoji 
Published: February 2007

AbstractThe effects of dehydroepiandrosterone (DHEA) with/without ribonucleoside (RNs) supplementation on butylated hydroxyanisole (BHA) bladder‐tumor promotion and forestomach carcinogenesis were investigated. Male F344 rats were given N‐butyl‐N‐(4‐hydroxybutyl)nitrosamine (BBN) in their drinking water for 4 weeks and then received basal diet or diet containing BHA, DHEA, a mixture of RNs, BHA + DHEA or BHA + DHEA + RNs for 32 weeks. The occurrences of papillomas and carcinomas in the urinary bladder were increased in the groups given BHA or BHA + DHEA + RNs, as compared with control group values. In comparison with the BHA group, the BHA + DHEA group incidences and numbers of these tumors were decreased. However, the incidence and multiplicity of papillomas in the group given BHA + DHEA + RNs were again elevated. DNA synthesis levels in normal‐appearing bladder epithelium, but not tumor cells, were closely correlated with the observed level of promotion in most groups. The case of DHEA alone proved exceptional in that DNA synthesis was markedly decreased without any significant influence on lesion development. In the forestomach, DHEA, which itself was associated with slight although non‐significant hyperplasia, enhanced BHA‐induced epithelial lesions, characterized by marked basal‐cell proliferation and keratin‐cyst formation, independently of additional RNs administration.Our results suggest that the anti‐promoting effects of DHEA in the bladder depend on a deficiency in the pentose phosphates necessary for production of nucleosides. Organ‐specific modulation is indicated by the enhancing effects of DHEA on BHA‐induced forestomach hyperplasia.
Binding of some metastatic tumor cell lines to fibrous elastin and elastin peptides
Authors: Svitkina Tatyana M. , Parsons Donald F. 
Published: February 2007

AbstractRecent suggestions that tumor‐cell targeting of elastin‐rich tissues (e.g., lung) correlates with the presence of surface elastin receptors have been investigated. Receptors for insoluble (fibrous) elastin and for soluble elastin peptides have been implemented in these correlations. A rapid assay for binding of insoluble elastin has been devised. Two of the cell lines tested (M27 and MAT‐LyLu), which metastasize to the lung, strongly bound fibrous elastin whereas a third (B16‐F10) did not. None of 4 metastatic cell lines that do not target the lung (A549,3LL, TA3, TA3‐iso2) bound fibrous elastin. The ability of cell lines to interact with soluble elastin was tested by cell attachment to high‐molecular‐weight soluble elastin peptides adsorbed on plastic surface. Three of 7 tested cell lines, B16‐F10, M27 and TA3, attached to a soluble elastin coating. In contrast to the rapid binding of insoluble elastin particles, the cell interaction with immobilized soluble elastin peptides was delayed, suggesting that induction of receptors for soluble elastin and/or modification of the elastin coat was occurring. Thus, all 3 tested cell lines where metastases target the lung, namely, MAT‐LyLu, B16‐F10 and M‐27, show soluble‐ or insoluble‐elastin interactions, whereas, of 4 cell lines not targeting lungs, only one, TA3, reacts with soluble elastin.
Cell culture of tumors alters endogenous poly(ADPR)polymerase expression and activity
Authors: Chabert Magali G. , Kopp Patrick C. , Bischoff Pierre L. , Mandel Paul 
Published: February 2007

AbstractPoly(ADP‐ribose)polymerase, a chromatin‐bound enzyme, actively participates in processes such as cell proliferation, differentiation, and DNA repair and replication. This enzyme is also implicated in cell transformation, and its inhibition has been proposed to potentiate anti‐cancer drug activity. Since cells prepared from tumor biopsies and established tumor cell lines are commonly used to evaluate the efficiency of anticancer therapies, we have compared poly(ADP‐ribose)polymerase activity in animal tumor cells growing in vivo and in cell culture. Three tumor types were tested: a mastocytoma (P815), a lymphoma (RDM4). and a glioma (C6). Our results show that cell culture alters poly(ADP‐ribose)polymerase levels and activity. Endogenous poly(ADP‐ribose) activity was several fold higher in exponentially growing cells than in cells freshly recovered from solid or ascitic tumors. Moreover, polymerase activity increased with culture time, reaching a maximum when cells became confluent. Measurements of poly(ADP‐ribose)polymerase gene expression and protein amount indicate that lower enzyme activity in tumors grown in vivo are sustained by decreases in poly(ADP‐ribose)polymerase mRNA and protein amount. In contrast, the increase in endogenous poly(ADP‐ribose)polymerase activity observed in cultured cells was due to enzyme activation and not to de novo protein synthesis. Such differences must be considered when assessing the applicability of cell‐culture results to in vivo situations.
Insulin dependence of murine T‐cell lymphoma. II. Insulin‐deficient diabetic mice and mice fed low‐energy diet develop resistance to lymphoma growth
Authors: Sharon Raphael , Pillemer Graciela , Ish‐Shalom Dvorah , Kalman Rony , Ziv Ehud , Berry Elliot M. , Naor David 
Published: February 2007

