bluuebunny/crossref_metadata_2025_split huggingface dataset:
The accelerating role of abelson murine leukemia virus in murine plasmacytoma development: in vitro infection of spleen cells generates donor‐type tumors after transfer to pristane‐treated BALB/c mice
Authors: Sugiyama Hiroyuki , Weber Günther , Silva Santiago , Babonits Magda , Wiener Francis , Klein George 
Published: February 2007

AbstractThe role of Abelson murine leukemia virus (A‐MuLV) in the accelerated development of murine plasmacytomas (PCs) (Potter et al., 1973: Science, 132, 592‐594) was studied in a new experimental system. Spleen cells from pristane‐treated or untreated BALB/c mice carrying Robertsonian 6;I5 fusion chromosomes were infected in vitro with helper‐free A‐MuLV overnight and subsequently transplanted into the peritoneal cavity of pristane‐treated or untreated BALB/c mice. Donor‐derived PCs developed in 4 out of 76 pristane‐treated recipients [latent periods: 38‐82 (mean 51) days] that had received spleen cells from pristane‐treated donors, and also in 2 out of 41 pristane‐treated recipients that had received untreated donor‐derived spleen cells (latent periods: 65 and 120 days). Three of the PCs in the former and both PCs in the latter group were tested for integration and expression of the v‐abl gene, with positive results. This indicates that the spleen contains PC‐precursor cells that can be activated by A‐MuLV even before the impact of pristane. All 6 donor‐origin PCs carried a translocation involving chromosone 15, band D2/3. Four of these corresponded to a typical 12; 15 translocation, one was a variant 6; 15 translocation and the 6th may represent a previously unidentified translocation between chromosome 15 and the λ gene‐carrying chromosome 16. No PCs developed among 29 pristane‐untreated recipients that had received pristane‐treated donor‐derived spleen cells. In addition to PCs, monocytic tumors developed in 37 (26%) of all recipients. Their development was independent of pristane treatment of recipients but was particularly frequent in those who had received spleen cells from pristane‐treated donors.
Increased CMP‐NeuAc:Galβ1,4GlcNAc‐R α2,6 sialyltransferase activity in human colorectal cancer tissues
Authors: Olio Fabio Dall , Malagolini Nadia , di Stefano Giuseppina , Minni Francesco , Marrano Domenico , Serafini‐Cessi Franca 
Published: February 2007

AbstractThe sialyltransferase activities of 10 human colorectal specimens were compared with those of the corresponding adjacent normal mucosa. Using asialofetuin as an acceptor we found, in tumor tissues of 9 out of 10 patients, an increased sialyltransferase activity towards the N‐linked chains as determined upon peptide‐N4‐(N‐acetyl‐β‐glucosaminyl)aspara‐gine amidase (PNGase) treatment. On the contrary, the activity towards the O‐linked chains was not significantly changed. When the specificity of the sialyltransferase acting on N‐linked chains was investigated by using N‐acetyl‐lactosamine (Galβ1,4GlcNAc) as an acceptor, we found that the α2,6 sialyltransferase activity expressed by both normal and tumor colorectal tissues was far higher than the α2,3‐activity and that α2,6 was the only sialyltransferase activity increased in tumor tissues. Kinetic analysis revealed that normal and tumor α2,6 sialyltransferases have the same apparent Km for the acceptor substrate (469 and 465 μ,M), but normal enzyme has a higher Km for CMP‐NeuAc (303 μM) than the tumor enzyme (50 μM). The higher affinity of tumor enzyme for the nucleotide‐sugar might partially explain its increased activity in tumor tissues. In addition, tumor tissues contain a lower amount of sialic acid despite the increase in α2,6 sialyltransferase activity.
Sera of children with renal tumours contain low‐molecular‐mass hyaluronic acid
Authors: Kumar S. , West D. C. , Ponting J. M. , Gattamaneni H. R. 
Published: February 2007

