bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoclonal antibody UJ13A recognizes the neural cell adhesion molecule (NCAM)
Authors: Patel K. , Rossell R. J. , Bourne S. , Moore S. E. , Walsh F. S. , Kemshead J. T. 
Published: February 2007

AbstractMonoclonal antibody (MAb) UJ13A, raised against 16‐week‐old human foetal brain, recognizes an antigen present on the majority of tissues of neuro‐ectodermal origin. The binding profile of this antibody is similar to the known distribution of the neural cell adhesion molecule (NCAM). Although detailed immunohistological and immuno‐cytochemical studies with the MAb have been published previously, we demonstrate here, through investigations of selected tissues and cell lines, that the binding profile of an anti‐NCAM antiserum is similar to UJ13A. Additional indirect evidence suggesting that UJ13A recognizes NCAM comes from Northern blot analysis of cell lines either binding or not binding UJ13A as determined by indirect immunofluorescence. Only those cell lines known to bind UJ13A express high levels of NCAM mRNA. Western blot analysis of extracts of human brain show that U J13A recognizes proteins of 180 and 140 kDa in addition to a very weak band of 120 kDa. This data corroborates the suggestion that UJ 13A recognizes NCAM as these 3 isoforms of the protein are identified in human brain. Final confirmation of the specificity of UJ 13A comes from the study of 3T3 fibroblasts transfected with a cDNA coding for the 125 kDa isoform of human muscle NCAM. UJ 13A selectively recognizes these transfectants and binds to a 125 kDa protein isolated from the cells by Western blot analysis. Thus we conclude from these immunological, biochemical and molecular studies that the antigen recognized by the UJ 13A MAb is the neural cell adhesion molecule.
Influence of cyclosporin a and α‐difluoromethylornithine, an inhibitor of polyamine biosynthesis, on two rodent T‐cell cancers in vivo
Authors: Smart L. M. , Maclachlan G. , Wallace H. M. , Thomson A. W. 
Published: February 2007

AbstractWe have examined the influence of cyclosporin A (CsA), administered together with the polyamine antimetabolite, a‐difluoromethylornithine (DFMO), on growth of the Roser acute T‐cell leukaemia in PVG rats and on growth of the EL4 lymphoma in C57BL/6 mice. CsA or DFMO alone, administered from the time of tumour injection, markedly reduced numbers of circulating lymphoblasts in leukaemic rats, although survival was prolonged only in those animals given DFMO. Drug combination further reduced blood‐borne tumour cells, but had no additional effects on tumour growth within organs or on host survival, compared to that achieved with DFMO treatment alone. Neither CsA nor DFMO, administered from the time of tumour‐cell injection, nor both drugs in combination, affected peritoneal growth of the EL4 lymphoma or organ infiltration. Host survival was prolonged by DFMO. As anticipated, DFMO inhibited polyamine synthesis in vivo, but the observed anti‐tumour effect of CsA was not accompanied by an alteration in polyamine biosynthesis. By reducing polyamine synthesis, however, DFMO may enhance the vulnerability of those malignant T cells which are susceptible to the as yet unexplained selective inhibitory action of CsA in vivo.
Increased drug cytotoxicity at reduced pH counteracts cyclophosphamide resistance in cultured rat mammary carcinoma cells
Authors: Jähde Fckhard , Geüsenkamp Karl‐Heinz , Rajewsky Manfred F. 
Published: February 2007