AbstractPhysiological concentrations of insulin support the in vitro growth of LB T‐cell lymphoma. We could not detect similar insulin dependence in other tumor cell lines. This study reports that insulin also enhances the growth of LB cells in vivo. Mice treated with Streptozotocin (SZ) developed partial resistance to LB lymphoma growth and they survived longer (p < 0.0025) than non‐diabetic mice after LB‐cell inoculation. A few diabetic mice developed complete tumor resistance, manifested by total regression of the lymphoma. SZ‐treated diabetic mice reconstituted with external insulin died as fast as non‐diabetic mice when both were inoculated with the same number of LB cells. The SZ‐treated diabetic mice did not develop resistance to the growth of BCLI B‐cell leukemia, which demonstrated only a marginal proliferative response to insulin in vitro. Mice fed a low‐energy diet exhibited low insulin levels and also developed resistance to lymphoma growth (50% survival 21 days vs. 15 days; p < 0.0005), supporting the concept that insulin enhances LB T‐cell tumor development in mice.
Expression of integrins and other adhesion molecules on NK cells; Impact of IL‐2 on short‐ and long‐term cultures
Authors: Mäenpää Anna , Jääskeläinen Juha , Carpén Olli , Patarroyo Manuel , Timonen Tuomo 
Published: February 2007

AbstractWe have investigated, using flow cytometry, the expression of 19 adhesion molecules on fresh and IL‐2‐activated NK cells. The study included β1, β2 and β3 integrins, CD2, CD54 and CD58 (belonging to the immunoglobulin superfamily), and CD44 and L‐selectin (homing receptors). α1 and α2 of the β1 integrins were non‐existant and α3 was weak on freshly isolated NK cells, but their expression increased after 4 weeks in culture with IL‐2. On the other hand, some down‐regulation of α4 and α5 and disappearance of α6 was detected. CD11a/CD18 was upregulated by IL‐2, whereas CD11b‐c/CD18 were down‐regulated. As a novel finding we detected β3 on IL‐2‐activated T and NK cells. CD2, CD44, CD54 and CD58 were increased by IL‐2 but L‐selectin was strongly down‐regulated on the long‐term‐activated NK cells. Although IL‐2‐activated lymphocytes are potent tumor‐lysing killer cells in vitro and therefore a potential modality in cancer treatment, the IL‐2 induced changes in lymphocyte adhesion molecule expression may also lead to undesired effects, such as altered untargeted distribution and compromised migratory capacity.
Camptothecin derivatives induce regression of human ovarian carcinomas grown in nude mice and distinguish between non‐tumorigenic and tumorigenic cells in vitro
Authors: Pantazis Panayotis , Kozielski Anthony J. , Mendoza John T. , Early Janet A. , Hinz Hellmuth R. , Giovanella Beppino C. 
Published: February 2007

AbstractWe have recently shown that the plant alkaloid 20(S)‐camptothecin and its derivatives 9‐nitro‐20(S)‐camptothecin(9NC) and 9‐amino‐2O(S)‐camptothecin(9AC) inhibit the growth of a variety of human tumors xenografted in nude mice. In this report, we demonstrate that 9NC and 9AC effectively inhibit growth, and subsequently induce regression, of human ovarian tumors grown in nude mice. Tumor regression is accompanied by degenerative changes in the tumor cells as assessed by microscopic observations of histological sections prepared from the tumors. Parallel experiments in vitro show that 9NC inhibits in a similar manner the growth of human ovarian carcinoma cells, regardless of their ability to induce tumors when xenografted in nude mice, and induces similar morphological changes in both non‐tumorigenic and tumorigenic cells, as assessed by microscopic observation. Flow cytometry studies show that 9NC‐induced growth inhibition of the non‐tumorigenic cells is associated with accumulation of these cells in G2. In contrast, 9NC‐induced growth inhibition of the tumorigenic cells is associated with the generation of cells containing a reduced DNA content, that is, cells programmed to die. In conclusion, camptothecins appear to be cytostatic for non‐tumorigenic, but cytotoxic for tumorigenic cells, an important finding from viewpoints of cell biology, pharmacology and cancer chemotherapy.
Immortalization of human cervical keratinocytes by human papillomavirus type 33
Authors: Gilles Christine , Piette Jacques , Rombouts Sonia , Laurent Christian , Foidart Jean‐Michel 
Published: February 2007

