bluuebunny/crossref_metadata_2025_split huggingface dataset:
Loss of HLA class‐I alleles, heavy chains and β2‐microglobulin in colorectal cancer
Authors: Kaklamanis Loukas , Gatter Kevin C. , Hill Ann B. , Mortensen Neil , Harris Adrian L. , Krausa Peter , McMichael Andrew , Bodmer Julia G. , Bodmer Walter F. 
Published: February 2007

AbstractUsing immunohistochemical methods, we have analysed colorectal biopsies of normal mucosa, metaplastic polyps (5 cases), adenomas (15 cases) and adenocarcinomas (70 cases) with 13 monoclonal antibodies (MAbs) to allelic products of the HLA‐A, B, C loci. Nine of the 70 carcinomas showed total loss of HLA Class‐I molecules due to an underlying defect regarding not only the expression of β2‐microglobulin (·β2‐m), but also the heavy chains of HLA A, B and C loci, or both. Much commoner was a loss of one or more Class‐I alleles as follows: Al/Aw36 (completely lost in 4 of 29 cases and focally lost in another 2), A2 (in 1 of 37 cases), A3 (in 2 of 14 cases), A11/28/31/33 (in 3 of 11 cases), B7 (in 3 of 13 and focally in 1 other case), B17 (in 1 case), Bw4 (in 8 of 45 and focally in another 6), Bw6 (in 9 of 62 and focally in another 3). Focal selective loss (Bw6 and a combined A1‐Bw6), was observed in 2 adenomas. Normal colonic mucosa, as well as stromal and lymphoid cells present between the neoplastic glands, were studied in each case as a control. A particular allele was only considered to be lost by the malignant cells if it was still expressed on these adjacent tissues.
Risk of lung cancer among cigarette and pipe smokers in Southern China
Authors: Lubin Jay H. , Jun‐Yao Li , Xiang‐Ghen Xuan , Kan Cai Shu , Qing‐Sheng Luo , Shen Yang Li , Jian‐zhang Wang , Lan Yang , Blot William J. 
Published: February 2007

AbstractStudies in Shanghai and in north‐east China indicate that cigarette smoking is a major contributor to the high rates of lung cancer in those areas, but doubts persist regarding the influence of cigarette use on lung cancer rates in other areas of China. In addition, the risk of lung cancer associated with other methods of tobacco consumption—in particular, the use of bamboo water‐pipes and long‐stem pipes—is uncertain. A population‐based case‐control study of 427 male lung cancer patients residing in a mining area of Southern China and 1,011 controls was carried out to address this and other issues. Of these patients, 63% smoked cigarettes and (water and longstem) pipes; 17% and 14% smoked only cigarettes or pipes, respectively; and 6% did not smoke. Compared to non‐smokers, smokers of cigarettes only, smokers of pipes only and mixed smokers were at increased risk; OR = 2.6 (95% CI 1.1–6.2), 1.8 (95% CI 0.8–4.2) and 4.1 (95% CI 2.3–9.2), respectively. Risk increased with duration of tobacco use; however, the rate of increase with years of cigarette use was significantly greater than for years of pipe use (p = 0.03). In addition, risks increased 8‐fold in the highest quartile of number of cigarettes per day compared to non‐cigarette smokers vs. 2.3‐fold for the highest quartile of number of liang (50 g) smoked per month compared to non‐pipe‐smokers; the trends in the ORs differed significantly (p < 0.001). Results suggest that, in this area of China, tobacco use is an important cause of lung cancer, and that smoking cigarettes may be more deleterious than smoking pipes (primarily water pipes).
Increased expression of αIIb β3 integrin in subpopulations of murine melanoma cells with high lung‐colonizing ability
Authors: Chang Y. S. , Chen Y. Q. , Timar J. , Nelson K. K. , Grossi I. M. , Fitzgerald L. A. , Diglio C. A. , Honn K. V. 
Published: February 2007

