bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human papillomavirus and cervical neoplasia: A case‐control study in Taiwan
Authors: Liaw Kai‐Li , Hsing Ann W. , Chen Chem‐Jen , Schiffmfman Mark H. , Zhang Tracy Y. , Hsieh Chang‐Yao , Greer Catherine E. , You San‐Lin , Huang Thomas W. , Wu Tzyy‐Choou , O'leary Timothy J. , Seidman Jeffrey D. , Blot William J. , Meinert Curtis L. , Manos M. Michele 
Published: February 2007

AbstractAs part of a large‐scale, community‐based cervical neoplastic screening project in rural Taiwan, a case‐control study was undertaken to evaluate the etiologic role of human papillomavirus (HPV) infection in this mainly monogamous (2% reported having multiple sexual partners) female population. A total of 88 biopsy‐confirmed cases and 261 cytologically normal controls were selected for the study. The case group included 40 cases of cervical intraepithelial neoplasia (CIN) 1, 9 of CIN 2, 36 of CIN 3 and 3 cases of invasive cancer. Cervical swabs collected at screening from study subjects were tested for HPV DNA by an LI consensus primer polymerase chain reaction (PCR)‐based technique. HPV DNA was found in 92% of high‐grade cases (CIN 2‐3 and invasive cancer); 54% of low‐grade cases (CIN I); and 9% of controls. HPV was significantly associated with both high‐grade and low‐grade cervical neoplasia. As reported in Western countries, HPV 16 was the predominant type among HPV‐positive high‐grade cases. However, HPVs 52 and/or 58 combined were the most common types among HPV‐positive low‐grade cases and controls. Among women without any high‐risk HPV infection (types 16, 18, 31 or 45), those with multiple‐type HPV infection had a higher risk for high‐grade cervical neoplasia than those with single‐type infection. Overall, 91% of high‐grade cases and 50% of low‐grade cases could be attributed to HPV infection. Our results show that, even in this monogamous population, HPV is the major risk factor for high‐grade cervical neoplasia. © 1995 Wiley‐Liss, Inc.
Sequence‐dependent antitumor activity of paclitaxel (taxol) and cisplatin in vivo
Authors: Milross Christopher G. , Peters Lester J. , Hunter Nancy R. , Mason Kathy A. , Milas Luka 
Published: February 2007

AbstractThe established antitumor efficacy of paclitaxel and cisplatin as single agents and their distinctly different mechanisms of action have prompted laboratory and clinical research into their use in combination. Our in vivo study was performed to investigate the importance of sequence of administration and inter‐agent interval. C3Hf/Kam mice bearing OCa‐1 tumors received paclitaxel and cisplatin. The antitumor efficacy of the combination, measured as re‐growth delay and expressed as the enhancement factor (EF), was determined for inter‐agent intervals of I, 9, 24, 48 and 72 hr. Morphometric analysis was used to determine the contribution of induced apoptosis. Our findings showed an additive effect when cisplatin preceded paclitaxel by 1 and 24 hr, producing EF of 1.1 and 1.0, respectively, and a greater than additive effect for 9 and 48 hr, producing EF of 1.3 and 1.8, respectively. This sequence, however, was associated with significant morbidity and mortality. When paclitaxel preceded cisplatin the effect was greater than additive with the EF for I, 9 and 24 hr, being 1.2, 1.5 and 1.5, respectively, and increasing to a maximum of 1.9 at 48 hr. Thus, for this combination, the therapeutic ratio was improved when paclitaxel preceded cisplatin and was greatest when a 48 hr interval was allowed between drugs. We were unable to attribute the efficacy of the drug combination to increased induction of apoptosis and suggest other possible mechanisms. © 1995 Wiley‐Liss, Inc.
Cloning of the gene encoding TROP‐2, a cell‐surface glycoprotein expressed by human carcinomas
Authors: Fornaro Mara , Arciprete Roberta Dell' , Stella Manuela , Bucci Cecilia , Nutini Michele , Capri Maria Grazia , Alberti Saverio 
Published: February 2007

