bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of a mouse‐human chimeric antibody to a cancer‐associated antigen
Authors: Orlandi R. , Figini M. , Tomassetti A. , Canevari S. , Colnaghi M. I. 
Published: February 2007

AbstractIn an attempt to obtain a therapeutic antibody, the murine monoclonal antibody (MAb) MBr 1 (IgM, k), directed against human carcinomas, was converted in a mouse/human chimeric MAb of γ I isotype. The chimeric MAb, γICHI‐MBr 1, retains the ability to specifically bind tumor cells and tissues with no modification in its binding to the normal material tested. γI CHI‐MBr 1 recognizes mucins and high‐molecular‐weight glycoproteins carrying the antigenic determinant and stains a neutral glycolipid extracted from MCF—7 cells. The chimeric and the murine MBr 1 efficiently cross‐inhibit each other on the reference cell line MCF‐7 and the calculated affinity constants amount to 3.8 × 107 and 1.7 × 108M−1, respectively. The human constant region allows γI CHI‐MBr 1 to bind with the FcR on the human monocytic cell line U937 and to efficiently mediate antibody‐dependent cellular cytotoxicity in the presence of human lymphocytes activated by IL2. In addition, γICHI‐MBr 1, like the murine MBr I, mediates complement‐dependent tumor‐cell lysis. Thus, by modelling a molecule with reduced size and increased functional characteristics, we have obtained a reagent which is more suitable for in vivo therapeutic approaches. © 1992 Wiley‐Liss, Inc.
Radiation‐induced lymphoid tumors and radiation lethality are inhibited by combined treatment with small doses of zinc aspartate and wr 2721
Authors: Floersheim G. L. , Christ A. , Koenig R. , Racine C. , Gudat F. 
Published: February 2007

AbstractCombined small doses of zinc aspartame and WR 2721 provided additive protection against radiation lethality in mice. Survival obtained with a small dose of WR 2721 which was ineffective alone could be enhanced to 83% by combining the drug with zinc aspartate, which on its own also displayed no effect. The survival of 25% provided by a higher dose of WR 2721 was increased significantly by adding zinc aspartate. Additivity was also tested in a model of radiation carcinogene‐sis. For this purpose, lethality and occurrence of lymphoid tumors induced by fractionated total‐body irradiation were studied in C57BI/6 mice treated with zinc aspartate and WR 2721. In order to reveal additive effects, both agents were used at sub‐optimal dosages. In mice subjected to 5 daily exposures of 1.9 Gy, the combination of zinc aspartate and WR 2721 was effective and enhanced the survival to 83% as compared with 25% afforded by WR2721 alone (p < 0.005). Similarly, histological assessment of organ involvement with lymphoma revealed that zinc aspartate and WR 2721 alone did not bring about a significant reduction of lymphoma incidence. On the other hand, the combined agents diminished organ involvement with lymphoma to 9.1 % as against 90% in the controls (p < 0.0005) and 62.5% with WR 2721 alone (p < 0.025). Thus, combined treatment with zinc aspartate and WR 2721 also inhibited radiation‐induced lymphoid tumors. © 1992 Wiley‐Liss, Inc.
Lung cancer following Hodgkin′s disease: A case‐control study
Authors: Kaldor J. M. , Day N. E. , Bell J. , Clarke E. A. , Landmark F. , Karjalainen S. , Band P. , Pedersen D. , Choi W. , Blair V. , Henry‐Amar M. , Prior P. , Assouline D. , Pompe‐Kirn V. , Cartwright R. A. , Koch M. , Arslan A. , Fraser P. , Sutcliffe S. B. , Host H. , Hakama M. , Stovall M. 
Published: February 2007