AbstractFour subpopulations of B16 amelanotic melanoma cells, possessing different abilities to induce platelet aggregation (TCIPA) and to form lung colonies, were isolated by centrifugal elutriation. The expression of αIIb, α3 and α5β1 integrins was examined in the 4 subpopulations in order to determine the relationship between integrin receptor expression and tumor‐cell metastatic potential. The mRNA of αIIb, α5, β1 and β3 was detectable in the 4 subpopulations by Northern blotting. A gradual increase in mRNAs and cell‐surface immunoreactivity of the αIIbβ3 receptor, but not in their gene copies, was observed from the low to the high metastatic subpopulations. The ability of tumor cells to adhere to fibronectin and subendothelial matrix (SEM) increased in parallel. In the high metastatic cells, the αIIbβ3 receptors, but not the α5β1 receptors, were localized to focal adhesion plaques. Incubation of the high metastatic cells with αIIbβ3‐specific antibodies reduced their matrix adhesion, TCIPA and lung‐colonizing abilities. In contrast, in the low met‐ astatic cells, SEM adhesion and lung‐colony formation were not affected by anti‐αIIbβ3 antibody treatment. Incubation of either the low or the high metastatic subpopulation with an α5β1‐specific antibody had no effect in vitro and showed a slight inhibition of lung colonization in vivo. Our results suggest that several phenotypic characteristics of the enhanced metastatic potential of B16a subpopulations may be mediated by increased expression of αIIbβ3 receptors and that expression of these receptors may be regulated at the transcriptional level.
Comparative anti‐viral and anti‐proliferative activity of PGA1 and PGJ2 against HTLV‐I‐infected MT‐2 cells
Authors: D'Onofrio C. , Amici C. , Puglianiello A. , Faraoni I. , Lanzilli G. , Santoro M. G. , Bonmassar E. 
Published: February 2007

AbstractProstaglandin (PG) A and J exert anti‐viral and anti‐proliferative effects in a number of experimental models. In particular, multiple treatments with PGAs prevent in vitro the clonal selection of HTLV‐l‐infected and potentially transformed cord‐blood‐derived mononuclear cells. Proliferation of HTLV‐I‐infected leukemic T cells is refractory in most cases to conventional anti‐blastic therapy. We examined whether these cyclo‐pentenone PGs might control cell proliferation and/or alter virus replication also in HTLV‐l‐transformed cells. We show that PGA1 and PGJ2 can exert powerful control of proliferation of the HTLV‐l‐immortalized, virus‐producing MT‐2 cell line, in a concentration‐dependent fashion. Cells were preferentially arrested at the G1/S interface by treatment with PGA1 or PGJ2 without any detectable cellular toxicity. The anti‐proliferative effect of PG treatment was independent of the growth phase of MT‐2 cells, since both asynchronous and synchronous cells were sensitive to treatment. This effect was accompanied by an increase in the synthesis of a 70 kDa heat‐shock protein (HSP70). However, synthesis of HSP70 was induced to a much greater extent by PGJ2 than by PGA1 at the same concentration. Neither PGA1 or PGJ2 inhibited the transcription of HTLV‐I in MT‐2 cells, but treatment with PGJ2, and not with PGA1, moderately inhibited the synthesis of viral proteins, i.e., p40 Tax and p19 core proteins. Moreover, infection of recipient K562 cells was significantly inhibited after pre‐treatment of MT‐2 cells with PGJ2 14 hr before or co‐treatment at the onset of the co‐culture with K562 cells. This effect was not obtained when MT‐2 cells were repeatedly pre‐treated with PGJ2 for I week before co‐culturing. This suggests that reduced infection could be related to impairment of some step in virus‐transmission phase.
High in vitro‐in vivo correlation of drug response using sponge‐gel‐supported three‐dimensional histoculture and the MTT end point
Authors: Furukawa Toshiharu , Kubota Tetsuro , Watanabe Masahiko , Takahara Tetsuya , Yamaguchi Hiroshi , Takeuchi Tooru , Kase Suguru , Kodaira Susumu , Ishibiki Kyuya , Kitajima Masaki , Hoffman Robert M. 
Published: February 2007

AbstractThe in vitro sponge‐gel‐supported three‐dimensional histoculture chemosensitivity assay (Hoffman assay) allows the in vivo‐like culture of human tumors. In this study, the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2H tetrazolium bromide (MTT) end point was applied to the Hoffman assay in an attempt to increase in vitro‐in vivo correlation. The chemosensitivities of 16 human tumor lines were determined in vitro by the histoculture assay, and retrospectively correlated to their in vivo chemosensitivity as xenografts in nude mice. The in vitro test was considered to be positive if tumor‐cell MTT reduction activity was lowered by more than 50%. The cutoff drug concentrations to determine sensitivity in vitro were determined for mitomycin C, doxorubicin, 5‐fluorouracil and cisplatin. Using these cutoff drug concentrations in vitro we found, as a function of time of exposure, a strong correlation between serum drug concentrations found in nude mice given maximum tolerated doses and drug concentrations found in the histoculture media in vitro, thereby establishing a relationship between the amounts of drugs to which tumors were exposed in vivo and in vitro. The overall correlation rate of the efficacy results of the drug‐response assay to in vivo chemosensitivities was 89.8%, with 90.0% true‐positive and 89.7% true‐negative rates, 81.7% sensitivity and 94.6% specificity, thereby indicating potential clinical use for tumor histoculture with the MTT end point.
Membrane association and shedding of the GPI‐anchored Ca‐MOv18 antigen in human ovary carcinoma cells
Authors: Miotti S. , Alberti S. , Facheris P. , Mantovani L. , Fornaro Mara , Stella Manuela , Ménard S. , Canevari S. , Colnaghi M. I. 
Published: February 2007

