bluuebunny/crossref_metadata_2025_split huggingface dataset:
A cell surface antigen (BAL) defined by a mouse monoclonal antibody inducing apoptosis in a human lymphocytic leukemia cell line
Authors: Wallén‐Öhman Marie , Borrebaeck Carl A. K. 
Published: February 2007

AbstractThe lack of apoptosis or programmed cell death in human tumor cells has been suggested to be one factor allowing uncontrolled growth of neoplasms. We have developed a mouse monoclonal antibody (MAb) that induces programmed cell death in a human acute leukemia cell line (KM‐3) of the pre B‐cell type. Stable, antibody‐producing hybridomas were produced by fusing mouse myeloma cells to spleen cells from mice immunized with viable KM‐3 cells. Incubation of KM‐3 cells with the MAb (designated anti‐BAL) resulted in growth inhibition and subsequent cell death within 2‐3 days. Anti‐BAL required cross‐linking with a rabbit anti‐mouse antibody to induce DNA fragmentation typical of apoptosis. Immunoblotting experiments with anti‐BAL identified a 37‐kDa protein, apparently different from any previously described apoptosis‐related surface antigen. Strongest expression of the antigen was generally found on cells of lymphoid or myeloid origin. However, several other cell types such as fibroblasts and endothelial cells were also stained by anti‐BAL in flow cytometry but less intensively. Despite the apparent presence of this cell surface‐bound 37‐kDa antigen on several normal and malignant cell types, anti‐BAL induced cell death only in human malignant cell lines expressing a more immature phenotype. © 1994 Wiley‐Liss, Inc.
Expression of uPA and its receptor by both neoplastic and stromal cells during xenograft invasion
Authors: Rømer John , Pyke Charles , Lund Leif R. , Eriksen Jens , Kristensen Peter , Rønne Ebbe , Høyer‐Hansen Gunilla , Danø Keld , Brünner Nils 
Published: February 2007

AbstractRecent studies have shown that molecules involved in generation and regulation of extracellular proteolytic activity are often expressed by non‐malignant stromal cells during human cancer invasion. We have studied the expression of the urokinase‐type plasminogen activator and the urokinase‐type plasminogen activator cell‐surface receptor in xenografts of human MDA‐MB‐231 mammary carcinoma cells growing invasively in nude mice. Northern analysis showed the presence of both human and mouse urokinase‐type plasminogen activator and urokinase‐type plasminogen activator receptor mRNA in tumor extracts. By in situ hybridization, mRNA for human urokinase‐type plasminogen activator and its receptor was detected in virtually all the cancer cells, while mouse urokinase‐type plasminogen activator and urokinase‐type plasminogen activator receptor mRNA was expressed by tumor‐infiltrating fibroblast‐like and macrophage‐like cells. In invasive areas the cells expressing the 2 murine mRNAs were either the same or located immediately adjacent to each other. This model system has several advantages for studies of the mechanism by which cancer cells induce or recruit stromal cells to produce molecules involved in proteolysis. © 1994 Wiley‐Liss, Inc.
Doxorubicin retention and chemoresistance in human mesothelioma cell lines
Authors: Isobe Hiroshi , Wellham Larry , Sauerteig Antonieta , Sridhar Kasi S. , Ramachandran Cheppail , Krishan Awtar 
Published: February 2007

AbstractEight cell lines were established from the pleural effusion of 4 patients with malignant mesothelioma. The most sensitive (FCCMES‐4) and the most resistant (FCCMES‐2) mesothelioma cell lines had IC50 of 0.66 and 1.85 μM for doxorubicin in clonogenic assays, respectively. In comparison with murine leukemic P388 cells, mesothelioma cell lines were 7.5‐ to 21 ‐fold more resistant to doxorubicin. Co‐incubation with verapamil significantly increased doxorubicin retention in one of the cell lines (FCCMES‐2) expressing P‐glycoprotein in 16.8% of the cells. These results indicate that doxorubicin resistance may be intrinsic in refractory mesothelioma patients and P‐glycoprotein‐mediated drug efflux may be involved in resistance of some of the mesotheliomas. © 1994 Wiley‐Liss, Inc.
Anti‐idiotypic monoclonal antibody AB3, reacting with the primary antigen (CEA), can localize in human colon‐carcinoma xenografts as efficiently as AB1
Authors: De Moraes Jane Z. , Gesztesi Jean‐Luc , Westermann Patrick , Le Doussal Jean‐Marc , Lopes José D. , Mach Jean‐Pierre 
Published: February 2007

