bluuebunny/crossref_metadata_2025_split huggingface dataset:
Improved detection of labile cell‐surface components with zinc chloride‐aprotinin: Demonstration of glycoprotein differences in K‐1735 metastatic melanoma variants
Authors: Rieber Manuel , Rieber Mary S. 
Published: February 2007

AbstractMetabolic labelling of K‐1735 melanoma variants with 3H‐glucosamine and cell harvesting with the commonly used protease inhibitor phenylmethylsulfonylfluoride revealed a Triton‐insoluble fibronection‐like 230 kd component in poorly metastatic cells. This component was not evident in highly metastatic cells. Significantly improved surface labelling and detection of the 230 kd glycoprotein in the highly metastatic variant was achieved by zinc chloride‐aprotinin treatment of cells prior to harvesting. This procedure also revealed an increase in a trypsin‐sensitive glycoprotein of higher molecular weight in the Triton‐insoluble fraction of the highly metastatic cell variant. Glycoprotein labelling in this fraction showed an electrophoretic pattern strongly resembling that reported by others for the high‐molecular‐weight human melanoma‐associated glycoprotein complex. The differential detection of the high‐molecular‐weight glycoprotein species in melanoma variants with differing metastatic abilities in an animal model provides a means of studying their possible relevance to metastatic melanoma. Our data also suggest that zinc chlorideaprotinin can be used to improve the detection of labile cell‐surface components.
Trends in morbidity and mortality for oesophageal cancer in linxian county, 1959–1983
Authors: Lu Jian‐Bang , Yang Wen‐Xian , Qin Yu‐Min , Lru Jin‐Ming , Li Yun‐Shu 
Published: February 2007

AbstractData on morbidity and mortality from oesophageal cancer (EC) over the 25 years from 1959‐1983 indicate that this malignancy has been the commonest cause of death in Linxian (LX) county during that period, accounting for 16% of deaths from all causes and 65% of deaths from cancer. Whereas incidence and mortality of EC were high but stable during this period, a decline in mortality has been noted recently in younger age groups, coinciding with an improvement in nutritional standards. Cohort analysis for the period 1879‐1954 demonstrates mortality peaks among individuals born late in the last century and early in the present one. It also shows that a decline in mortality appears to have started among natives of the county born during the period 1935‐1954.
Prevalence of HTLV‐I in arctic regions
Authors: Robert‐Guroff Marjorie , Clark Jeffrey , Lanier Anne P. , Beckman Gunhild , Melbye Mads , Ebbesen Peter , Blattner William A. , Gallo Robert C. 
Published: February 2007

AbstractSera of native inhabitants of Arctic regions were assayed for antibodies to HTLV‐I by the ELISA technique followed by competition experiments to confirm antibody specificity. Residents of 7 widely separated Alaskan villages exhibited prevalence rates of 0 to 12% for HTLV‐I antibodies. Less than 1 % of Greenland Eskimos were HTLV‐I antibody‐positive. Residents of 3 northern Swedish regions ranged in HTLV‐I antibody prevalence from 0 to 5%. Sera of healthy native inhabitants of Alaska and northern Sweden were similarly assayed for antibodies to HTLV‐II. No additional sera were shown to be positive for HTLV‐II antibodies. While some of the HTLV‐I antibody‐positive sera exhibited cross‐reactivity with HTLV‐II antigens, competition experiments using disrupted HTLV‐II or purified HTLV‐I p24 as test antigens indicated that the primary antibody response in all cases tested was elicited by HTLV‐I. Our results show that HTLV‐I distribution is not restricted to endemic areas in warm, humid climates, but extends to Arctic regions. Within these regions, HTLV‐I exhibits the same restricted distribution seen in other areas where virus infection is prevalent. The Arctic does not seem to be a reservoir for HTLV‐II infection. The origin of HTLV‐I in Arctic areas is not known. One may speculate that foreign visitors introduced the virus into Aleut and Lapp populations, and that it has been maintained there and restricted in its distribution as a result of close familial relationships.
Possible association of a new translocation, t(7; 11)(p15;p15), with Ph1 chromosome‐negative chronic myelogenous leukemia
Authors: Kaneko Yasuhiko , Maseki Nobuo , Takasaki Nobuko , Sakurai Masaharu , Kawai Kazuo , Sakurai Minoru 
Published: February 2007