AbstractThe sensitivity of a cyclophosphamide (CP)‐resistant MIR rat mammary carcinoma cell variant (MIRCPr) in monolayer culture towards the cytotoxic effect of mafosfamide (an analogue of “activated” CP) was measured as a function of extracellular pH (pHe). An inverse correlation was found between cell survival and the H+ ion concentration in the culture medium. At pHe 7.4, the fraction of clonogenic MIRCPrcells exposed to mafosfamide (7.S üg/ml) for 24 hr was 1 ± 10−1 in relation to untreated control cells. At pHe6.2, however, this value was reduced to 3 ± 10−4, i.e., a value equal to that for the CP‐sensitive parental MIR cells exposed to the same concentration of mafosfamide at pHe 7.4. Our data indicate complete compensation of CP resistance in MIRCPrcells at pHe 6.2. MIRCPr cells were not resistant to the cytotoxic effect of nornitrogen mustard. This suggests that resistance to CP in MIRCPr cells is due to enzymatic inactivation of the primary intermediates in CP bioactivation. The alkylating activity of nornitrogen mustard (and less so that of phosphoramide mustard) is strongly enhanced at low pH. In MIRCPr cells shifted to an acidic environment, therefore, a (putative) decrease in the intracellular concentration of alkylating CP metabolites may be counteracted by an enhancement of their alkylating activity (on a molar basis). By parenteral administration of glucose, the pH in malignant tumors of both animal and human origin can be lowered to values between 5.6‐6.6. Our data suggest that an upshift of H+ ion concentration in malignant tissues may at least partially counteract CP resistance in cancer cells in vivo.
Effects of disseminative route on the liver‐ and lung‐colonizing efficiencies of B16 melanoma and colon‐26 carcinoma in mice
Authors: Weiss L. , Ward P. M. 
Published: February 2007

AbstractTumor‐colony formation in the liver and lungs of mice was assessed, after delivery of equal numbers of B16 melanoma or colon‐26 carcinoma cells via the portal vein or the hepatic artery, and via the pulmonary artery or the bronchial artery. Significantly greater lung involvement occurred after delivery of both cell types Wa the bronchial artery than via the pulmonary artery. In the case of colon‐26 cells, liver colonization via the hepatic artery was more efficient than via the portal vein. In the case of B16 cells, no route‐dependent differences in liver colonization were detected. Our results indicate that during hematogenous metastasis, the vascular route taken by some cancer cells to the same target organ may considerably modify the efficiency with which they form metastases.
Anti‐tumor effects of interleukin‐2 and interleukin‐1 in mice transplanted with different syngeneic tumors
Authors: Belardelli F. , Ciolli V. , Testa U. , Montesoro E. , Bulgarinl D. , Proietti E. , Borghi P. , Sestili P. , Locardi C. , Peschle C. , Gresser I. 
Published: February 2007

AbstractWe have studied the anti‐tumor effects of human recombinant IL‐2, alone or in association with LAK cells, in mice transplanted subcutaneously (s.c.) with the following syngeneic tumors: highly metastatic Friend leukemia cells (FLC), non‐metastatic FLC, lymphoma RBL‐S cells and HeJ16 fibrosarcoma cells. In these tumor models, peri‐tumoral injections of IL‐2 were more effective in inhibiting tumor growth than a systemic treatment. Although s.c. IL‐2 treatment resulted in marked inhibition of tumor growth in mice injected s.c. with highly metastatic FLC, it was not effective in inhibiting growth of FLC in the liver and spleen. IL‐2 therapy was more effective at increasing survival time in mice transplanted with non‐metastatic FLC or with RBL‐5 cells. In mice transplanted wth HeJ16 fibrosarcomas, s.c. IL‐2 treatment resulted in highly significant anti‐tumor effect and survival of 70% of tumor‐injected mice. No general correlation was found between in vitro sensitivity or resistance to the cytolytic activity of LAK cells and the anti‐tumor effects observed in vivo. Subcutaneous injection of IL‐1β in mice transplanted with highly metastatic FLC resulted in a marked increase in survival time and inhibition of metastatic tumor growth in liver and spleen. Combined treatment of IL‐1β and IL‐2 produced a synergistic anti‐tumor effect: 60% of mice injected with highly metastatic FLC survived. Combined IL‐1/IL‐2 treatments exerted no anti‐tumor activity either in DBA/2 mice injected with antibody to Thy 1.2 antigen or in nude mice, indicating that T cells play important roles during IL‐1/IL‐2 therapy. In vitro treatment of FLC with IL‐1β resulted in a slight inhibition of cell multiplication, whereas even high doses of IL‐2 did not affect FLC multiplication. Our results indicate that local combined treatments with IL‐1 and IL‐2 can induce potent, host‐dependent (T cell‐mediated) anti‐tumor effects against highly malignant tumors.
Cytogenetic analysis of eight human papillomavirus immortalized human keratinocyte cell lines
Authors: Smith Patricia P. , Bryant Eileen M. , Kaur Pritinder , McDougall James K. 
Published: February 2007