AbstractBALB/c mice were immunized with anti‐idiotypic monoclonal (MAb) antibody (anti‐Id or Ab2) directed against an ABI Mab anti‐carcinoembryonic (CEA) in order to obtain AB3 MAbs (anti‐anti‐Id). AB3 MAbs were shown to recognise the primary antigen (CEA) and one of them was tested extensively in vitro and in vivo. This AB3 MAb was shown to bind specifically to CEA on frozen sections of a human colon carcinoma by immunoper‐oxidase. Scatchard plot analyses showed that the affinity of this AB3 was of the same order of magnitude as the ABI. In vivo experiments, in nude mice bearing CEA‐producing human colon‐carcinoma xenografts showed that up to 30% of the intravenously injected dose of 125I‐labelled AB3 were localized per gram of tumour tissue. Furthermore, calculation of the ratios of AB3 concentration in the tumour over those in normal organs such as lung, liver, kidney, spleen and bone gave relatively high values similar to results obtained with ABI. All together our results show that AB3 can localize as efficiently and specifically in the tumour as ABI, despite the fact that the mice from which it was derived were immunized with a mouse MAb (AB2) and had never been exposed to CEA. © 1994 Wiley‐Liss, Inc.
The induction of apoptosis is a common feature of the cytotoxic action of ether‐linked glycerophospholipids in human leukemic cells
Authors: Diombde Luisa , Piovani Bianca , Re Fabio , Principe Paola , Colotta Francesco , Modest Edward J. , Salmona Mario 
Published: February 2007

AbstractThe ability of 2 recent ether‐lipid derivatives, aza‐phospholipids BN52205 and BN522II, to induce apoptosis in different leukemia cell lines was investigated using I‐octadecyl‐2‐methly‐rac‐glycero‐3‐phosphocholine (ET‐18‐OCH3) as a positive control. HL60, K562, Molt‐4 and U937 cells were exposed for 24 hr to 20 μM of drug. The 2 aza‐derivatives were as cytotoxic as ET‐18‐OCH3: BN52205 and BN522II selectively induced apoptotic death in HL60, Molt‐4 and U937 cells, but not in the KS62‐resistant cell line. Around 50% of DNA was fragmented in HL60 cells after exposure to the aza‐derivatives, and 34% and 20% of DNA was fragmented in Molt‐4 and U937 cells respectively. Similar results were obtained when cells were exposed to ET‐18‐OCH3. Our data confirm that ether lipids induce apoptosis in a variety of human leukemic cells, providing a possible explanation for their selectivity and mechanism of action.
Establishment and in vivo characterization of multidrug‐resistant dunning R3327 rat prostate‐carcinoma cell‐lines
Authors: Bashir Imtiaz , Sikora Karol , Abel Paul , Foster Christopher S. 
Published: February 2007