AbstractA Ph1 chromosome‐negative chronic myelogenous leukemia (CML) with t(7;11)(p15;p15) in a 6‐year‐old girl is reported. Three cases of 7;11 translocation have been reported so far. The patients concerned were between 37 and 72 years of age; 2 of them had CML and the other had acute myelomonocytic leukemia. Data from these 4 cases suggest that the 7;11 chromosome translocation may be related to a subgroup of Ph1‐negative CML, specifically to one that may easily proceed to blast phase, or to „subacute”︁ myelogenous leukemia. The present case demonstrates that CML with this chromosome abnormality is not restricted to adults but also affects children. The t(1;11)(q21or23;p15) reported in another case with Ph1‐negative CML may be a variant of this translocation.
06‐Methyldeoxyguanosine in oesophageal dna among individuals at high risk of oesophageal cancer
Authors: Umbenhauer D. , Wild C. P. , Montesano R. , Saffhill R. , Boyle J. M. , Huh N. , Kirstein U. , Thomale J. , Rajewsky M. F. , Lu S. H. 
Published: February 2007

AbstractA radioimmunoassay using monoclonal antibodies (MAb) against 06‐medGuo and 06‐etdGuo enabled the presence of these DNA adducts to be detected in human tissues. With this methodology and with I mg of hydrolysed DNA it is possible to detect approximately 25 fmol 06‐medGuo or 12.5 fmol 06‐etdGuo per mg DNA. The analysis comprised a total of 37 human tissue specimens derived from patients who underwent surgery for cancer of the oesophagus in Linxian County (People's Republic of China); for comparison 12 tissue samples obtained from hospitals in Europe were similarly analysed. Seventeen samples from Linxian County showed a level of 06‐medGuo ranging from 15 to SO fmol/mg DNA, 10 showed higher levels up to 160 fmol/mg DNA, and the remaining 10 samples were below the limit of detection. All the tissue samples from Europe showed levels below 45 fmol 06‐medGuo/mg DNA, 7 being below the limit of detection. No 06‐etdGuo was detected in any of the samples. 06‐alkylguanine DNA alkyltransferase activity observed in tissue extracts from Linxian County. ranged from 190 to 326 fmol (mean values) of 06 medGuo removed per mg protein and lower values were obtained for the removal of 06‐etdGuo. The findings obtained using this approach appear promising in assessing the role of alkylating agents, e.g. nitrosamines, in the aetiology of human cancer.
Evidence for increased epidermal growth factor receptors in human sarcomas
Authors: Cowley Gerard , McIlhinney Jeffrey , Gusterson Barry , Ozanne Bradford , Fisher Cyril , Reeves Brian 
Published: February 2007

AbstractThe results of an immunocytochemical study of the epidermal growth factor receptor (EGFR) in 35 human soft‐tissue sarcomas, using a murine monoclonal antibody (MAb) EGF‐RI, are reported. In many of the tumours staining was stronger than in the adjacent stroma, suggesting increased levels of receptor. Particularly strong staining was seen in one epithelioid sarcoma and in the spindle‐cell component of a synovial sarcoma. Binding studies carried out on an epithelioid sarcoma cell line established from one of the specimens, using radiolabelled EGF, showed that approximately 8% of the receptors were of high affinity with a dissociation constant (Kd) of approximately 10−10m, while the remainder were of lower affinity with a Kd of 10−9m. The cells expressed a total of 1.7 × 106 receptors/cell which is equivalent to that found in some epidermoid tumours where gene amplification has been demonstrated. These data suggest that, as with other tumours recently reported, increased levels of epidermal growth factor receptor may be related to transformation.
Mast cells and tumour angiogenesis: The tumour‐mediated release of an endothelial growth factor from mast cells
Authors: Roche William R. 
Published: February 2007

AbstractExposure to tumour cells has previously been shown to induce mast cells to degranulate and release heparin. Isolated mast‐cell granules were found to be mitogenic for endothelial cells in vitro. This effect was a property of mast‐cell heparin, whose potency as a mitogen exceeded that of commercial heparins. The basis of this difference lay in the proteoglycan structure of the molecule. The release of heparin in mastcell‐tumour co‐cultures was examined by both endothelial cell proliferation and isotopic techniques. The kinetics and mode of release are described. The results are discussed in relation to the role of the mast cell in angiogenesis assays and tumour neovascularization.
Estrogen and progesterone receptors in benign breast tumors and lesions: Relationship with histological and cytological features
Authors: Giani C. , D'Amore E. , Delarue J. C. , Mouriesse H. , May‐Levin F. , Sancho‐Garnier H. , Breccia M. , Contesso G. 
Published: February 2007