AbstractCytogenetic analysis was performed on human papillomavirus (HPV)‐immortalized cell lines. Lines were established by co‐transfection of primary human keratinocyte cells with HPV type 16 or 18 DNA and pSV2neo. The resulting clonal lines contained integrated HPV DNA and exhibited extended life spans in culture but were non‐tumorigenic in nude mice. Two HPV16‐immortaiized lines (FEPEIL8 and FEPEIL9) and 4 HPV18‐immortalized lines (FEA, FEH18L, FEP18‐5 and FEP18‐11) were established. Two additional lines were derived by subsequent treatment of the FEA line with TPA and by further transfection with HSVII DNA. Cytogenetic analysis revealed that all lines were abnormal, containing a variety of numerical and structural aberrations. Six of the 8 lines were hyper‐triploid and 2 were near‐diploid. Examination of lines FEA, FEH18L and FEP18‐II at multiple passages in culture revealed that the lines were clonal and chromosomally stable over extended passage in culture. Structural rearrangements were most common in chromosomes 1 and 3 but also occurred in chromosomes 5, 7, 8, 12, 16 and 22. Marker chromosomes were present in all cell lines. A small metacentric marker, possibly an isochromosome for the short arm of chromosome 5, was consistently present in the FEA line and its derivatives (FEAB10 and FEAT) as well as the FEH 18L line. A loss or reduction in copy number of chromosome 13 was seen in 5 of the 8 cell lines.
Use of monoclonal antibodies to human breast‐tumor‐associated antigens in the diagnosis of fine‐needle aspirates of breast nodules: Results of a multicenter study
Authors: Natali P. G. , Mottolese M. , Perrone Donnorso R. , Buffa R. , Bussolati G. , Coggi G. , Corradi G. , Coscia‐Porrazzi L. , Ferretti M. , Rondanelli E. , Castagna M. , Vecchione A. , Siccardi G. A. 
Published: February 2007

AbstractFine‐needle aspiration (FNA) cytology is being increasingly employed in conjunction with physical examination and mammography in the pre‐surgical diagnosis of breast nodules. In the present study, we have submitted to multicenter validation an immunocytochemical test which employs monoclonal antibodies (MAbs) to breast‐tumor‐associated antigens (BTAA) for the diagnosis of breast cancer. The results of this analysis, which has evaluated 846 FNAs, show that the immunological test has a sensitivity of 88.62%, a specificity of 97.9% and an accuracy of 92.4%. The predictive value of a positive and a negative finding were 98.4% and 85.57% respectively. Comparison between the cytological and immunocytochemical diagnosis displayed a higher sensitivity, accuracy and predictive value of a negative result with the latter method (p <0.01). Our findings clearly indicate that immunocytochemical methods can complement and improve the diagnostic accuracy of FNA cytology of breast nodules.
Frequency and degree of aneuploidy in benign and malignant thyroid neoplasms
Authors: Schelfhout Lodewijk J. D. M. , Cornelisse Cees J. , Goslings Bernard M. , Hamming Jacob F. , Kuipers‐Dijkshoorn Nel J. , van de Velde Cornelis J. H. , Fleuren Gert Jan 
Published: February 2007