AbstractWe describe the selection of 3 new multidrug‐resistant cell lines derived from tumor cells of different metastatic phenotypes within the Dunning R3327 model of rat prostatic carcinoma. Cell lines of weak (AT2) and strong (AT3 and MAT‐LyLu) metastatic behavior were cultured in vitro and challenged with doxorubicin at progressively increasing concentrations. Chemosensitivity was determined colorimetrically by release of precipitated formazan pigment (MTT assay). Expression of the multidrug‐resistance glycoprotein (P‐170) was monitored immunocytochemically and by Western blotting using monoclonal antibody C219. The behavior of the parental and resultant drug‐resistant cells was assessed by their growth in syngeneic rats. Doxorubicin challenge of the initially drug‐sensitive parental prostatic carcinoma cell lines resulted in the rapid development of multidrug resistance together with simultaneous expression of P‐glycoprotein. While lung and lymph‐node metastases developed in host animals inoculated with parental AT3 and MAT‐LyLu cells, no metastases developed in the multidrug‐resistant progeny of these cell lines. This study has shown that Dunning rat prostate‐carcinoma cell lines, previously sensitive to different cytotoxic agents, rapidly become multidrug‐resistant and express P‐glycoprotein following exposure to doxorubicin. Further more, development of multidrug resistance is associated with a less aggressive tumor phenotype and loss of metastatic potential. Nevertheless, it is unlikely that the non‐metastatic phenotype of Dunning rat prostatic carcinoma cells is solely associated with expression of P‐glycoprotein. These new multidrug‐resistant cell lines exhibiting an altered behavioral phenotype will provide a valuable mode with which to analyze the relationship between expression of P‐glycoprotein and the metastatic phenotype of prostatic carcinoma cells.
Inhibition of metastasis of lewis lung carcinoma by a synthetic peptide within growth factor‐like domain of urokinase in the experimental and spontaneous metastasis model
Authors: Kobayashi Hiroshi , Gotoh Junko , Fujie Michio , Shinohara Hiromitsu , Moniwa Nobuhiko , Terao Toshihiko 
Published: February 2007

AbstractFour synthetic peptides (residues 20‐30 and 17‐34) within the growth factor‐like domain (GFD) of murine and human urokinase‐type plasminogen activator (uPA) were examined to determine whether they inhibit production of experimental and spontaneous lung metastasis by murine Lewis lung carcinoma (3LL) cells. In an in vivo experimental metastasis assay, which determines mainly the later steps of the metastatic migration process (extravasation from the bloodstream and then growth into pulmonary tumor), none of the peptides introduced by i.v. single co‐injection into syngeneic C57B1/6 mice inhibited pulmonary metastasis, when 3LL cells were pre‐incubated with the peptides followed by i.v. co‐injection of the peptide and cells. In addition, none of the peptides, when injected i.p. daily for 7 days after i.v. tumor cell inoculation, reduced the number of lung tumor colonies. In a second in vivo assay that measures metastasis from a primary tumor (spontaneous metastasis model), multiple i.p. injections of the mouse peptide 17‐34 for 7 days after s.c. tumor cell inoculation significantly inhibited metastatic lung tumor colonization in a dose‐dependent manner, whereas human peptide 17‐34 had no effect. Mouse and human peptide 20‐30 had no effect either. The inhibition of lung metastasis was not due to direct antitumor effects of mouse peptide 17‐34. Our results indicate that occupation of uPA receptors on 3LL cells by the enzymatically inactive mouse peptide 17‐34 or prevention of rebinding of uPA synthesized by tumor cells to their receptor specifically reduced tumor cell invasion and formation of metastasis and that uPA may regulate more efficiently the mechanism involved in the entry of tumor cells into vascular circulation than extravasation during the metastatic process.
T‐helper‐ and accessory‐cell‐independent cytotoxic responses to human tumor cells transfected with A B7 retroviral vector
Authors: Döhring Christian , Angman Lena , Spagnoli Giulio , Lanzavechia Antonio 
Published: February 2007

AbstractAs a means to increase the immunogenicity of tumor cells, we have developed a retroviral vector to transfect human B7, a molecule capable of delivering co‐stimulatory signals to T cells. Three different tumors, a melanoma, an ovarian carcinoma and a myelomonocytic leukemia, were transfected with high efficiency. When compared for their capacity to stimulate allogeneic T cells, B7+ but not B7− tumor cells were able to stimulate strong proliferative and cytotoxic responses. The effector CTL generated recognised B7+ and B7− cells as well as untransfected tumor cells, indicating that B7 is required in the inductive but not the effector phase of the response. Remarkably, B7+ tumor cells were able to induce cytotoxic responses both by CD4‐depleted and by CD8‐purified T cells, demonstrating that expression of B7 is at the same time necessary and sufficient to induce a cytotoxic response in the absence of T‐helper cells and accessory cells.
Esophageal balloon cytology and subsequent risk of esophageal and gastric‐cardia cancer in a high‐risk chinese population
Authors: Liu S. F. , Shen Q. , Dawsey S. M. , Wang G. Q. , Nieberg R. K. , Wang Z. Y. , Weiner M. , Zhou B. , Cao J. , Yu Y. , Guo W. D. , Li J. Y. , Blot W. J. , Li B. , Taylor P. R. 
Published: February 2007