AbstractThe pattern of estrogen (ER) and progesterone receptors (PR) and their relationship to histo‐ and cytopathological parameters has been studied in 97 cases of benign breast disease and benign phyllode tumors (95 women, of whom 76 were premenopausal, and 2 men). Total (cytosolic + nuclear) ER and PR were assayed by a single‐saturating dose method using a tris‐KCI buffer. The cut‐off between positive and negative ER and PR assay was 100 femtomoles/g tissue. All specimens were processed for histological examination: epithelial and fibroblastic proliferation, epithelial/stromal ratio and presence of focal or diffuse hyalinosis. In 33% of the 46 cases of fibrocystic disease one receptor at least was present (13% ER+, 31% PR+). All the 8 cases in which infiltrating epitheliosis was present were PR+ and 4 of them were also ER+. In 72% of the 31 fibroadenomas one receptor at least was present (19% ER+, 71% PR+). In all these cases levels of receptors were lower than in malignant tumors. An inverse correlation between PR + prevalence and fibrohyalinosis was observed; on the other hand a positive relationship between PR + and fibroblastic (p<0.001) or epithelial (p<0.01) proliferation was found. In all 5 benign phyllode tumors examined PR + were present at a very high level, almost as high as in malignant tumors. Of the 15 other benign breast lesions, all but one (I hamartoma) were ER− and PR−.
Invasion of lung tissue by bronchogenic squamous‐cell carcinomas: Interaction of tumor cells and lung parenchyma in the tumor periphery
Authors: Dingemans Koert P. , Mooi Wolter J. 
Published: February 2007

AbstractWe collected multiple samples from 43 human bron‐chogenic squamous‐cell carcinomas and studied the ultrastructure of the tumor‐cell‐lung parenchyma interaction in the tumor periphery. Since, in the periphery of a growing tumor, the surrounding tissue has only recently been reached by the tumor cells, it is the initial stage of interaction which can be observed here. The main findings were: (1) The tumor cells in the tumor periphery always penetrated the lung parenchyma along the epithelial side of the alveolar basal lamina. (2) The non‐neoplastic alveolar epithelial cells were either detached from their basal lamina or overgrown by the tumor cells, without being visibly damaged or destroyed. When the alveolar epithelial cells were overgrown by the tumor, they retracted and formed extra‐ or intracellular lumina much smaller than the original alveoli. (3) The contact between tumor cells and alveolar epithelial cells resulted in the formation of common desmosomes and complete junctional complexes and the common lining of lumina. (4) Although the tumor cells extended small pseudopods through the basal lamina, they virtually never migrated through it to reach the interstitial compartment. These results indicate that the initial invasion of lung parenchyma is characterized by a smooth integration of tumor cells and elements of the preexisting tissue, leading to orderly associations of neoplastic and non‐neoplastic cells, rather than by tissue destruction by the tumor cells.
Parity and breast cancer risk: Possible effect on age at diagnosis
Authors: Pathak Dorothy R. , Speizer Frank E. , Willett Walter C. , Rosner Bernard , Lipnick Robert J. 
Published: February 2007

AbstractWe examined the effect of parity on breast cancer risk on the basis of information from 107,146 married female nurses followed prospectively between 1976–1980. For everparous women, a significant protective effect against breast cancer was observed with increasing parity (χ 2for trend = 14.2, ρ<0.001). Adjustment for age at first birth and other potential confounders by multiple logistic regression did not materially affect this trend. After controlling for these risk factors, the overall relative risk of breast cancer for women with four or more pregnancies lasting 6 months or longer was 0.68 (95% confidence limits 0.51‐0.90) compared with women with only one pregnancy. When nulliparous and everparous women were compared, an interaction of age and everparous status in 1976 was observed. The logistic regression coefficient for the interaction was 0.3419 (95% confidence limits 0.0374‐0.6464). Specifically, for women of parity 2 relative to nulliparous, the relative risk of breast cancer and the 95% confidence intervals were 1.85 (1.09, 3.14), 1.32 (0.92, 1.89), and 0.93 (0.62, 1.41) for 30‐39, 40‐49 and 50‐55‐year‐old women, respectively. This points to the need of presenting age‐specific, rather than age‐adjusted, relative risks in future studies of breast cancer and parity.
Antigens related to three core proteins of HTLV‐I (p24, p19 and p15) and their intracellular localizations, as defined by monoclonal antibodies
Authors: Tanaka Yuetsu , Lee Bunsho , Inoi Takeshi , Tozawa Hideki , Yamamoto Naoki , Hinuma Yorio 
Published: February 2007