AbstractTen immortalized cell lines were established by transfection of human cervical keratinocytes (CK) with HPV‐33 DNA and some of their characteristics were investigated. The following observations were made: (a) several cell lines have reached over 100 population doublings in vitro; (b) 3 transcripts were observed, 2 being encoded by the E6/E7 open reading frames (ORFs); (c) cytogenetic analyses showed important genetic modifications such as aneuploidy and isochromosome formation of the q arm of chromosome 8; (d) 2 of the 10 cell lines developed colonies in soft agar but none was able to form tumors when injected S.C. into nude mice; (e) Southern analysis suggested that a single copy of HPV‐33 is integrated at a single common site within the genome of the 10 cell lines. These immortalized cell lines should be useful for studying mechanisms involved in proliferation, differentiation and neoplastic transformation of CK by HPV‐33.
In vitro anti‐tumor activity of eosinophils from cancer patients treated with subcutaneous administration of interleukin 2. Role of interleukin 5
Authors: Rivoltini Licia , Colombo Mario Paolo , Parmiani Giorgio , Viggiano Vincenzo , Spinazzè Silvia , Santoro Armando , Takatsu Kiyoshi 
Published: February 2007

AbstractInterleukin 2 (IL‐2) administration is known to induce marked eosinophilia. To evaluate the potential role of eosinophils as anti‐tumor effectors and to understand the direct or indirect effects of IL‐2 on eosinophils, the physical and functional characteristics of eosinophils obtained during IL‐2 therapy were compared with those of eosinophils obtained from the same patients before IL‐2 administration, or from healthy donors. The treatment schedule consisted of subcutaneous (s.c.) injections of IL‐2, and was performed in 7 patients with small‐cell lung cancer (SCLC) in advanced stage. A marked increase of hypodense cells in peripheral blood was found to correlate with eosinophil activation in patients undergoing IL‐2 therapy. Cyto‐toxic activity of eosinophils against allogeneic tumor cells (SCLC, K562 and melanoma lines), as assessed by direct and antibody(Ab)‐dependent cellular cytotoxicity (ADCC), was markedly increased during IL‐2 therapy. Conversely, eosinophils obtained before treatment, like those of healthy donors, lacked any activity against tumor cells. Sera from IL‐2‐treated, but not from untreated, patients, significantly improved the in vitro survival and anti‐tumor cytotoxicity of eosinophils from healthy donors. Comparable effects were obtained with eosinophils cultured with interleukin 5 (IL‐5), granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) and, to a lesser extent, by tumor necrosis factor‐α (TNFα), while no direct activity was mediated by IL‐2. A 91% inhibition of eosinophil ADCC was found after pre‐incubation of the sera of IL‐2‐treated patients with anti‐IL‐5 but not with anti‐GM‐CSF or anti‐TNFα Ab. IL‐5 mRNA expression was detected in peripheral‐blood lymphocytes (PBL) obtained 4 hr after IL‐2 injection during the second and third week of IL‐2 therapy. Phenotypic analysis of eosinophils from IL‐2‐treated patients showed enhanced expression of activation markers, including Fcγ RII (CD32), HLA‐DR, CR3 (CD I lb) and CRI (CD35). These findings suggest that a significant cytotoxicity against tumor cells can be mediated by eosinophils after indirect, IL‐5‐mediated in vivo activation by IL‐2, and that eosinophils may be involved in the anti‐tumor response(s) induced in vivo by IL‐2.
Absence of HTLV‐I infection among seronegative subjects in an endemic area of Japan
Authors: Kinoshita Tomohiro , Imamura Jun , Nagai Hirokazu , Shimotohno Kunitada , Ito Mizuko , Ito Shin‐Ichiro , Ikeda Shuichi , Nagatomo Masazumi , Tajima Kazuo 
Published: February 2007