AbstractLinxian, China has some of the highest rates of esophageal/gastric cardia cancer in the world. In 1983, esophageal balloon cytology screening was performed in 3 communes in northern Linxian. Of the participants, 10,066 with no evidence of cancer were followed prospectively for 71/2 years to evaluate the ability of the initial cytologc diagnoses to identify individuals at increased risk for developing cancer of the esophagus or gastric cardia. A total of 747 incident cases of esophageal or cardia cancer and 322 deaths due to these tumors were identified during the follow‐up period and used in this analysis. The risks for esophageal or cardia cancer incidence and mortality increased in parallel with the presumed severity of the 1983 Chinese cytologic diagnoses. After adjusting for potential confounding factors, relative risks for esophageal or cardia cancer incidence, by initial cytologic diagnosis, were normal = 1.00 (reference), hyperplasia = 1.25, dysplasia 1 = 2.20, dysplasia 2 = 4.22 and near‐cancer = 5.96. Our results suggest that esophageal balloon cytology, as performed and interpreted in Linxian in 1983, successfully identified individuals at increased risk for developing cancer of the esophagus or gastric cardia. © 1994 Wiley‐Liss, Inc.
Enhancement of radioimmunotherapy by drugs modifying tumour blood flow in a colonic xenograft model
Authors: Pedley R. Barbara , Begent Richard H. J. , Boden Joan A. , Boxer Geoffrey M. , Boden Robert , Keep Patricia A. 
Published: February 2007

AbstractRadioimmunotherapy (RIT) is hampered clinically by poor tumour localization of antibody. In order to enhance localization we have investigated the concomitant use of RIT with 2 drugs, fiavone‐8‐acetic acid (FAA) and its analogue 5,6‐dimethylxanthenone‐4‐acetic acid (XAA), which both reduce tumour blood flow and induce immunomodulation. A single i. v. dose of 0.5 mCi (18.5 MBq) intact 131 I anti‐CEA antibody significantly delayed growth and prolonged survival over that of untreated controls, in an established LSI74T colon xenograft model in nude mice. The adjuvant use of a single i. p. dose of either FAA or XAA, given 24 or 48 hr after 131 I‐A5B7 to allow maximum tumour levels of antibody to be attained before drug‐induced blood‐flow inhibition, significantly enhanced the RIT. FAA caused entrapment of antibody within the tumour in relation to the time allowed for localization before drug administration. Repeated doses of FAA prolonged tumour growth inhibition but did not enhance the therapy achieved after a single dose. Although both drugs alone induced massive tumour necrosis of all but a thin peripheral rim of viable cells, tumour regrowth was inhibited for a few days only, with no effect on survival. Drug‐induced tumour necrosis, immunomodulation and retention of higher doses of 131 I‐A5B7 within the tumour may contribute to the enhanced RIT produced by this combined therapy. © 1994 Wiley‐Liss, Inc.
Anti‐Tac(Fab)‐PE40, a recombinant double‐chain immunotoxin which kills interleukin‐2‐receptor‐bearing cells and induces complete remission in an in vivo tumor model
Authors: Kreitman Robert J. , Chang Chung Nan , Hudson Dehra V. , Queen Cary , Bailon Pascal , Pastan Ira 
Published: February 2007