AbstractThe antigen recognized by the MOvl8 MAb (Ca‐MOvl8) was recently shown to be a glycosylphosphatidylinositol (GPI)‐linked protein. In this report we show that GPI‐anchorage is not limited to IGROVI cells nor to other ovary carcinoma cell lines, but Ca‐MOvl8 was also found to be sensitive to phosphatidylinositol‐specific phospholipase C (PI‐PLC) treatment on fresh ovarian cancer cells. Furthermore, we found a heterogeneous sensitivity of Ca‐MOv18 to PI‐PLC cleavage, not only among the different cells studied but also in different experiments performed on the same cell line, during extended periods of time in culture. Sensitivity to PI‐PLC cleavage was determined by immunofluorescence on live cells and by double‐determinant radioimmunoassay of the antigen released in the supernatant. The specificity of the PI‐PLC cleavage was demonstrated as follows: (a) TX114 solubilized Ca‐MOv18 shifts from the detergent to the aqueous phase after treatment with PI‐PLC; (b) on membrane preparations, PI‐PLC specifically released a fraction of the antigen, which is distinct from the weakly associated form released by high‐salt treatment; (c) Ca‐MOvI8 from IGROVI expressed the cross‐reacting determinant (CRD), which is characteristic of GPI‐linked molecules. The absence of CRD expression on the spontaneously released protein and the possibility of artificially inducing antigen shedding during the resynthesis of Ca‐MOvI8 which follows bacterial PI‐PLC treatment are interesting points which need to be further investigated in order to understand the physiology of the Ca‐MOvI8 tumor antigen.
Human papillomavirus (HPV) infection, hiv infection and cervical cancer in Tanzania, East Africa
Authors: Meulen J. Ter , Eberhardt H. C. , Luande J. , Mgaya H. N. , Chang‐Claude J. , Mtiro H. , Mhina M. , Kashaija P. , Ockert S. , Yu X. , Meinhardt G. , Gissmannl L. , Pawlita M. 
Published: February 2007

AbstractThe presence of HPV‐DNA was determined in tumor biopsies of cervical‐cancer patients and in cervical swabs of non‐cancer patients from Tanzania, East Africa, by Southern blot hybridization and/or PCR. HPV types 16 and 18 were detected in 38% and 32%, respectively, of 50 cervical‐carcinoma biopsies. A consensus primer PCR capable of detecting a broad spectrum of HPV types revealed the presence of HPV‐DNA in 59% of 359 cervical swabs of non‐cancer patients. Type‐specific PCR showed that types 16 and 18 accounted for 13.2% and 17.5%, respectively, of all HPV infections. Therefore we concluded that HPV 18 is more prevalent in Tanzania than in any other geographical location so far reported. The strongest risk factors for the presence of any HPV‐DNA in the 359 female non‐cancer patients were young age and HIV infection. The epidemiology of HPV types 16 and 18 was found to differ from that of other HPV types, being associated in univariate analysis with trichomonas vaginalis infection, marital status (single/divorced), age at first intercourse, and young age at menarche. However, young age at menarche accounted for most of the effects of all other variables in multivariate analysis. Of the non‐cancer patients, 12.8% had antibodies against HIV I (no patient being severely symptomatic), and HIV infection was highly correlated with the presence of HPV‐DNA, especially types 16 and 18. While HPV‐DNA of any type was detectable 1.4‐fold more often in HIV‐positive patients than in HIV‐negative patients, evidence of an infection with HPV types 16 or 18 was found 2.2‐fold more often in the HIV‐positive patients. The HIV‐positive women did not show an increased rate of cervical cytological abnormalities as assessed by PAP staining of a single cervical smear, the overall rate of abnormalities being 2.8%. Furthermore, the age‐adjusted prevalence of HIV antibodies was found to be considerably lower in 270 cervical‐carcinoma patients (3% HIV‐positive) in comparison with non‐cancer patients. Thus there was no association observable between the prevalence of HIV infections and the frequency of cervical cytological abnormalities or cervical cancer in the setting of this cross‐sectional study.
Expression of Cx26, Cx32 AND Cx43 gap junction proteins in normal and neoplastic human tissues
Authors: Wilgenbus Klaus K. , Kirkpatrick Charles J. , Knuechel Ruth , Willecke Klaus , Traub Otto 
Published: February 2007