AbstractTo examine the prevalence of infection by human T‐cell leukemia virus type I (HTLV‐I) among seronegative subjects, healthy subjects on Tsushima Island, Japan, where the infection is endemic, were evaluated. A total of 209 healthy adults were examined for HTLV‐I provirus in peripheral blood mononuclear cells by the polymerase chain reaction (PCR), as well as for anti‐HTLV‐I antibodies by the particle agglutination (PA) method, the enzyme‐linked immunosorbent assay (ELISA) and by immunofluorescence analysis (IF). A total of 76 subjects were positive and 133 were negative for the provirus, showing a close correlation with the results of 3 assays for anti‐HTLV‐I serum antibodies. None of the seronegative subjects reacted positively on PCR analysis. These observations indicate that seronegative HTLV‐I carriers are rare in an area of Japan in which this viral infection is endemic.
High incidence of monoclonal EBV episomes in Hodgkin's disease and anaplastic large‐cell ki‐1‐positive lymphomas in HIV‐1‐positive patients
Authors: Boiocchi Mauro , De Re Valli , Doixetti Riccardo , Marzorro Alessandra , Gloghini Annunziata , Carbone Antonino , Vaccher Emanucla , Bertola Giulio 
Published: February 2007

AbstractA series of selected lymphoid malignancies (LMs) occurring in Italian HIV‐1‐infected (HIV+) patients, principally intravenous drug users, was investigated. In addition to small non‐cleaved‐cell (SNCC) and large‐cell immunoblastic (LCI) non‐Hodgkin's lymphomas (NHLs), a relatively high occurrence of anaplastic large‐cell Ki‐1‐positive (ALC Ki‐1+) lymphomas and Hodgkin's disease (HD) was observed, at variance with other reported series of HIV+ patients. Combined results of in situ hybridization and Southern‐blot analyses, in conjunction with immunohisto‐chemical detection of Epstein‐Barr virus (EBV)‐encoded latent membrane protein‐1 (LMP‐1), showed an almost complete association of ALC Ki‐1+ lymphomas and HD cases with EBV. The neoplastic cells of both these LMs also showed common immunophenotypic features such as frequent absence of B‐ and T‐cell differentiation markers and expression of the Ki‐1 activation marker, while SNCC and LCI lymphomas were mainly of mature B‐cell origin and Ki‐1‐. The concomitant high incidence of ALC Ki‐1+ lymphomas and HD in a specific group of HIV+ patients, their almost complete association with EBV in clonal and episomal form and the great similarity in differentiation, activation and virological markers which they display suggest that these LMs are pathological variants of a continuous spectrum of HIV‐1‐associated disorders etiopathologically linked to EBV.
Analysis of T‐cell‐receptor variable gene segment usage in peripheral‐blood lymphocytes of advanced cancer patients
Authors: Angevin Eric , Farace Françoise , Genevée Catherine , Caignard Anne , Dietrich Pierre‐Yves , Hercend Thierry , Triebel Frédéric , Henry‐Amar Michel , Escudier Bernard 
Published: February 2007

AbstractAdvanced cancer patients generally display impaired T‐cell immune functions. The underlying mechanisms are not well understood. The aim of this study was to analyze whether major alterations of TCR variable gene segment usage could be detected in the blood of these patients. Seventeen individuals with various malignancies were tested using PCR and a panel of V‐gene‐segment‐sub‐family‐specific (Vα1‐w29/Vβ1‐w24) oligonucleotide primers. The results indicate that these cancer patient lymphocytes expressed most Vα and Vβ sub‐family specificities, similarly to the lymphocytes of healthy donors (n = 10). This suggests that immunodepression in advanced cancer patients is not related to major deletions in their T‐cell repertoires. We also compared the mean relative expression of each V‐sub‐family specificity of patients and healthy donors by quantitative densitometric analysis. We found significant differences in 4 Vβ specificities (and no Vα). Our analysis identified unique T‐cell sub‐sets putatively involved in the mechanisms leading to immunodepression in advanced cancer patients. Alternatively, the observed differences in terms of Vβ specificity expression may reflect the host response against the tumor.
Integrin expression in cutaneous malignant melanoma: Association of the α3/β1 heterodimer with tumor progression
Authors: Natali P. G. , Bartolazzi A. , Cavaliere R. , Bigotti A. , Nicotra M. R. 
Published: February 2007