AbstractIt is recognized that survivors of Hodgkin's disease are at a substantially increased risk of lung cancer. A collaborative group of population‐based cancer registries and major treatment centers carried out a case‐control study, in which 98 cases of lung cancer were identified in patients who had survived at least 1 year following a diagnosis of Hodgkin's disease. A total of 259 matched controls were selected from patients with Hodgkin's disease who did not develop subsequent lung cancer, and for both cases and controls detailed information was abstracted from medical records concerning stage and treatment of Hodgkin's disease. Patients treated with chemotherapy alone had about twice the risk of developing lung cancer than those treated by radiotherapy alone or both modalities. There was no increase in risk with cumulative number of cycles of chemotherapy. Among patients treated with radiotherapy alone, there was an increase in risk related to estimated radiation dose to the lung. There was also a strong association between cigarette smoking and the risk of lung cancer. The finding of a higher risk following chemotherapy than following radiotherapy was unexpected, but could not be explained by any identified methodological flaws. A plausible inference from the study is that all forms of Hodgkin's disease therapy are carcinogenic to the lung and that, in particular, chemotherapy is associated with an increase in risk which is at least comparable to and perhaps higher than the risk produced by radiotherapy. © 1992 Wiley‐Liss, Inc.
Viral CO‐infections in human papillomavirus‐associated anogenital lesions according to the serostatus for the human immunodeficiency virus
Authors: Bernard Catherine , Mougin Christiane , Madoz Laurence , Drobacheff Christine , van Landuyt Hervé , Laurent Rene , Lab Michel 
Published: February 2007

AbstractIn HIV‐infected men, human papillomavirus (HPV) infection is strongly linked with the development of anogenital lesions but is not a sufficient factor to explain the neoplastic transformation of such lesions. We investigated the association between HPV and herpesvirus infections in penile and anal lesions from 54 HIV‐seronegative and 54 HIV‐seropositive men by means of colposcopy, histopathology andin situhybridization. Our patients showed condyloma acuminata (39%), papular warts (35%) and macular warts (26%). High‐grade lesions were predominant in the HIV+men, whereas low‐grade lesions were more frequent in the HIV−men. In the HIV+group, potential oncogenic HPV were the most frequently detected (83.4%) whereas the “low‐risk” HPV were found chiefly in HIV−men (62.1%). The CD4 number was lower in patients showing “high‐risk” HPV than in men showing lesions without HPV or with non‐oncogenic HPV. HPV types 6/11 were found mainly associated with koilocytosis or with AIN(PIN)I. Oncogenic HPV were more often detected in AIN(PIN)II‐III. The herpesviruses DNA detection revealed a higher prevalence of HSV1 and ‐2 than CMV and EBV in the studied biopsies. The frequency of HSV and CMV detection was higher in the HIV+than in the HIV−men. A link was found between the “high‐risk” HPV and the CMV detection whatever the population considered. The detection in HPV lesions of other sexually transmitted viral agents could therefore represent an important means of preventing progression of the anogenital disease, especially in immuno‐suppressed patients. © 1992 Wiley‐Liss, Inc.
Suppression of basal, PMA‐and IFN‐α‐, but not IFN‐γ‐induced expression of HLA class I in v‐myc‐transformed U‐937 monoblasts
Authors: Larsson L.‐G. , Öberg F. , Stöckbauer P. , Masucci M. G. , Nilsson K. 
Published: February 2007

AbstractRecent studies have suggested that certain oncogenes, in particular members of the myc family, may be involved in the down‐regulation of HLA class‐1 antigen expression observed in many types of tumor. We report that constitutive expression of an OK 10 v‐mye gene in human monoblastic U‐937 cells results in a reduced expression of HLA class‐1 cell‐surface expression and decreased levels of HLA class‐1 protein and mRNA. All class‐1 alleles, with the possible exception of HLA A3, were affected, as shown by one‐dimensional isoelectric focusing (ID‐IEF). Basal expression of the β2m chain was also reduced, although to a lesser extent. In addition, we show that the PMA‐, and at least partially the IFN‐α‐induced increase in HLA class‐1 antigen expression, was inhibited in U‐937‐myc cells both at the protein and the mRNA level. In contrast, the response to IFN‐γ was normal. Another important difference in the response to IFN‐γ and a was that, while IFN‐γ abrogated the v‐myc block of PMA‐induced differentiation of U‐937 cells, as previously reported, IFN‐α did nat. Our data show that v‐myc negatively affects the regulation of both basal and inducible HLA class‐1 antigen expression. © 1992 Wiley‐Liss, Inc.
Regulation of androgen receptor gene expression by steroids and retinoic acid in human breast‐cancer cells
Authors: Hall Rosemary E. , Tilley Wayne D. , McPhaul Michael J. , Sutherland Robert L. 
Published: February 2007