AbstractThree distinct monoclonal antibodies (MAbs) specific for human T‐cell leukemia virus type‐I (HTLV‐I) core proteins with molecular weights of 24 kDa (p24), p19 or p15 were produced, characterized and compared. These antibodies were named NOR‐I (anti‐p24, IgG2a). GIN‐7 (anti‐p19, IgG2b) and FR‐45 (anti‐p15, IgG2a). Immunofluorescence assay showed that they reacted specifically with methanol‐fixed cells of virus‐bearing cell lines, and that only GIN‐7 bound, albeit weakly, to the surface of a small percentage of viable cells. Like natural antibodies to HTLV‐I in human serum, GIN‐7 stained the fixed cells brightly and diffusely, and gave more intense fluorescence than NOR‐I and FR‐45, which stained restricted areas of the cells. NOR‐I, GIN‐7 and FR‐45 specifically precipitated core proteins p24, p19 and p15, respectively, from a lysate of HTLV‐Imt‐2 labelled with 35S‐cysteine. NOR‐I precipitated p53, p36, and p24, GIN‐7 precipitated p53, p32, p28 and p19, and FR‐45 precipitated p53, p36, and p15 from a lysate of 35S‐cysteine‐labelled MT‐2 cells. GIN‐7 also precipitated p32, p28 and p19 from a lysate of MT‐2 cells, labelled by surface iodination, but NOR‐I and FR‐45 did not detect any proteins in this lysate. GIN‐7 also detected p28 in 3H‐glucosamine‐labelled MT‐2 cells. Antibody binding competition assay showed that the sera of ATL patients significantly interfered with the binding of NOR‐I and GIN‐7 but not with that of FR‐45, to antigens of disrupted virus of MT‐2 cells. This complete set of MAbs against the HTLV‐I gag gene products is useful for biological and functional studies of the HTLV‐I core proteins.
Cytotoxic t‐cell precursors against non‐immunogenic rat tumors: Limiting dilution analysis
Authors: Zöller M. 
Published: February 2007

AbstractAfter in vitro stimulation of lymphocytes with syngeneic tumor cells in the presence of interleukin 2 (IL‐2), a cytotoxic T‐cell response was observed against these spontaneously arising BDX tumors, which are non‐immunogenic in the syngeneic host. The response was due to cytotoxic T‐cells (CTL), which were specific for syngeneic tumor cells, i.e. neither syngeneic lymphoblasts, allogeneic lymphoblasts, allogeneic tumor cells, nor NK targets were lysed. The frequencies of anti‐tumor lymph‐node (LN) and spleen CTL precursors (CTLp) against a panel of syngeneic tumors of different histology varied between 1/6,000 and 1/16,000. Further analysis of the reactivity pattern of anti‐tumor CTL revealed some degree of cross‐reactivity within the syngeneic system. By a limiting dilution (LD) split culture approach in combination with cold target (CT) inhibition, it could be shown that tumors carry a panel of tumor‐associated antigens (TAAs). Some tumors express individually specific as well as cross‐reactive TAAs, while others carry cross‐reactive TAAs only.
Treatment of murine L1210 lymphoid leukemia and melanoma B16 with lipophilic cytosine arabinoside prodrugs incorporated into unilamellar liposomes
Authors: Rubas W. , Supersaxo A. , Weder H. G. , Hartmann H. R. , Hengartner H. , Schott H. , Schwendener R. 
Published: February 2007

AbstractLipophilic prodrugs of 1‐β‐D‐arabinofuranosyl cytosine (Ara‐C), namely N4‐ and 5′‐oleyl‐1‐β‐D‐arabinofuranosyl cytosine (N4‐oleyl‐ara‐C, 5′‐oleyl‐ara‐C) and N4‐palmitoyl‐1‐β‐D‐arabinofuranosyl cytosine (N4‐palmara‐C) were incorporated into liposomes of various lipid compositions. The phospholipid vesicles were prepared by controlled dialysis of lipid/prodrug/detergent micelles yielding homogeneous and stable unilamellar liposomes. The liposome size ranged from 70 to 120 nm depending on the lipid composition and the amounts of prodrug incorporated. Depending on the total amount of micellized Ara‐C prodrugs, a maximal incorporation rate of 250 μg prodrug per mg egg phosphatidylcholine was achieved. The incorporation efficiency was in the range of 85 to 97%. The in vivo antitumor activity of the liposome preparations against L1210 lymphoid leukemia was clearly superior by factors of 2–8 depending on the therapy schedule and route of drug application. The treatment of melanoma B16 with free Ara‐C as well as with the prodrug‐liposomes exhibit rather weak antitumor activity. Drug application by means of prodrug‐liposomes yields equal or higher tumor‐inhibitory effects at drug concentrations which were 2 ‐ 4 times lower than those of free Ara‐C. Although drug tolerance and myelosuppression studies with Swiss albino mice revealed that the prodrug‐liposomes were 5–10 times more toxic than free Ara‐C, a substantial improvement of efficiency could be observed. The incorporation of the ara‐C prodrugs into liposomes provides protection against fast degradation and systemic elimination which might be an explanation for the improved antitumor effect of these preparations.
Tissue‐specific markers in flow cytometry of urological cancers. II. Cytokeratin and vimentin in renal‐cell tumors
Authors: Feitz W. F. J. , Karthaus H. F. M. , Beck H. L. M. , Romijn C. , van der Meyden A. P. M. , Debruyne F. M. J. , Vooijs G. P. , Ramaekers F. C. S. 
Published: February 2007