AbstractThe frequency and degree of aneuploidy in 44 benign and 124 malignant thyroid neoplasms were analyzed by DNA flow cytometry. Single aneuploid cell populations were found in 72% of the undifferentiated carcinomas, 64% of the follicular carcinomas, 24% of the papillary carcinomas and in 24% of the follicular adenomas. Multiple aneuploid cell populations were detected in 4% of the papillary and in 36% of the follicular carcinomas but not in undifferentiated carcinomas. A low degree of aneuploidy was found in well differentiated papillary carcinomas (mean DNA index of aneuploid populations; DI =1.17; SD ± 0.09). Significantly higher values were found for aneuploid moderately differentiated papillary carcinomas (DI =1.46; SD ± 0.29), well and moderately differentiated follicular carcinomas (DI =1.61; SD ± 0.33 and DI =1.60; SD ± 0.30, respectively) and undifferentiated carcinomas (DI =1.72; SD ± 0.19). High DNA indices were also found in several follicular adenomas (DI =1.49; SD ± 0.22). Comparison of the 10‐year survival rates of patients with moderately versus well differentiated papillary carcinoma (79 vs. 98 months, respectively) indicates that loss of differentiation and progression of aneuploidy in this tumour type is associated with more aggressive clinical behaviour. Similarly, the high frequency and degree of aneuploidy in undifferentiated carcinomas is in agreement with the very poor survival rate (0% at 10 years) in this group of patients. However, the occurrence of highly aneuploid adenomas and (near)‐diploid undifferentiated carcinomas does not point to a direct causal relationship between DNA‐ploidy changes and clinical behaviour of these thyroid tumours.
Human papillomavirus (HPV) DNA in esophageal precancer lesions and squamous cell carcinomas from China
Authors: Chang Fuju , Syrjänen S. , Shen Qiong , Ji Hongxiu , Syrjänen K. 
Published: February 2007

AbstractA series of 51 biopsies derived from the same number of patients with established invasive squamous‐cell carcinoma of the esophagus in Linxian, a high‐risk area for esophageal cancer in China, were analyzed histologically and by in situ DNA hybridization to demonstrate human papillomavirus (HPV) infection. Epithelial changes suggesting HPV infection within or adjacent to the carcinoma lesions were found in 25 cases (49.0%). Esophageal lesions with HPV morphology showed both flat (25 cases) and inverted condylomas (2 cases) resembling those found in the genital tract. HPV 6, 11, 16 or 18 DNA sequences were detected in 22/51 (43.1%) of the esophageal specimens. HPV DNA was most frequently localized in epithelium adjacent to carcinomas in areas showing either epithelial hyperplasia (36.1%) or dysplasia (22.2%). Of the lesions with morphological HPV changes, 64% (16/22) were shown to contain HPV DNA. In 2 specimens, HPV DNA was found in frankly malignant cells. High‐risk types HPV 16 and/or 18 DNA sequences were found in 16 of the 22 HPV DNA‐positive cases (72.7%). Our results confirm previously reported HPV involvement in esophageal squamous‐cell lesions, and support the hypothesis of HPV as a possible etiological agent in esophageal carcinogenesis.
Lack of benefit from semi‐annual screening for cancer of the lung: Follow‐up report of a randomized controlled trial on a population of high‐risk males in czechoslovakia
Authors: Kubik A. , Parkin D. M. , Khlat M. , Erban J. , Polak J. , Adamec M. 
Published: February 2007

AbstractCigarette‐smoking males (6,364), aged 40–64, were randomized into an intervention group which received 6‐monthly screening by chest X‐ray and sputum cytology, and a control group which received no asymptomatic investigation. After 3 years, both groups entered a follow‐up period during which they received annual chest X‐rays. Lung cancer cases detected by screening were identified at an earlier stage, more often resectable, and had a significantly better survival than “interval” cases diagnosed mainly because of symptoms. Comparison of the 2 groups showed a higher incidence of lung cancer in the intervention group, despite the follow‐up period when both groups received annual examinations. There was no significant difference in mortality between the 2 groups.
Prognostic significance of dna‐ploidy in a series of 690 primary breast cancer patients
Authors: Beerman H. , Kluin Ph. M. , Hermans J. , Van de Velde C. J. H. , Cornelisse C. J. 
Published: February 2007