AbstractThis report concerns the expression of the gapjunction proteins Connexin (Cx)26, 32 and 43 in different malignant and nonmalignant human tissues. Affinitypurified polyclonal antibodies against Cx26, 32 and 43 were used for immunohistochemical as well as immunoblot analysis. Cx32, the major gapjunction protein in rat and mouse liver, was detected in human liver and kidney. By contrast, Cx43 was expressed in epithelial and mesenchymal tissues and Cx26 was detected in different epithelia. Whereas all of the benign tumors studied, and some malignant ones, showed stable expression of gapjunction proteins, breast cancer, renalcell cancer and sarcomas showed a significant decrease in gapjunction proteins as opposed to normal tissue. Cx43, not detected in human normal liver, was found in human hepatocellular carcinoma and Cx26, not detected in human adult skin, was observed in tissue samples of basalcell carcinoma. In immunoblot analysis, Cx32 antibodies recognized a 27‐kDa protein in human liver and hepatocellular carcinoma. A 43‐kDa polypeptide was detected in human kidney, renalcell carcinoma, normal breast, connective tissue of invasiveduct carcinoma of the breast and hepatocellular carcinoma. © 1992 Wiley‐Liss, Inc.
Basement membrane collagen‐IV synthesis in colorectal tumours
Authors: Hewitt Robert E. , Powe Desmond G. , Carter G. Ian , Turner David R. , Price Janet E. 
Published: February 2007

AbstractMany studies suggest that increased proteolysis accounts for the epithelial basement membrane (EBM) breaks commonly seen in carcinomas. As failure to produce or maintain EBM may also be important, we chose to investigate synthesis of basement membrane collagen‐IV in human colorectal carcinomas. First, to determine the cellular origin of EBM collagen‐IV, speciesspecific antibodies were used to analyse caecal xenografts of 4 different human colorectalcarcinomaderived cell lines. The results of this study suggest an exclusively stromal cell origin for EBM collagen‐IV. Next, the distribution of periglandular myofibroblasts in carcinomas was examined, since in normal mucosa their location and ultrastructural features suggest that they play a role in EBM maintenance. They were generally abundant in normal mucosa and adenomas, but sparsely distributed in carcinomas, particularly at the invasive periphery where EBM collagen‐IV immunostaining is most deficient. Finally, the in situ hybridization technique was used to define cell populations synthesizing collagen‐IV. In normal mucosa, no collagen‐IV mRNA was detected in any component, while in carcinomas, the mRNA was clearly detectable in vascular endothelial cells but not in any other cell type. Increased vascular collagen‐IV production in carcinomas may be at least partly due to tumourinduced angiogenesis, since new bloodvessel formation requires the synthesis of new vascular basement membranes. © 1992 Wiley‐Liss, Inc.
Alcohol consumption as A risk factor for hepatocellular carcinoma in urban Southern African blacks
Authors: Mohamed Abdulla E. , Kew Michael C. , Groeneveld Hendrik T. 
Published: February 2007

AbstractOur purpose was to ascertain whether alcohol abuse is a risk factor for the development of hepatocellular carcinoma in urban southern African blacks and, if so, to relate alcohol consumption to other possible risk factors such as persistent hepatitis‐B‐virus infection, smoking, male sex, in this subpopulation. A prospective, hospitalbased, casecontrol format involving 101 patients with hepatocellular carcinoma and 101 controls was used. The mean age of the patients was 53.7 ± 1.85 years and the male:female ratio 3.2:1. An increased risk was found, but only in urban men over the age of 40 years who habitually drank more than 80 g of ethanol daily. The risk remained after adjusting for chronic hepatitis‐B infection, smoking, and sex (odds ratio 4.4, 95% confidence interval 1.3 to 16.6; p = 0.003). Smoking proved not to be a risk factor, either alone or in concert with alcohol consumption. Hepatitis‐B infection was confirmed as a major risk in younger men and in women, but in urban men over the age of 40 years alcohol abuse was a greater risk. Current hepatitis‐B infection and alcohol abuse were additive risks. © 1992 Wiley‐Liss, Inc.
An attempt to define sets of cooperating genetic alterations in human breast cancer
Authors: Cheickh Meryem Ben , Rouanet Philippe , Louason Geneviève , Jeanteur Philippe , Theillet Charles 
Published: February 2007