AbstractWe have cloned by expression the cDNA encoding Trop‐2, a cell‐surface glycoprotein expressed by most human carcinomas. Formal proof of the identity of the clone is the hybridization to DNA and RNA from genomic TROP2 transfectants. TROP2 is a single‐copy gene in human cells, hybridizes to a single 1.8‐kb mRNA from expressing sources and encodes a 35,709 Da type‐1 transmembrane protein with a single transmembrane domain. TROP2 is essentially identical to GA733‐1. Thus, we have proven that GA733‐1, for which a protein product had not been identified, is a functional gene. TROP2 is also homologous to TROPI/KSA/GA733‐2, confirming the serological similarities between the 2 molecules. The homology between the Trop‐1 and Trop‐2 peptides is clustered in 2 extracytoplasmic domains and in the transmembrane/cytoplasmic region. Twelve cysteines and a potential cytoplasmic tyrosine phosphorylation site are also conserved. Trop‐1 and Trop‐2 are homologous to serum IGF‐11‐binding proteins and appear as signal transducers. Thus, they likely represent novel cell‐surface receptors and may play a role in regulating the growth of carcinoma cells. On the other hand, we have found no evidence for a role of Trop‐2 and Trop‐1 as homophilic adhesion molecules. © 1995 Wiley‐Liss, Inc.
Butyrate regulates gene expression of the plasminogen activating system in colon cancer cells
Authors: Antalis Toni M. , Reeder Jennifer A. 
Published: February 2007

AbstractButyrate is a potent differentiating agent present in high concentrations in colonic lumen as a result of metabolic breakdown of dietaiy fibre and, as such, may directly influence colonic cancer progression. We have investigated the effects of butyrate on an enzyme system important in colonic tumour progression, the plasminogen‐activating system, in a poorly differentiated colon cancer cell. Butyrate was found to induce a rapid and transient increase in plasminogen activator inhibitor type 1 (PA1‐1) mRNA while concomitantly suppressing the constitutive production of both urokinase‐type plasminogen activator (uPA) and uPA receptor (uPAR) mRNA transcripts. We have investigated the mechanisms involved in mediating these effects by run‐on transcription and RNA stability analyses. Our data show that PA1‐1 mRNA induction occurs through both regulation of the stability of the alternately spliced 3.3 kb PA1‐1 mRNA transcript and induction of the 2.4 kb PA1‐1 mRNA transcript. Studies using modulators of signal transduction pathways demonstrate that induction of PA1‐1 mRNA synthesis is independent of protein kinase C but dependent on the activation of protein kinase A. Suppression of uPA mRNA by butyrate was found to occur by down‐regulation of gene transcription through a process independent of de novo protein synthesis. The transcription rate of the uPAR gene was not modulated by butyrate, but rapid turnover of the uPAR gene by butyrate was dependent on ongoing protein synthesis. Our results demonstrate that butyrate can effect rapid changes in the expression of genes of the plasminogen‐activating system through several different mechanisms in a gene‐specific manner. © 1995 Wiley‐Liss, Inc.
Anti‐tumor efficacy of an anti‐epidermal‐growth‐factor‐ receptor monoclonal antibody and its F(ab′)2 fragment against high‐ and low‐egfr‐expressing carcinomas in nude mice
Authors: Tosi Emanuela , Valota Olga , Negri Donatella R. M. , Adobati Elena , Mazzoni Alessandra , Meazza Raffaella , Ferrini Silvano , Colnaghi Maria I. , Canevari Silvana 
Published: February 2007