AbstractAlthough the androgen receptor (AR) has been detected by ligand‐binding assays, there is little known about the expression and regulation of the AR gene in human breast‐cancer cells. AR mRNA, measured by Northern analysis in 18 cell lines, was found to be expressed predominantly in oestrogen‐ and progesterone‐receptor‐positive (ER+, PR+) lines as a single species of approximately 10.5 kb but was also comparatively abundant in I ER‐ and PR‐negative cell line, MDA‐MB‐453. Dexamethasone (Dex), Organon 2058 (Org 2058), dihydrotestosterone (DHT), and all‐trans‐retinoic acid (RA) down‐regulated AR mRNA levels in T‐47D (ER+, PR+) cells 6 hr after treatment, whereas oestradiol (E2) had no effect. In MDA‐MB‐453 (ER−, PR−) cells, regulation of AR mRNA by RA differed from the other cell lines: RA increased the level of AR mRNA. DHT‐binding assays indicated a corresponding increase in AR protein. Transfection of the androgen‐responsive mouse mammary tumour virus long‐terminal repeat (MMTV LTR) linked to a chloramphenicol acetyltransferase (CAT) reporter gene was used to examine the effect of altered AR levels on androgen action. The increased level of AR following RA pre‐treatment in MDA‐MB‐453 cells resulted in enhanced induction of CAT activity by DHT and, conversely, a decrease in the level of AR following RA pretreatment in T‐47D cells resulted in reduced induction of CAT activity by DHT. These data demonstrate that AR is expressed predominantly in ER+ and PR+ cell lines and its expression is regulated by ligands also known to regulate ER or PR, including progestins and retinoids. Androgen responsiveness measured by a transfected reporter gene was altered according to the extent of up‐ or down‐regulation of AR expression, demonstrating that responsiveness is dependent on receptor concentration. © 1992 Wiley‐Liss, Inc.
Inhibition by 6‐hydroxydopamine of enhanced gastric carcinogenesis induced by N‐methyl‐N′‐nitro‐N‐nitrosoguanidine in spontaneously hypertensive rats
Authors: Tatsuta Masaharu , Iishi Hiroyasu , Baba Miyako , Taniouchi Haruo 
Published: February 2007

AbstractThe effects of chemical sympathectomy induced by 6‐hydroxydopamine (6‐OHDA) on the enhanced induction of gastric carcinogenesis by N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG) in spontaneously hypertensive rats (SHR), and the norepinephrine (NE) concentrations in their gastric wall and the labeling index of gastric epithelial cells were investigated. SHR rats and normotensive Wistar Kyoto rats (WKY) as controls were given MNNG (25 μ/ml) in their drinking water for 25 weeks and then i.p. injections of 6‐OHDA (42 mg/kg twice within 24 hr, and then 105 mg/kg every 2 weeks from I week later). In control group (WKY rat + NaCI), gastric cancers were found in 2 (11%) of 18 rats examined in week 52. In SHR rats treated with NaCI solution only, the incidence of gastric cancers significantly increased, to 53% compared with that in control WKY rats. Treatment of SHR rats with 6‐OHDA significantly decreased its incidence to 12% compared with the value in SHR rats treated with NaCI solution only. Prolonged administration of 6‐OHDA to SHR rats significantly reduced the NE concentration in the antral portion of the gastric wall and the labeling index of antral epithelial cells. These findings indicate that prolonged i.p. treatment with 6‐OHDA attenuated the normally higher incidence of MNNG‐induced gastric cancer in SHR rats. © 1992 Wiley‐Liss, Inc.
Expression and function of VLA‐α2, ‐α3, ‐α5 and ‐α6‐integrin receptors in pancreatic carcinoma
Authors: Weinel R. J. , Rosendahl A. , Neumann K. , Chaloupka B. , Erb D. , Rothmund M. , Santoso S. 
Published: February 2007