AbstractThe molecular mass of hyaluronic acid (HA) rather than its serum concentration alone may be a hallmark of certain types of malignancy. A radiometric assay was used to measure HA levels in 35 children with renal tumours [33 Wilms' tumours and 2 bone metastasizing renal tumours of childhood (BMRTC)] and 20 normal siblings of children with cancer. The HA level in the sera of normal children was barely detectable and had a molecular mass of 1–5 × 105. In both Wilms' and BMRTC patients, very high levels of HA were found in preoperative serum samples; these fell dramatically following surgical excision of the tumours. A novel finding of our study was the presence of low‐molecular‐mass HA (similar to the angiogenic fragments of HA) in the sera of BMRTC patients. In contrast, high‐molecular‐mass HA (which is not angiogenic) was found in the sera of Wilms' patients (2 × 106 kDa). Following surgery in BMRTC patients, not only did serum HA levels fall to a value within normal ranges, but also the HA which remained was of high molecular mass.
Insulin receptor expression in burkitt lymphoma cell lines
Authors: Newman Julie D. , Harrison Leonard C. 
Published: February 2007

AbstractThe specific binding of insulin to 7 different Burkitt lymphoma cell lines containing chromosomal translocations t(8; 14), t(8;2) and t(8;22) was markedly decreased when compared to binding to lymphoblastoid cells of normal karyotype derived from Burkitt lymphoma patients or the human IM‐9 lymphoblastoid line. The number of insulin‐binding sites on intact Burkitt cells was decreased by >90% compared to lymphoblastoid cells, with no change in affinity. This decrease in binding was paralleled by reduced amounts of insulin receptor α (Mr 130,000) and β (Mr 95,000) subunits detected by cell‐surface‐labelling and insulin receptor mRNA transcripts, indicating that transcription of receptor mRNA is decreased in Burkitt cells compared to lymphoblastoid cells and/or that receptor mRNA is less stable. Burkitt cells displayed negligible insulin‐stimulated β subunit auto‐phosphorylation, which could reflect either their decreased number of receptors or a defect in signal transduction. Structural analysis also revealed that the Burkitt cells had an increase in a precursor form (Mr210,000) of the receptor, suggesting that decreased expression of the receptor may be associated with defective processing. Four Burkitt cell lines with t(8;l4) also had reductions of 45–100% in expression of class‐l major histocompatibility (MHC) antigens. The expression of insulin receptors in both Burkitt and lymphoblastoid cells correlated with the expression of class‐l MHC antigens. There was also an inverse correlation between the expression of c‐myc and both insulin receptors and class‐l MHC antigens. As the insulin receptor is absent on resting B cells and is induced after cell activation, the decrease in receptor expression on Burkitt cells may reflect their less activated phenotype compared to lymphoblastoid cells.
Discrepancy in the abilities of lymphokines and bacteria to mediate tumor protection in vivo and/or tumoricidal activity by macrophages in vitro
Authors: Keller R. , Keist R. , Schwendener R. A. 
Published: February 2007

AbstractIn the present study, the ability of lymphokines (MAF and IFNγ) and microbial agents (CP and LM) to induce and maintain tumoricidal activity in BMMP in vitro and to enhance local resistance to the DA rat D‐12 ascites tumor in vivo was assessed comparatively. Under standard conditions in vitro, i.e., when present during the 24‐hr induction and the 36‐hr effector phase, both lymphokines and microbes were similarly potent for eliciting tumoricidal activity in BMMP. When the activating agents were present only during the induction phase, and effector cells were interacted with tumor targets after a 24‐hr interval, clear differences were observed: BMMP which had been incubated with lymphokines had largely if not completely lost their tumoricidal activity; in contrast, BMMP which had been incubated with microbes still manifested considerable tumoricidal activity. Experiments performed to assess the in vivo significance of the discrepancy established in vitro have shown that resistance to the D‐12 ascites tumor was markedly enhanced after local inoculation of microbes but was affected very little or not at all by soluble lymphokines. The causes responsible for the discrepancy in the antitumor potential of lymphokines vs. microbes are probably manifold. Extensive attempts to improve the efficacy of lymphokines by repeated administration or by incorporation into liposomes were not successful.
Integrin‐receptor‐mediated differentiation and growth inhibition are enhanced by transforming growth factor‐β in colorectal tumour cells grown in collagen gel
Authors: Pignatelli Massimo , Bodmer Walter F. 
Published: February 2007