AbstractNine primary human renal‐cell tumors (RCT), one lymph‐node metastasis, 4 human xenografts of a RCT in nude mice and a rat RCT line were analyzed by flow cytometry (FCM) using propidium iodide for DNA analysis and antibodies to cytokeratin and vimentin in the indirect immunofluorescence technique for labelling of specific tumor‐cell populations. By means of 2‐dimensional FCM analysis, vimentin‐ and cytokeratin‐positive (tumor) cells were compared and their DNA content and proliferative fraction analyzed separately from those of cytokeratin‐negative stromal and inflammatory cells. In primary human RCT, 2 subpopulations of cells were detected and analyzed separately. Small numbers of tumor cells with an abnormal DNA stemline were also detected. In addition, co‐expression of intermediate filament proteins of both the cytokeratin and the vimentin types was detected in the aneuploid cell population. Comparison of 2 model systems of RCT with primary human RCT revealed a similar pattern of tumor‐cell subfractions within these tumors. The 2‐parameter FCM analysis permits the detection of subpopulations in complex cell suspensions and the quantification of these fractions, as well as analysis of their cellular DNA content.
Media conditioned by human leukemic T‐cells induce expression of IL2 receptors and proliferation of normal T lymphocytes
Authors: Kosmatopoulos Constantinos , Allouche Michèle , Triebel Frédéric , Zanti Maria , Clemenceau Corine , Gluckman Jean‐Claude , Jasmin Claude , Georgoulias Vassilis 
Published: February 2007

AbstractPeripheral blood T‐colony‐forming cells (T‐CFC) from patients with T‐cell acute lymphoblastic leukemias (T‐ALL) and T‐cell non‐Hodgkin lymphomas (T‐NHL) can generate colonies in methylcellulose in the absence of added growth factors and/or mitogenic stimulation. In the present study, we show that media conditioned (LCM) by unstimulated mononuclear cells (MNC) from these patients can induce proliferation (proliferating inducing activity; PIA) and promote colony growth (T‐cell colony promoting activity; T‐CPA) of normal T lymphocytes in the absence of any other mitogenic stimulation. Preincubation of normal E+ lymphocytes with some TCPA+, PIA−‐LCM for 48 hr leads to IL2‐induced cell proliferation in the absence of any other stimulation. Moreover, staining of the cells with anti‐Tac monoclonal antibody (Mab) reveal 9%‐26% Tac+ cells. Both PIA and IL2 receptor‐inducing activities were abrogated by treatment of LCM with proteolytic enzymes or by heating at 47°C for 30 min. Modulation of the T3 molecule by OKT3 MAb on normal E+ cells did not abrogate the capacity of LCM to induce expression of IL2‐receptors, suggesting that this activity was not mediated by triggering the Ti‐T3 molecular complex. These activities were detected in media conditioned by both unfractionated MNC and blast‐enriched cell fractions, and their production required DNA and RNA synthesis by actively dividing cells. Taken together, these findings indicate that human leukemic T cells spontaneously release activites which can activate normal resting T lymphocytes.
Immunological consequences of tumor excision: From active immunity to immunological memory
Authors: Bursuker Isia , North Robert J. 
Published: February 2007

AbstractExcision of the immunogenic Meth‐A fibrosarcoma during generation by the host of concomitant antitumor immunity resulted in the appearance in sequence of two qualitatively distinct states of post‐excision immunity. Immunity expressed on the day of excision was dependent on Ly‐I−2+, cyclophosphamide‐sensitive T cells, whereas immunity expressed 2 weeks later was dependent on cyclophosphamide‐resistant T cells which can be functionally eliminated by either anti‐Ly‐1 or anti‐Ly‐2 monoclonal antibody and complement. The data suggest that antitumor immunity expressed shortly after tumor excision represents active concomitant immunity that is acquired by the host before excision is performed. In contrast, immunity expressed 2 weeks later is based on immunological memory.