AbstractMonoclonal antibody (MAb) MINTS specifically detects the epidermal‐growth‐factor receptor (EGFR). In vitro analyses of intact MINTS (IgG,) and its F(ab′)2 fragment indicated that both forms of the MAb inhibited binding of ′25l‐mEGF to EGFR, induced receptor internalization and blocked EGF‐induced EGFR tyrosine‐kinase activation in A431 cells. Both forms of the MAb also inhibited to the same extent the proliferation of the carcinoma cell lines A431 and IGROVI, despite the difference in EGFR levels on the cells. The detection of TGFα mRNA and the inhibition of cell growth in EGF‐free conditions by anti‐EGFR MAb indicated the involvement of an EGFR/TGFα autocrine/ paracrine pathway in the in vitro growth of both cell lines. Analysis of mice xenotransplanted s.c. with A43I cells and treated with MINTS revealed a block in A431 tumor take in 6 of 10 animals when intact MAb was administered from day 0 to day 11. On a molar basis, F(ab)2 at the same dose was ineffective, although at a 7‐fold higher dose F(ab′)2 reduced s.c. tumor growth by 80%. At the same dose, intact MINTS MAb reduced s.c. growth of the EGFR‐negative MeWo cell line by 5%. Survival of mice bearing IGROV I i.p. xenotransplants and treated locally with either form of MAb was significantly prolonged even when treatment was initiated on day 3. Corrected doses of intact and F(ab′)2 fragment, which accounted for the difference in serum half‐lives of the MAb forms, resulted in similar survival rates in the tumor‐bearing mice. These pre‐clinical results suggest that MINTS MAb might be safely used for systemic therapy of EGFR‐over‐expressing tumors. Loco‐regional therapy might be contemplated in the case of tumors with moderate/low EGFR expression. © 1995 Wiley‐Liss, Inc.
Detection of an epstein‐barr‐virus variant in T‐cell‐lymphoma tissues identical to the distinct strain observed in nasopharyngeal carcinoma in the taiwanese population
Authors: Chang Yu‐Sun , Su Ih‐Jen , Chung Pei‐Jung , Shu Chih‐Hung , Ng Cheng‐Koon , Wu Shao‐Jung , Liu Shih‐Tung 
Published: February 2007

AbstractAn EBV variant has been identified in NPC tissues in Taiwan. This EBV variant contains a point mutation in exon I of the LMP I gene. This mutation results in the loss of an Xhol site at nt 169,426, which is present in strain B9S‐8. In addition, this variant contains a 30‐bp deletion in exon 3 of the gene. The recent demonstration of the prevalence of EBV‐containing nasal and peripheral T‐cell lymphoma in this region drove us to evaluate the presence of this NPC‐EBV strain in 7 cases of T‐cell lymphoma, as well as in 48 NPC tissues, 2 cases of Hodgkin's disease and I B‐cell lymphoma. Four samples of normal lymph‐ node tissue, 40 of normal nasopharynx tissue and 78 throat washings of healthy individuals were included for comparison. We used sequence‐specific primers and the polymerase chain reaction (PCR) method to amplify LMP I gene fragments containing these variations. Mutations were then confirmed by restriction‐enzyme digestion and the DNA sequencing analysis. Our results showed that 57 of 58 tumor‐tissues samples were EBV‐positive. Among them, 56, including 6 T‐cell‐lymphoma samples, belonged to the NPC strain. This strain of EBV was also present in 92% of EBV‐positive normal nasopharynx tissues and in 84% of EBV‐positive throat washings of the healthy individuals tested. These results suggest that the NPC‐EBV strain is prominently present in Taiwan. © 1995 Wiley‐Liss, Inc.
Interleukin‐6 inhibits the potent stimulatory action of androgens, glucocorticoids and interleukin‐1α on apolipoprotein D and GCDFP‐15 expression in human breast cancer cells
Authors: Blais Yves , Sugimoto Keiko , Carrière Marie‐Claude , Haagensen Darrow E. , Labrie Fernand , Simard Jacques 
Published: February 2007