AbstractFlow cytometric DNA‐ploidy measurements were performed on paraffin‐embedded and fresh tumor specimens from 690 patients with Stage I‐III breast cancer. The conventional classification of DNA‐ploidy (diploid versus aneuploid) was compared with a division of tumor ploidy into 5 classes based on DNA index (DI) range. The DI‐classification showed a better correlation with tumor size and TNM stage than the conventional classification. Aneuploidy was associated with an impaired survival and distant relapse‐free survival (p =0.02) but the DI‐classification improved the discrimination between different prognostic groups of patients. In general, this indicated a more aggressive phenotype for tumors evolved via polyploidization. Hyper‐tetraploidy (DI >2.10) indicated a very poor prognosis in pre‐menopausal patients. No prognostic effect of aneuploidy and DI‐class was found in node‐negative and TI patients. Cox multivariate regression analysis showed that aneuploidy was an additional prognostic factor to nodal status (1 < N < 3, N > 3 vs. N =0) and tumor size (T2‐4 vs. T1) for overall and distant relapse‐free survival. Subdivision according to DI‐class did not improve the prognostic power of DNA‐ploidy due to stronger correlations with established prognostic factors.
Two new human papillomavirus types (HPV54 and 55) characterized from genital tumours illustrate the plurality of genital HPVs
Authors: Favre Michel , Kremsdorf Dina , Jablonska Stefania , Obalek Slavomir , Pehau‐Arnaudet GÉRard , Croissant Odile , Orth GÉRard 
Published: February 2007

AbstractThe genomes of two new human papillomavirus (HPV) types, named HPV54 and HPV55, were cloned from penile lesions of 2 patients. HPV54 was isolated from a verrucous carcinoma (Buschke‐Löwenstein tumour) together with fulllength HPV6 genomes and HPV6 DNA molecules with a deletion of about 0.3 kb located in the non‐coding region. HPV55 was isolated from a condyloma acuminatum. No crosshybridization was observed between HPV54 DNA and the DNAs of the known cutaneous and genital HPVs by blot hybridization experiments performed under stringent conditions. In contrast, significant cross‐hybridization was detected between HPV55 DNA and the DNA of HPV13, associated with benign oral lesions, and, to a lesser extent, with the DNAs of HPV6, 11, and 44, associated with benign genital proliferative lesions. The DNA sequence homology between HPV55 and HPV6, 11, and 13 was estimated at 12%, 12%, and 20%, respectively, by hybridization in liquid phase at saturation, followed by nuclease SI analysis. The physical maps of HPV54 and 55 were aligned with the genetic maps of HPV16 and 11, respectively, by heteroduplex mapping and partial DNA sequencing. HPV54 is thus only weakly related to the known HPVs, while HPV55 represents an additional HPV6‐related HPV type. HPV54 and HPV55 are uncommon genital HPV types since, in a survey of a large series of specimens of benign, pre‐malignant or malignant anogenital and orolaryngeal tumours, HPV54 was not detected, and HPV55 was found in another case of condyloma acuminatum.
The neu‐oncogene protein as a predictive factor for haematogenous metastases in breast cancer patients
Authors: De Potter Christian R. , Beghin Catherine , Makar Amin P. , Vandekerckhove Dirk , Roels Hendrik J. 
Published: February 2007

AbstractIn a prospective study with a median follow‐up of 13 months on a series of 71 breast cancer patients, 9 developed haematogenous metastases. The neu protein was found on the cell membranes in 27 of the 71 carcinomas (38%) by an immunohistochemical technique using a monoclonal antibody (MAb). Eight of the 9 patients with haematogenous metastases showed overexpression of the neu protein. Immunohistochemical staining of the cell membrane was inversely correlated with the oestrogen and the progesterone receptor status. There was no correlation with lymph‐node involvement. The immunohistochemical detection of the neu protein in breast adenocarcinomas is an independent factor in predicting the patients at risk for haematogenous tumour spread and is therefore correlated with unfavourable prognosis.
A population‐based case‐control study of colorectal cancer in majorca. I. Dietary factors
Authors: Benito E. , Obrador A. , Stiggelbout A. , Bosch F. X. , Mulet M. , Muñoz N. , Kaldor J. 
Published: February 2007