AbstractThe extent and the variation of losses of genetic material were examined in a series of 191 human breast cancers by means of a set of 18 polymorphic DNA probes, specific of 7 chromosomal arms (1p, 1q, 3p, 11p, 13q, 17p and 18q) known to be frequently affected by allele losses. Frequencies of losses of heterozygosity ranged from a low of 3.5% (chromosome 13q) to a high of 27% (chromosome 3p). The number of sites involved in breast cancer added to the frequent occurrence of concomitant losses at several chromosomal arms within the same tumor suggest cooperative effects of these LOHs. We were therefore interested in assessing the existence of preferential associations between sets of LOHs in our panel of tumors. Statistically significant associations were found between LOHs at chromosomes Ip and 17p, and between LOHs at chromosomes 11p and 17p. Furthermore, since all the tumors presently studied had previously been analyzed for protooncogene amplification at 5 distinct chromosomal sites, we tested for associations between LOH and DNA amplification. Such associations were indeed observed as exemplified by the correlations observed between the LOH at 11p and amplification of the erbB2 gene and LOH at 17p and the amplification of the fig gene. The only correlation with clinicopathological parameters that could be observed linked the occurrence of LOHs on 11p with recurrent breast cancer (p = 0.015). Sets of several LOHs or LOHs and gene amplifications could not be significantly related to any marker of tumor aggressiveness. © 1992 Wiley‐Liss, Inc.
DNA flow cytometry, nuclear morphometry, mitotic indices and steroid receptors as independent prognostic factors in female breast cancer
Authors: Eskelinen Matti , Lipponen Pertti , Papinaho Sari , Aaltomaa Sirpa , Kosma Veli‐Matti , Klemi Pekka , Syrjänen Kari 
Published: February 2007

AbstractClinical features, 8 histological variables, 7 nuclear morphometric variables, 2 mitotic indices, oestrogen‐receptor (ER) and progesterone‐receptor content (PR), DNA ploidy and S‐phase fraction (SPF) were entered in a Cox's model to assess their independent predictive value in 216 breast‐cancer patients followed up for over 9 years. In the whole series, histological type (p = 0.007), volume‐corrected mitotic index (M/V index) (p = 0.01), axillary‐lymph‐node (pN) status (p = 0.024) and the year of treatment (p = 0.045) predicted independently the recurrence‐free survival (RFS). In a sub‐analysis including SPF (n = 148), the year of treatment (p = 0.003), tumour diameter (p = 0.004), SPF (p = 0.022) and nuclear pleomorphism (p = 0.056) independently predicted the RFS. In a Cox's analysis of the whole series, tumour diameter (p < 0.001), pN status (p = 0.001), PR status (p = 0.002) and the year of treatment (p = 0.021) were independent predictors of survival. In a separate analysis including also SPF (n = 148), tumour diameter (p < 0.001), SPF (p = 0.003), pN status (p = 0.008) and the year of treatment (p = 0.015) proved to be independent prognostic factors. The results show that tumour diameter, pN status, M/V‐index, histological type, SPF and PR status comprise a sufficient combination of prognostic factors in female breast cancer. In pN patients, age and SDPE may be of additional prognostic significance. The prognostic scores combining the independent prognostic variables reflecting both the proliferative rate and metastatic potential of the tumours are accurate predictors of the RFS and overall survival.
Human papillomavirus (hpv) DNA in penile carcinomas and in two cell lines from high‐incidence areas for genital cancers in Africa
Authors: Tornesello Maria L. , Buonaguro Franco M. , Beth‐giraldo Elke , Kyalwazi S. K. , Giraldo Gaetano 
Published: February 2007

AbstractBiopsies of 13 penile cancers (PC), from patients living in regions of Uganda with a high incidence of genital cancers, were studied for the presence, molecular characteristics and physical state of DNA related to that of human papillomavirus (HPV) types 6, 11, 16, 18, 31 and 33. HPV DNA sequences were detected in all PC specimens by dot/Southern blot analyses and by gene amplification of DNA sequences highly conserved among several HPVs. HPV 16 DNA sequences were found in one PC; DNA sequences with low homology to HPV 16 or HPV 18 were present in all other samples. Viral DNA is primarily integrated in the cellular DNA. To isolate and characterize a possible highly oncogenic HPV, a genomic library of the DNA extracted from the PC‐8 biopsy has been constructed in the EcoRI arms of the EMBL4 phage. A single phage containing 8.30‐kb HPV16‐related sequences has been identified and the 3 segments of 0.45, 0.65 and 7.2 kb, released by EcoRI digestion, have been independently subcloned in pUCI8 for further analysis.