AbstractOur study was designed to investigate the potential interaction between steroid hormones and interleukin‐6 (IL‐6) in the regulation of apolipoprotein D (apo‐D) and gross cystic disease fluid protein 15 (GCDFP‐15) expression in ZR‐75‐1 human breast cancer cells. We first observed that exposure to IL‐6 for 6–14 days decreased basal apo‐D and GCDFP‐15 secretion by 50% and 23%, respectively. In the same experiment, such treatment with IL‐6 decreased cell proliferation by approximately 40% after 6 and 14 days of incubation. Exposure to IL‐6 markedly decreased dihydrotestosterone (DHT)‐induced apo‐D and GCDFP‐15 release, with a half‐maximal effect measured at 13 U/ml. A similar inhibitory action of IL‐6 was observed on the glucocorticoid dexamethasone (DEX)‐induced apo‐D and GCDFP‐15 secretion. The sensitivity of the apo‐D and GCDFP‐15 response to the stimulatory action of DHT or DEX was, however, not changed by concomitant exposure to IL‐6. The inhibitory effect of IL‐6 on the secretion of these two biochemical markers was additive to that of 17β‐estradiol. In addition, IL‐6 blocked the stimulatory effect of interleukin‐1α (IL‐1α) on apo‐D and GCDFP‐15 secretion. Our results show that IL‐6 is a potent inhibitor of basal as well as androgen‐, glucocorticoid‐ and IL‐1α‐induced apo‐D and GCDFP‐15 secretion in ZR‐75‐1 human breast cancer cells, while cell proliferation is inhibited by this cytokine. © 1995 Wiley‐Liss, Inc.
Modulation of heparan‐sulphate/chondroitin‐sulphate ratio by glycosaminoglycan biosynthesis inhibitors affects liver metastatic potential of tumor cells
Authors: Tímár József , Diczházi Csaba , Bartha Irén , Pogány Gábor , Paku SÁNdor , Rásó Erzsébet , Tóvári József , Ladányi Andrea , Lapis Károly , Kopper László , Jeney András 
Published: February 2007

AbstractPrevious data have indicated that the proteoglycan (PG) pattern is different on tumor cells with different liver metastatic potential. We selected “conventional” glycosaminoglycan (GAG) biosynthesis inhibitors, β T‐D‐xyloside (BX), 2‐deoxy‐D‐glucose (2‐DG), ethane‐1‐hydroxy‐1, 1‐diphosphonate (ETDP) and the newly discovered 5‐hexyl‐2‐deoxyuridine (HUdR), to modulate PGs on highly metastatic/liver‐specific 3LL‐HH murine carcinoma and HT168 human melanoma cells and to influence their liver colonization potential. These compounds all induced remarkable changes in GAG biosynthesis, but to varying degrees: glucosamine labelling was affected mainly by 2‐DG, and HUdR and sulphation by BX and HUdR. Furthermore, the ratio of he paran sulphate/chondroitin sulphate (HS/CS) of PGs was increased by ETDP and decreased after treatment by HUdR. In addition to changes in PG metabolism, tumor‐cell proliferation and adhesion to fibronectin were affected; BX and 2‐DG stimulated cell proliferation and adhesion, while HUdR inhibited both proliferation and adhesion. Most interestingly, HUdR, the most effective inhibitor of HS/HSPG, depressed the formation of liver colonies, while ETDP, the most effective inhibitor of CS/CSPG, stimulated the appearance of liver colonies. These observations indicated that, at least in these experimental systems, tumor cells with a high HS/CS ratio are more likely to form liver metastases; consequently, anti‐HS agents could also be anti‐metastatic. © 1995 Wiley‐Liss, Inc.
Amphiregulin anti‐sense oligodeoxynucleotides inhibit growth and transformation of a human colon carcinoma cell line
Authors: Normanno Nicola , Selvam Mouna P. , Bianco Caterina , Damiano Vincenzo , de Angelis Ernesto , Grassi Michele , Magliulo Gabriella , Tortora Giampaolo , Salomon David S. , Ciardiello Fortunato 
Published: February 2007