AbstractThe expression of the VLA‐integrins α2, α3, v5 and α6 was studied immunohistochemically in tissue samples from ductal pancreatic cancer, chronic pancreatitis, normal pancreas and in 8 cell lines of ductal human pancreatic cancer. Furthermore, adhesion assays on purified extracellular matrix (ECM)‐compounds were used to define the function of α2, α3, α5 and α6in pancreatic cancer cells. Immunohistochemically, VLA α2 and VLA α6 were moderately to strongly expressed on the basal surface of ductal and acinar cells in normal pancreatic tissue, while centro‐acinar cells predominantly expressed VLA α3 and VLA α5. Pancreatic carcinoma showed intense staining for VLA α2 and VLA α6 with a diffuse distribution on the cell surface. The redistribution of VLA α2 and VLA α6 may reflect a loss of spatial arrangement of tumor cells and their ability to interact randomly with extracellular matrix structures during invasion and metastasis. Expression of VLA α3 and VLA α5 in pancreatic carcinoma was heterogeneous, ranging from moderate to weak, and was lost in about 50% of the cells. Two pancreatic carcinoma cell lines (PC 3, PC 44) were further investigated in adhesion assays. Monoclonal antibodies (MAbs) against α2 (Gl 9, 10‐G‐11) were able to inhibit tumor‐cell adhesion to collagen IV (59%‐72%) in both cell lines. A MAb against α6 (GoH3) inhibited tumor‐cell adhesion to laminin (52%‐86%) in both cell lines. These results suggest that α2 is a collagen‐binding site and α6 a laminin‐binding site in pancreatic cancer cells. The anti‐α5‐MAb SAM I inhibited adhesion of PC3 to fibronectin (76%), being without effect in PC44. Adhesion of both cell lines to fibronectin was almost completely inhibited by RGDS (85%‐88%). Thus, α5is a functionally important fibronectin binding site in some pancreatic carcinoma cells, suggesting further RGD‐dependent fibronectin binding sites in other pancreatic carcinoma cells. © 1992 Wiley‐Liss, Inc.
Cell kinetics evaluation of colorectal tumors after in vivo administration of bromodeoxyuridine
Authors: Roncucci Luca , Pedroni Monica , Scalmati Alessandra , Bormioli Maria Luisa , Sassatelli Romano , Fante Rossella , Losi Lorena , di Gregorio Carmela , Petocchi Benedetta , de Leon Maurizio Ponz 
Published: February 2007

AbstractAlthough several biomarkers have been tested, Dukes' (or TNM) stage at diagnosis is still considered the only prognostic factor of clinical relevance in colorectal cancer. Among the various biomarkers, the fraction of cells engaged in DNA synthesis has been extensively investigated as an indicator of tumor aggressiveness. Bromodeoxyuridine (BUdR) is a non‐radioactive thymidine analogue which is incorporated into DNA during the S‐phase of cycling cells. In order to evaluate the relationships between cell kinetics and morphologic variables, 500 mg of BUdR were given i.v. to 46 patients with colorectal cancer prior to surgery. After operation, a large tumor sample was taken and processed for immunohistochemical detection of BUdR‐labeled cells in various regions of the neoplasm and in normal colorectal mucosa. Smaller superficial tumor specimens were also incubated with 3H‐thymidine (3H‐TdR) for the autoradiographic identification of labeled cells. In the 43 evaluable tumors, the overall BUdR labeling index (BLI, percent of labeled cells) was significantly higher in carcinoma (20.30 ± 0.86%, SEM) than in normal colonic mucosa (6.51 ± 0.49%). BLIs in central and peripheral regions of carcinoma were closely correlated (r = 0.48, p = 0.003). In 21 neoplasms a high correlation between overall BUdR and 3H‐TdR labeling index in the same tumor was observed (r = 0.57, p = 0.007). No evident association between overall BLI and clinical or morphologic parameters of the tumor was seen, including number of capillaries and ras‐p2l protein expression. We conclude that BUdR immunostaining after in vivo administration of BUdR is a simple method for studying cell kinetics in various regions of colorectal cancer. BUdR labeling data are comparable to those obtained with in vitro incorporation of 3H‐TdR. © 1992 Wiley‐Liss, Inc.
Antibody against p58 surface antigen of RA‐2 rat rhabdomyosarcoma cells inhibits their metastatic activity
Authors: Guzhova Irina V. , Margulis Boris A. , Kaminskaya Elena V. 
Published: February 2007