AbstractWe have studied the role of cell‐matrix interactions and the modulating effect on these of transforming growth factor‐βs (TGF‐βs) in controlling differentiation and proliferation in a series of human colorectal carcinoma cell lines. Two (SW1222 and SW480) out of 7 cell lines specifically bound type‐1 collagen, via integrin‐like (SW1222) and non‐integrin‐like (SW480) collagen receptors. Binding of these receptors may be responsible for regulating the degree of epithelial differentiation of the cells when grown in a 3‐dimensional (3D) collagen gel. We have also shown that TGF‐βs enhance the binding of SW1222 cells to collagen and that this is accompanied by greatly increased crypt‐like glandular differentiation and inhibition of cell proliferation. Inhibition of cell proliferation was only seen when cells were grown in 3D collagen gel and were thus expressing a fully differentiated phenotype. The enhanced collagen binding induced by TGF‐βs was partially inhibited by an Arg‐Gly‐Asp (RGD)‐containing peptide which is a cell recognition signal for collagen binding. This suggests that TGF‐βs mediate their effects on differentiation of SW1222 cells specifically by modulating the expression of the integrin‐like collagen receptor. The other colorectal carcinoma cell lines which lack this integrin‐like receptor either failed to bind collagen or, in the case of SW480 binding, exhibited differentiation and proliferation which were not affected by TGF‐βs. This suggests that cell responsiveness to TGF‐βs may depend, at least in part, upon the cell‐matrix interaction.
Localization and imaging of radiolabelled monoclonal antibody against squamous‐cell carcinoma of the head and neck in tumor‐bearing nude mice
Authors: Quak J. J. , Balm A. J. M. , Brakkee J. G. P. , Scheper R. J. , Haisma H. J. , Braakhuis B. J. M. , Meijer C. J. L. M. , Snow G. B. 
Published: February 2007

AbstractNude mice carrying human squamous‐cell carcinoma xenografts were given i.v. injections of radiolabelled monoclonal antibodies (MAbs). MAb E 48, which reacts with squamous‐cell carcinomas, was labelled with 131l,while a second control MAb of similar immunoglobulin subclass was labelled with 125l. Both antibodies were injected simultaneously, then the mice were scanned with a gamma camera or their tissues were removed and antibody uptake was calculated as a percentage of the injected dose. Uptake of E 48 reached a peak value of 16%/g on day 3, while uptake of the control antibody was less than 1.8%/g. By 24 hr after injection tumor could be visualized without subtraction techniques. At days 3 and 7, only xenografts were visible on imaging. These findings suggest that E 48 is capable of high specificity in targeting isotopes to squamous‐cell carcinomas in an experimental setting.
Doxorubicin resistance in P388 leukemia—evidence for reduced drug influx
Authors: Ramu Avner , Pollard Harvey B. , Rosario Luis M. 
Published: February 2007

AbstractMulti‐drug resistance (MDR) in cancer cells is associated with reduced drug accumulation. Although intensively studied, the mechanism of this process remains ill‐defined. We have now developed a new, rapid and quantitative method of measuring uptake of doxorubicin by these cells, in which the fluorescence of accumulated drug is rapidly quenched by DNA in the cell nucleus. Pre‐treatment of cells with deoxyribonuclease eliminates DNA from non‐viable, permeable cells, and this obviates the spurious fluorescence quenching that made previous application of this technique useless. Our data strongly suggest that the drug passively diffuses into cells. The rate of this diffusion into drug‐resistant cells is considerably lower than that found in drug‐sensitive cells. The ratio of the rates of drug entry in these cell types could fully account for the differences between the cell lines in doxorubicin growth‐inhibitory activity. In these experiments no evidence for the previously proposed active efflux mechanism was found in either cell line.
Differential modulation by tumor necrosis factor and immune interferon of HLA class‐II antigens expressed by melanoma cells
Authors: Maio Michele , Gulwani Beena , Morgano Anna , Ferrone Soldano 
Published: February 2007