AbstractWe have produced a single plasmid encoding both the heavy chain Fd domain (VH + CHl) of the anti‐interleukin‐2 receptor (IL2R) monoclonal antibody anti‐Tac, and the anti‐Tac light chain fused to PE40, a truncated derivative of Pseudomonas exotoxin. The active immunotoxin anti‐Tac(Fab)‐PE40 could be recovered from E. coli from either periplasm or renatured inclusion bodies. The double‐chain immunotoxin was very cytotoxic toward IL2R‐bearing cell lines, human activated T cells and fresh adult‐T‐cell‐leukemia cells. The cytotoxicity was similar to that of anti‐Tac(Fv)‐PE40, the single‐chain recombinant toxin containing only the variable domains of anti‐Tac. IL2R‐binding affinity was also equivalent to that of anti‐Tac(Fv)‐PE40, which is one‐third that of anti‐Tac. The serum half‐life in mice was significantly prolonged as compared with anti‐Tac(Fv)‐PE40, with a β phase of 430 vs. 57 minutes, but the LD50s were equivalent when the immunotoxins were administered in 3 daily doses. Anti‐Tac(Fab)‐PE40 was very cytotoxic in vitro toward transfected ATAC‐4 carcinoma cells which express IL2Rs. In mice bearing ATAC‐4 tumors, anti‐Tac(Fab)‐PE40 showed significant anti‐tumor activity, inducing complete remissions in 80 and 100% of treated animals at approximately 7 and 14% respectively of the LD50. Anti‐Tac(Fab)‐PE40 was much more effective in vitro and in vivo than chemical conjugates between anti‐Tac and truncated PE molecules. The recombinant Fab toxin should be studied further as potential treatment for IL2R‐related malignancies, particularly if smaller recombinant immunotoxins have insufficient half‐life in humans. © 1994 Wiley‐Liss, Inc.
Analysis of proviral integration in human mammary epithelial cell lines immortalized by retroviral infection with a temperature‐sensitive SV40 T‐antigen construct
Authors: Stamps Alasdair C. , Davies Susan C. , Burman Jacqueline , O'Hare Michael J. 
Published: February 2007

AbstractA panel of eight conditionally immortal lines derived by infection of human breast epithelial cells with an amphotropic retrovirus transducing a ts mutant of SV40 large T‐antigen was analyzed with respect to individual retroviral integration patterns. Each line contained multiple integration sites which were clonal and stable over extended passage. Similar integration patterns were observed between individual lines arising separately from the same stock of pre‐immortal cells, suggesting a common progenitor. Retroviral integration analysis of preimmortal cells at different stages of pre‐crisis growth showed changes indicative of a progressive transition from polyclonality to clonality as the cells approached crisis. Each of the immortal lines contained a sub‐set of the integration sites of their pre‐immortal progenitors, with individual combinations and copy numbers of sites. Since all the cell lines appeared to originate from single foci in separate flasks, it is likely that each set arose from a common clone of pre‐immortal cells as the result of separate genetic events. There was no evidence from this analysis to suggest that specific integration sites played any part either in the selection of pre‐crisis clones or in the subsequent establishment of immortal lines. © 1994 Wiley‐Liss, Inc.
The state of differentiation of HT‐29 colon carcinoma cells alters the secretion of cathepsin D and of plasminogen activator
Authors: Huet Guillemette , Zerimech Farid , Dieu Marie‐Claire , Hemon Brigitte , Grard Georges , Balduyck Malika , Janin Anne , Lafyatis Robert , Degand Pierre 
Published: February 2007