AbstractAmphiregulin (AR) is a secreted heparin‐binding growth factor that is structurally and functionally related to epidermal growth factor (EGF) and transforming growth factor a (TGFα). GEO cells are from a human colon cancer cell line that expresses high levels of AR protein and mRNA. To assess the role of AR in colon‐cancer cell proliferation and transformation, 2 different anti‐sense 20‐mer phosphorothioate oligodeoxy‐nucleotides (AR AS‐1 and AR AS‐2 S‐oligos) complementary to the 5′ sequence of AR mRNA were synthesized. Both AR AS S‐oligos were able to inhibit the anchorage‐dependent growth (ADG) of GEO cells. The 2 AR AS S‐oligos were equipotent when used in equimolar concentrations. In particular, a 40% growth inhibition was observed at a concentration of 10 μM, while a mis‐sense S‐oligo used as control had no effect on GEO cell growth. The AR AS‐1 S‐oligo used at the same concentration also inhibited by 40% the 3H‐thymidine incorporation by DNA of GEO cells. The anchorage‐independent growth (AIG) of GEO cells was even more significantly affected by AR AS S‐oligo treatment. In fact, up to 80% inhibition of the AIG of GEO cells was observed when cells were treated with 10 μM of both AR AS S‐oligos. Finally, the AR AS S‐oligos were able to specifically inhibit AR protein expression in GEO cells, as assessed by immunocytochemistry. These data suggest that AR is involved in colon‐cancer cell transformation, and that AR may represent a suitable target for gene therapy in human colon carcinomas. © 1995 Wiley‐Liss, Inc.
Paradoxical effects of bleomycin and heavy water (D2O) in mice
Authors: Gaeng Dominique P. , Geiser Marianne , Cruz‐Orive Luis‐Manuel , Larsen Soren E. , Schaffner Thomas , Laissue Jean A. , Altermatt Hans J. 
Published: February 2007

AbstractBleomycin (BLM) lacks many side effects of other cytostatic drugs. Pulmonary toxicity is the major dose‐limiting effect of BLM. This is based in part on generation of free radicals. It is conceivable that deuterium in body fluids lessens the production of free radicals, thus preventing or diminishing the morphologic expression of pulmonary BLM toxicity. We therefore studied the effect of moderate deuteration of body fluids on BLM‐induced lung damage in BALB/c‐mice. In addition to conventional histopathological methods, we used a vertical sectioning design for stereological estimation of pulmonary volumes and surface areas. BLM (low/medium/high dose: 25/50/75 IU/kg body weight) was injected i.p. once a week for 6 weeks. Half the mice drank deuterated water before, during and after BLM treatment. Three weeks after the last injection, the lungs were fixed by airway instillation. Deuterated animals treated with BLM lacked signs of irreversible BLM‐induced pulmonary damage. Conversely, focal sub‐pleural fibrosis and fibrosing alveolitis were present in BLM‐treated mice drinking tap water. Deuterated mice had stereological values for almost all lung parameters that were lower than in non‐deuterated mice. The organ‐specific advantage of deuteration was offset by marked enhancement of systemic toxicity of BLM. We conclude that (I) moderate concentrations of deuterium may prevent the development of fibrosing alveolitis in BLM‐treated mice, possibly by reducing proliferation of alveolar fibroblasts, and, less probably, by impairing generation or enhancing capture of free radicals; (2) the toxicity of BLM was enhanced by ingestion of deuterium, resulting in morphological liver alterations and increased mortality. © 1995 Wiley‐Liss, Inc.
Irradiation induces Up‐regulation of E9 protein (CD105) in human vascular endothelial cells
Authors: Wang Ji‐Min , Kumar Shant , Van Agthoven Andre , Kumar Pat , Pye David , Hunter Robin D. 
Published: February 2007