AbstractTumor necrosis factor (TNF‐α) was compared to immune interferon (IFN‐γ) for its ability to modulate the expression and shedding of HLA antigens, of intercellular adhesion molecule I (ICAM I) and of high‐molecular‐weight melanomaassociated antigen (HMW MAA) by a panel of melanoma cell lines. The latter included the melanoma cell line MeWo and its metastatic variant MeM 50–10, which display differential susceptibility to modulation of HLA class‐ll antigens by IFN‐γ and the cell lines SK‐MEL‐93‐DX‐2 and SK‐MEL‐93‐DX‐3, which originated from anatomically distinct metastases in patient DX. TNF‐α enhanced the expression of HLA class‐l antigens on all 7 melanoma cell lines tested, although to a lower extent than IFN‐γ and the combination of IFN‐γ and TNF‐α. TNF‐α displayed a differential effect on the expression of HLA class‐ll antigens by the 7 melanoma cell lines: it enhanced it on 3 out of the 4 cell lines with constitutive expression of HLA class‐ll antigens and induced them on I of 3 cell lines without detectable expression of these antigens. The effects of IFN‐γ were different since it enhanced HLA class‐ll antigens on the 4 cell lines with constitutive expression of these antigens and induced them on 2 out of the remaining 3 lines. Interestingly, both TNF‐α and IFN‐γ enhanced the expression of HLA class‐ll antigens by SK‐MEL‐93‐DX‐3 cells. On the other hand only TNF‐α induced the expression of HLA class‐ll antigens by MeWo cells and only IFN‐γ induced such expression by MeM 50–10 cells and by SK‐MEL‐93‐DX‐2 cells. The effect of the combination of TNF‐α and IFN‐γ was similar to that of the individual cytokines. Both TNF‐α and IFN‐γ displayed a differential effect on the expression of the gene products of the HLA‐D region by the melanoma cell lines. Northern blot analysis with HLA‐DR β‐, DQ β‐ and DP β‐specific probes suggests that the modulation of HLA class‐ll antigens by both cytokines reflects transcriptional and posttranscriptional events. TNF‐α enhanced the expression of ICAM‐I on all the melanoma cell lines, although to a lower extent than IFN‐γ and the combination of IFN‐γ and TNF‐α. Lastly, neither TNF‐α nor IFN‐γ displayed a marked effect on the expression of HMW‐MAA by the melanoma cell lines tested.
Neural cell adhesion molecule (NCAM) is the antigen recognized by monoclonal antibodies of similar specificity in small‐cell lung carcinoma and neuroblastoma
Authors: Patel K. , Moore S. E. , Dickson G. , Rossell R. J. , Beverley P. C. , Kemshead J. T. , Walsh F. S. 
Published: February 2007

AbstractWe describe reagents from 2 workshops which had been identified as recognizing the same or very similar antigens based on their tissue reactivity. Examination of their tissue specificity led us to the conclusion that this was similar to the expression of the neural cell adhesion molecule (NCAM). We also describe the use of a transfection‐based assay to show that these reagents do recognize NCAM. 3T3 cells were trans‐fected with a full‐length clone of human NCAM. Indirect immunofluorescence studies showed binding of all related antibodies to the transfectants, but not to the control 3T3 cells. In addition, biochemical analysis using certain antibodies in the cluster confirm that they detect NCAM in the transfectants. Our study shows the benefits of using workshops to compare monoclonal antibodies and a molecular approach to define the antigens recognized by such reagents.
Increase in murine monoclonal‐antibody‐defined urinary antigens in patients with bladder cancer and benign urogenital disease
Authors: Masuko Takashi , Sugahara Kunio , Kamiya Takashi , Hashimoto Yoshiyuki 
Published: February 2007

AbstractMonoclonal antibodies (MAbs) were obtained from hybrid‐oma clones established by cell fusion between P3X63Ag8.653 mouse myeloma cells and spleen cells of mice or rats hyper‐immunized against human bladder cancer tissue or BC47 rat bladder cancer cells. RBS‐31 and RBS‐85 mouse MAbs and RBA‐1 rat MAb were raised against BC47 cells and HBP‐1 MAb was raised against human bladder cancer tissues. Urinary antigens detected by these MAbs were quantitatively assayed by means of ELISA using 50 μ1 of 1:2 diluted urine samples. The cut‐off value of the assay was set up as the mean + 4 × SD of the mean using data from the healthy individual urine samples. The reactivity of all healthy control urine samples were under the cut‐off value (negative). By contrast, urine from bladder cancer patients reacted positively with the RBS‐31 MAb at 72%, with the RBS‐85 MAb at 63%, with the RBA‐1 MAb at 51% and with the HBP‐1 MAb at 35%. The urine samples from some patients with renal calculi, acute cystitis or complicated urinary tract infections showed only a weak reactivity with our MAbs. As for extra‐bladder cancers, some patients with renal, renal pelvis, prostate or ureter cancer, but no patients with esophageal, gastric, colon or liver cancer or leukemia, had reactive urinary antigens.
Diet and pharyngeal cancer
Authors: Rossing Mary Anne , Vaughan Thomas L. , McKnight Barbara 
Published: February 2007