AbstractA population‐based case‐control study was conducted between July 1984 and February 1988 in the Spanish island of Majorca; 286 incident colorectal cancer cases, 295 population controls and 203 hospital controls were interviewed using a food frequency questionnaire. In a multivariate analysis, an increased risk of colon cancer was found for high consumption of fresh meats (RR =2.87) while a high consumption of cruciferous vegetables afforded protection (RR =0.48). For rectal cancer an increased risk was associated with dairy products (RR =3.08) while a protection was afforded by consumption of cruciferae (RR =0.50). For colorectal cancer, the cereal food group also showed an increase in risk (RR =1.92). When cases were compared to hospital controls, the effects of cruciferae in colon and rectum and those of dairy products in rectal cancer remained. The magnitude of the RR estimates was decreased for most comparisons, although in general terms the direction of the associations was the same. In addition, univariate analyses of food groups also suggested significant increases in risk of colorectal cancer for increasing consumption of cereals, potatoes, pastry, eggs and number of meals per day. An indication was found of a reduction in risk for consumers of coffee. An analysis based on risk scores was also conducted and a 4‐fold increase in the risk of colorectal cancer and a highly significant statistical trend was found for high consumption of fresh meat, dairy products and cereals combined with low consumption of cruciferae.
Establishment and characterization of two epithelial tumor cell lines (hne‐1 and hone‐1) latently infected with epstein‐barr virus and derived from nasopharyngeal carcinomas
Authors: Yao Kaitai , Zhang Hai‐Ying , Zhu He‐Cheng , Wang Fu‐Xi , Li Gui‐Yuan , Wen Dong‐Seng , Li Ying‐Ping , Tsai Ching‐Hwa Ann , Glaser Ronald 
Published: February 2007

AbstractTwo epithelial tumor cell lines were established from biopsy specimens of 2 nasopharyngeal carcinomas (NPC) and designated HNE‐1 and HONE‐1. Uncloned HNE‐1 cells were found to be Epstein‐Barr virus (EBV) DNA‐positive when examined by Southern blot analysis up to passage 35, after which the EBV genome could no longer be detected. A similar loss of EBV DNA took place in uncloned HONE‐1 cells. However, HONE‐1 clone 40 cells are still EBV DNA‐positive up to passage 42 thus far and cell cultures contain 85–90% EBV nuclear antigen (EBNA)‐positive cells. The HNE‐1 cell line has been passaged more than 100 times and the uncloned HONE‐1 cells more than 90 times. The tumorigenicity of the HNE‐1 and HONE‐1 cells was demonstrated by tumor induction in nude mice. Karyotypic analysis of the HNE‐1 cells demonstrated an aneuploidy with a modal chromosomal number of 74 at passages 5 and 101 at passage 20; 18 marker chromosomes were identified. We have continued to map the EBV genome latently associated with the HNE‐1 and HONE‐1 cells using the Bam HI, EcoRI or Hind III restriction enzymes. Using EcoRI fragments A‐K as probes, we found that HNE‐1 EBV DNA is different from B95‐8 and HR‐1 EBV DNA in the EcoRI‐C region. The Bam HI map for HONE‐1 EBV DNA is very similar to the B95‐8 map; it contains the Bam HI‐Y fragment but without Bam HI B' and WI'. Differences were observed between HONE‐1 EBV DNA and B95‐8 DNA using the Hind III restriction enzyme. There was no evidence of spontaneous expression of the latent EBV genome in HNE‐1 cells, and attempts to induce replication of the latent EBV genome and rescue infectious virus have failed, suggesting a tightly restricted virus genome.