AbstractAntibodies generated against the whole membrane preparation isolated from rhabdomyosarcoma RA‐2 cells were shown by immunoblotting and immunoaffinity chromatography to recognize 58‐kDa polypeptide, p58. The latter was confirmed to be a surface molecule in a test of radioiodination of RA‐2 membrane by lodogen. The antibodies added to a suspension of RA‐2 cells before their inoculation into rats decreased metastatic activity 50‐fold without any noticeable influence on RA‐2 proliferation level and viability. The data indicate that masking of p58 surface antigen by antibodies could make RA‐2 cells unable to form experimental metastases in lung. We suggest that p58 may participate in the specific recognition by RA‐2 of lung endothelial cells. © 1992 Wiley‐Liss, Inc.
VLA‐4 integrin on sarcoma cell lines recognizes endothelial VCAM‐1. Differential regulation of the VLA‐4 avidity on various sarcoma cell lines
Authors: Mattila Pirkko , Majuri Marja‐Leena , Renkonen Risto 
Published: February 2007

AbstractOsteosarcomas and rhabdomyosarcomas are vigorously invading tumors. Before they can extravasate to the parenchymal organs and form metastases, they have to adhere to the endothelial cells lining the blood vessels and then penetrate through the endothelium. We show that several human sarcoma cell lines, osteosarcomas HOS, MG‐63, U2‐OS, and a rhabdomyosarcoma RD, express VLA‐4 molecule on their surface and bind to the VCAM‐1 ‐expressing activated endothelial cell line Ea.hy 926. The increased sarcoma‐cell adhesion could be abolished by treating the sarcoma cells with monoclonal antibodies (MAbs) VLA4 (both α‐ and β‐chain, HP2/1 and 4B4 respectively) or treating endothelial cells with VCAM‐1 antibody (4B9). Furthermore, we show that sarcoma cells adhere to recombinant soluble VCAM‐1 protein. On the other hand, these sarcoma cell lines do not express marked amounts of other ligands (such as CD11/18 or sialyl‐Lex) for other endothelial adhesion molecules (ICAM‐1, ICAM‐2, E‐ and P‐selectin) indicating that the VLA‐4‐VCAM‐1 dependent pathway might be of major importance in sarcoma extravasation. VLA‐4 is not always in an avid form and therefore the expression of VLA‐4 does not directly predict adherence to VCAM‐1. The avidity of VLA‐4 (measured by adherence to soluble VCAM‐1) of MG‐63 and U2‐OS cells could be increased by a 30‐min PMA treatment, whereas the avidity of VLA‐4 on HOS cells increased only after 48 hr of PMA induction. Our results show that sarcoma cell lines (HOS, MG‐63, U2‐OS and RD) adhere to stimulated endothelium via VLA‐4‐VCAM‐1 adhesion molecules and that VLA‐4 avidity on sarcoma cells can be differentially modulated by PMA. © 1992 Wiley‐Liss, Inc.
Protection by muscimol against gastric carcinogenesis induced by N‐methyl‐N′‐nitro‐N‐nitrosoguanidine in spontaneously hypertensive rats
Authors: Tatsuta Masaharu , Iishi Hiroyasu , Baba Miyako , Uehara Hiroyuki , Nakaizumi Akihiko , Taniguchi Haruo 
Published: February 2007