AbstractThe use of MAb E‐9 raised against tissue‐cultured endothelial cells (EC) has shown marked heterogeneity in vascular EC lining the blood vessels of normal and tumour tissues. MAb E‐9 is human EC‐specific and the protein recognized by it is a homodimer with a molecular mass of 97 kDa. The E‐9 protein is resistant to treatment by 3 mM sodium periodate, but is sensitive to 10% trichloroacetic acid and 70% ethanol. E‐9 protein has been assigned to a new cluster, CD 105, and mapped to human chromosome 9q3. It has approximately 70% homology with type‐III cell‐surface receptor for transforming growth factor beta (TGF‐β). Recently CD 105 has been reported to be the gene in patients with hereditary haemorrhagic telangiecta‐sia. We have examined the effects of radiation on its expression in normal human umbilical‐vein endothelial cells (HUVEC) and brain‐tumour‐derived endothelial cells (BTEC). Irradiation induced dose‐and time‐dependent up‐regulation in the expression of the E‐9 protein on the plasma membranes of EC, and also resulted in greater increase in the expression of the E‐9 protein in semi‐confluent (proliferating) as compared with confluent (non‐proliferating) EC. It may well be that, following radio‐therapy in cancer patients, E‐9 protein is also up‐regulated. The presence of increased amounts of E‐9 protein in EC makes it an attractive target in the control of angiogenesis, especially after radiotherapy in cancer patients. The time scale involved in the up‐regulation of E‐9 protein following irradiation has led us to suggest that it may be a secondary event, the primary being the production and release of mitogenic factors (such as basic fibroblast growth factor) from irradiated EC. © 1995 Wiley‐Liss, Inc.
Cancer in the european population of harare, Zimbabwe, 1990–1992
Authors: Bassett M. T. , Levy L. , Chokunonga E. , Mauchaza B. , Ferlay J. , Parkin D. M. 
Published: February 2007

AbstractThe data presented from the population‐based cancer registry in Harare, Zimbabwe, represent the first information on the incidence of cancer in a population of European origin living in Southern Africa for over 30 years. Their cancer pattern is more or less typical of white populations of high socio‐economic status living in Europe or North America, with elevated incidence rates of breast cancer, large‐bowel cancer and, in women, lung cancer. However, there are also several unusual features, with extremely high incidence rates of skin cancers, including melanomas, and higher rates of liver and bladder cancer than normally seen in white populations.
Cancer in the african population of harare, Zimbabwe, 1990–1992
Authors: Bassett M. T. , Chokunonga E. , Mauchaza B. , Levy L. , Ferlay J. , Parkin D. M. 
Published: February 2007

AbstractThe data presented from the population‐based cancer registry in Harare, Zimbabwe, represent the first information on the incidence of cancer in Southern Africa for almost 20 years. In the African population in Zimbabwe there are several features in common with other countries in sub‐Saharan Africa: high rates of liver, prostate and cervix cancer, low rates of large‐bowel cancer and breast cancer. Also, as reported from southern and south‐eastern Africa, there are relatively high incidence rates of cancers of the oesophagus, bladder and (in men) lung. The AIDS epidemic has given rise to a striking increase in incidence of Kaposi's sarcoma (now the commonest cancer of African men), but there is not much evidence for an increase in incidence of non‐Hodgkin lymphomas nor, although rates are very high, of cervical cancer.
Association of herpesvirus infection with the development of genital cancer
Authors: Koffa Maria , Koumantakis Eugenios , Ergazaki Maria , Tsatsanis Christos , Spandidos Demetrios A. 
Published: February 2007

AbstractClinical observations and epidemiological studies on genital cancer have revealed an association with sexual behavior, thus motivating research into sexually transmitted agents which may be responsible for the neoplasia. In this study, we used the PCR technique to examine the presence of CMV, HSV and EBV viruses in 187 cases of human genital lesions and found that infection with CMV or HSV was associated with cervical cancer. When we stratified according to HPV status this association was found only for HPV‐DNA‐negative cases. These findings indicate that past infection with CMV or HSV could be interpreted as a surrogate marker of HPV infection. However, these viruses may play an important role themselves in cervical cancer.