AbstractThe cell‐surface heterodimers of the integrin family of molecules, which mediate cell‐cell and cell‐substratum interactions, are likely to be functionally relevant in local and metastatic tumor growth. In the present study we have analyzed whether the α3/β1 receptor for collagen, laminin and fibronectin undergoes changes in expression during tumor progression in cutaneous malignant melanoma (CMM). The results of this study have demonstrated that, while low levels of VLA3 expression are detectable in benign lesions, in primary melanomas the heterodimer undergoes progressive increase in expression which correlates with the degree of dermal invasiveness. Metastatic lesions were found VLA3 positive in 82% of cases. Furthermore, the heterodimer is homogeneously expressed in multiple autologous metastases. The presence of VLA3 correlates with detection of at least one of the ligands in 45% of the cases studied. These findings provide additional evidence that tumor progression in CMM is associated with changes in integrin phenotypes which include the α3/β1 heterodimer.
Regulation of urokinase‐type plasminogen activator expression in squamous‐cell carcinoma of the oral cavity
Authors: Clayman G. , Goepfert H. , Boyd D. D. , Wang S. W. , Nicolson G. L. , El‐Naggar A. , Mazar A. , Henkin J. , Blasi F. 
Published: February 2007

AbstractWe undertook a study to determine the role and regulation of expression of urokinase‐type plasminogen activator in squamous‐cell carcinoma of the oral cavity. The contribution of urokinase to the invasive process was clearly demonstrated in experiments in which in vitro invasion by a cultured squamous‐cell carcinoma cell line was substantially reduced by a monoclonal antibody directed at the catalytic site of urokinase. The conditioned medium from 2 invasive cell lines contained high levels of urokinase. Examination of resected tumors for urokinase revealed (a) localization of the antigen to the tumor cells and (b) higher levels of the plasminogen activator in tumor tissue than in adjacent non‐malignant tissue. These results suggested that elevated expression of urokinase is a common feature of this malignancy. The mRNA half‐lives of cell lines expressing high and low levels of urokinase were similar, indicating that elevated levels of mRNA for the plasminogen activator were not a consequence of a more stable transcript. No evidence of u‐PA gene amplification was obtained by Southern blotting of DNA derived from the cell lines expressing high urokinase levels. Transfection of squamous‐cell carcinoma cells, which express high levels of urokinase, with a construct bearing the chloram‐phenicol acetyl transferase gene driven by the full‐length (2345 bp) urokinase promoter indicated activation of the urokinase promoter in trans. In conclusion, our results suggest that transcriptional activation of the urokinase gene, in squamous‐cell carcinomas of the oral cavity, leads to elevated levels of urokinase mRNA/protein which, in turn, can promote the invasive phenotype.
Allelic loss on chromosome 17 in human ovarian cancer
Authors: Phillips Nancy , Ziegler Michelle , Saha Bratin , Xynos Francisco 
Published: February 2007

AbstractIn order to identify a common region of deletion on chromosome 17 potentially containing a tumor‐suppressor gene, 27 ovarian carcinomas and 3 ovarian tumors of low malignant potential (LMP) were examined for loss of heterozygosity (LOH) at 6 p arm and 10 q arm loci. Ninety percent of all tumors had deletions at one or more loci. On the p arm, there was a single near‐common region of deletion on 17p 13.3 (D/7S30/ pYNZ22.1; 86% LOH), an intervening locus with a low LOH rate, and a more proximal locus on 17p11.2 (D/7S58/pEW301; 82% LOH) with a high LOH rate. In less aggressive tumors, LOH at Df 7S30 was not accompanied by LOH at p53. The q arm had a common region of deletion for high‐stage carcinoma at D/7S579 (Mfd 188; 74% LOH) on q21, a locus tightly linked to the familial breast‐ovarian‐cancer syndrome (BRCAI) locus. D/7S579 was lost in all informative high‐stage carcinomas and retained in all low‐stage carcinomas and tumors of LMP. There may be at least 2 tumor‐suppressor genes, an early‐acting gene on the p arm and a gene on the q arm involved in tumor progression and metastasis.