AbstractThe effects of prolonged administration of the gamma‐aminobutyric acid receptor agonist muscimol on enhanced induction of gastric carcinogenesis by N‐methyl‐N′‐nitro‐N‐nitrosoguanid ine (MNNG) in spontaneously hypertensive rats (SHR), and on the norepinephrine concentration in the gastric wall and the labeling index of gastric mucosa were investigated. SHR and normotensive Wistar Kyoto (WKY) rats as controls were given a solution of MNNG (25 fig/ml) for 25 weeks and then i.p. injections of 0.5 mg/kg body weight of muscimol every other day. In control WKY rats, gastric cancers were found in I (7%) of 14 rats examined at week 52. In SHR treated with NaCI solution only, the incidence of gastric cancers was significantly increased to 50% compared with that in control WKY rats. However, treatment of SHR with muscimol significantly increased its incidence to 12% compared with the value in SHR treated with NaCI solution only. The norepinephrine concentration in the gastric wall and the labeling index of the gastric mucosa were significantly greater in SHR than in WKY rats. Prolonged administration of muscimol to SHR significantly reduced the norepinephrine concentration in the antral portion of the gastric wall or the labeling index of the antral epithelial cells. These findings indicate that long‐term treatment of SHR with muscimol attenuated the enhancement of gastric carcinogenesis in SHR. © 1992 Wiley‐Liss, Inc.
Second‐messenger pathways involved in the regulation of survival in germinal‐centre B cells and in burkitt lymphoma lines
Authors: Knox Kirstine A. , Finney Michael , Milner Anne E. , Gregory Christopher D. , Wakelam Michael J. O. , Michell Robert H. , Gordon John 
Published: February 2007

AbstractSpontaneous apoptosis in germinal‐centre (G.C) B cells can be prevented by treatment with anti‐immunoglobulin (Ig). By contrast, susceptible group‐l Burkitt lymphoma (BL) cells can be driven to apoptosis by anti‐lg. The second‐messenger pathways involved in the regulation of apoptosis in GC B lymphocytes and in BL cell lines were studied using pharmacological agonists or inhibitors of intracellular calcium ([Ca2+],) and protein kinase C (PKC). Anti‐lg was found to mobilize Ca2+ in group‐l cells. Pre‐incubation with the Ca2‐ chelator EGTA partially reduced apoptosis induced by anti‐lg or by Ca2+ionophore in group‐l BL cells. Activation of PKC with phorbol ester reduced such Ca2+‐driven programmed cell death (PCD) to control levels of apoptosis. Apoptosis in group‐l BL cell lines could also be triggered by the kinase inhibitors staurosporine and Ro‐31 ‐8220 at concentrations selective for PKC activity. Expression of the bcl‐2 protein in BL group‐l cells following gene transfer affords protection from apoptosis induced by ionomy‐cin or anti‐lg. In the present study, bcl‐2 was additionally found to protect from apoptosis driven by staurosporine. The high levels of spontaneous apoptosis exhibited fay normal GC 6 cells were reduced, but not abrogated, by co‐culture with phorbol ester. These results indicate that, in group‐l BL cells, imbalance in the phosphoinositide pathway of signalling, in favour of [Ca2+], and away from PKC, results in apoptosis: constitutive phosphorylation of key proteins by PKC may therefore suppress apoptosis in BL as well as in GC B cells. © 1992 Wiley‐Liss, Inc.
p53 mutations and aflatoxin B1 exposure in hepatocellular carcinoma patients from thailand
Authors: Hollstein Monica C. , Wild Christopher P. , Bleicher Françoise , Chutimataewin Sopa , Harris Curtis C. , Srivatanakul Andpetcharin , Montesano Ruggero 
Published: February 2007

AbstractThe prevalence and type of mutations in the p53 tumoursuppressor gene have been determined in 15 hepatocellular carcinomas (HCC) originating from Thailand. Direct sequencing of exons 5‐8 revealed 2 mutations, an AGG to AGT (Arg → Ser) transversion at codon 249, and an ATC → AAC (lle → Asn) transversion at codon 254. Samples from the Thai patients were analyzed for the presence of aflatoxin‐liver DNA and aflatoxinserum albumin adducts, and all but one were found negative. All the patients were genotyped for glutathione‐S‐transferase (GST) μ, an enzyme possibly involved in the detoxification of AFB1, and 12 out of 15 had the null genotype. In general, the level of aflatoxin‐albumin adducts in sera and the prevalence of p53 mutation at codon 249 in HCC were lower than in other areas at high risk of HCC, including southern China and parts of Africa.