AbstractWe have studied the cellular content and the extracellular release of cathepsins B and D, and of plasminogen activator, in 2 different tumor cell populations before confluence and after late confluence: the HT‐29 colon carcinoma cell line, which contains primarily undifferentiated cells, and a subpopulation derived from this cell line, which contains cells committed to differentiation into mucus‐secreting goblet cells after confluence. In both populations, cellular cathepsin‐B activity increased after confluence, and latent cathepsin B was found in all culture media. In the parental cell line, cellular cathepsin D activity decreased after confluence; however, cathepsin D was secreted at high levels into the extracellular medium. In contrast, in the subpopulation of cells committed to differentiation, cellular cathepsin D activity increased after confluence, and cathepsin D was not secreted into the extracellular medium, but was immunolocalized in the apical brush border of the differentiated cells. Plasminogen activator of urokinase type was identified by immunocytochemistry. Both subconfluent cell populations, and the post‐confluent undifferentiated cell population, produced plasminogen activator activity at similar levels. In contrast, in the differentiated postconfluent cells, the production of plasminogen activator activity was markedly lower. Our data show that the differentiation of HT‐29 colon carcinoma cells into mucus‐secreting cells impairs the secretion of plasminogen activator and cathepsin D, but does not affect cathepsin B. © 1994 Wiley‐Liss, Inc.
Evaluation of a new photosensitizer, meso‐tetra‐hydroxyphenyl‐chlorin, for use in photodynamic therapy: A comparison of its photobiological properties with those of two other photosensitizers
Authors: Ma Liwei , Moan Johan , Berg Kristian 
Published: February 2007

AbstractThe properties of a new photosensitizer, meso‐tetra‐hydroxyphenyl‐chlorin (mTHPC), were studied using V79 cells (Chinese‐hamster lung fibroblasts). Comparisons were made with 2 other photosensitizers: photofrin II (PII) and meso‐tetra‐hydroxyphenyl‐porphyrin (mTHPP). A main advantage of mTHPC is that it has a strong absorption at 652 nm. Maximal cellular uptake of the dye was observed after 24 hr incubation of the cells with the drug. Using a confocal laser‐scanning fluorescence microscope, we observed a diffuse distribution of m THPC in the cytoplasm. Furthermore, the lipophilicity of mTHPC was compared with that of the components of PII by means of high‐pressure liquid chromatography (HPLC). Absorption and fluorescence spectroscopy indicated that aggregated as well as monomeric mTHPC was bound to the cells. The action spectrum for photo‐inactivation of the cells showed that aggregated mTHPC did not contribute significantly to its photosensitizing effects. In the present cellular system, the efficiency of photodynamic therapy (PDT) with mTHPC (cells were irradiated at a wavelength of 652 nm) was higher than with PII (irradiation at 630 nm) or with mTHPP (648 nm). The quantum yield for photo‐inactivation of cells was smaller for mTHPC than for mTHPP and PII. The addition of 1,3‐diphenylisobenzofuran (DPBF) reduced cell inactivation during PDT. Thus, PDT with mTHPC seems to act at least partlyviaa type‐II process. © 1994 Wiley‐Liss, Inc.
Caffeine attenuates the action of amsacrine and etoposide in U‐937 cells by mechanisms which involve inhibition of RNA synthesis
Authors: Pérez Concepción , Pelayo Francisco , Vilaboa Nuria E. , Aller Patricio 
Published: February 2007

AbstractPulse treatments of U‐937 human promonocytic leukemia cells with the DNA topoisomerase‐II inhibitors 4′‐(9‐acridynilamino)methanesulfon‐m‐anisidide (amsacrine, mAMSA) or etoposide (VP‐16) caused growth inhibition, G2‐arrest, increase in cell size and expression of differentiation markers. All these effects were greatly reduced by the presence of 5–10 mM caffeine. In addition, caffeine partially prevented the increase in the number of topoisomerase‐DNA cleavable complexes caused by the topoisomerase inhibitors, as determined by SDS/CIK precipitation assays; it caused chromatin condensation, as determined by flow cytometry assays, and interacted with mAMSA in solution, as suggested by spectrophotometric assays. Pulse treatment with caffeine greatly inhibited RNA synthesis but not DNA or protein synthesis, as indicated by labelled precursor incorporation assays. The transcription inhibitor 5,6‐dichloro‐1‐β‐D‐ribofuranosylbenzymidazole reduced the mAMSA‐ and VP‐16‐produced growth inhibition in a similar manner. It is concluded that RNA synthesis inhibition is one of the possible mechanisms by which caffeine protects cells from the action of topoisomerase‐II inhibitors. © 1994 Wiley‐Liss, Inc.