AbstractA population‐based case‐control study was conducted to examine the effect of ingestion of vitamin C, carotenoids and retinol on risk of pharyngeal cancer. Data were available from 166 cases of pharyngeal cancer or their next‐of‐kin, and from 547 controls similar in age and sex to the cases. Odds ratios (ORs) relating consumption of vitamin C, carotenoids and retinol from foods and vitamins C and A from supplements to risk of pharyngeal cancer were calculated using multiple logistic regression analysis. After adjustment for smoking and alcohol consumption, a significant increase in risk associated with low intake of vitamin C from foods was observed. Compared to the highest quartile, the OR for the lowest quartile of intake was 2.5 (95% confidence interval, 1.5‐4.2). No overall effect of dietary carotenoid or retinol consumption was noted after adjustment for smoking and alcohol. Decreasing use of either vitamin C or vitamin A supplements was associated with increasing cancer risk among the case group as a whole. However, the effect of vitamin C supplement use was substantially lower when next‐of‐kin respondents were excluded from analysis. Also, the OR for use of vitamin A supplements is based on a very small number of cases reporting use, and must be viewed with caution. The results of our study suggest that intake of vitamin C may be protective against pharyngeal cancer, and are consistent with the results of previous studies which reported a decreased risk of pharyngeal cancer associated with intake of fruits and vegetables.
Tobacco and bladder cancer in males: Increased risk for inhalers and smokers of black tobacco
Authors: Clavel J. , Cordier S. , Boccon‐Gibod L. , Hemon D. 
Published: February 2007

AbstractRelationships between risk of bladder cancer and tobacco smoking were assessed from a hospital‐based case‐control study conducted in France from 1984 to 1987. Smoking history was analyzed for 954 male patients (477 cases and 477 controls). The odds ratio (OR) of bladder cancer was estimated at 3.95 for all smokers vs. non‐smokers. The risk increased with duration of smoking and with average daily cigarette consumption, but there was a significant interaction between these 2 parameters, since the risk only increased with average daily consumption when the duration exceeded 20 years. Black tobacco consumption and inhaling were both found to double the risk when analyzed separately, but their respective effects appeared to interact, and an elevated risk for smokers of black tobacco was only observed among inhalers. Smokers of black and blond tobacco also differed in the way in which the risk evolved with time after cessation of smoking. The OR decreased faster after cessation of smoking among smokers of black tobacco than among smokers of blond tobacco, but the residual risk was higher 15 years after cessation among the former than among the latter.
A case‐control study of gastric cancer and diet in Italy
Authors: Buiatti Eva , Palli Domenico , Decarli Adriano , Amadori Dino , Avellini Claudio , Bianchi Simonetta , Biserni Roberta , Cipriani Francesco , Cocco Pierluigi , Giacosa Attilio , Marubini Ettore , Puntoni Riccardo , Vindigni Carla , Fraumeni Joseph , Blot William 
Published: February 2007

AbstractA case‐control study was conducted in high‐ and low‐risk areas of Italy to evaluate reasons for the striking geographic variation in gastric cancer (GC) mortality within the country. Personal interviews with 1,016 histologically confirmed GC cases and 1,159 population controls of similar age and sex revealed that the patients were more often of lower social class and resident in rural areas and more frequently reported a familial history of gastric (but not other) cancer. After adjusting for these effects, case‐control differences were found for several dietary variables, assessed by asking about the usual frequency of consumption of 146 food items and beverages. A significant trend of increasing GC risk was found with increasing consumption of traditional soups, meat, salted/ dried fish and a combination of cold cuts and seasoned cheeses. The habit of adding salt and the preference for salty foods were associated with elevated GC risk, while more frequently storing foods in the refrigerator, the availability of a freezer and use of frozen foods lowered risk. Reduced GC risk were associated with increasing intake of raw vegetables, fresh fruit and citrus fruits. Lowered risk was also related to consumption of spices, olive oil and garlic. Neither cigarette smoking nor alcoholic beverage drinking were significantly related to GC risk. The case‐control differences tended to be consistent across geographic areas, despite marked regional variations in intake levels of certain foods. The high‐risk areas tended to show higher consumption of food associated with elevated risk (traditional soups, cold cuts) and lower consumption of foods associated with reduced risks (raw vegetables, citrus fruits, garlic). Our findings indicate that dietary factors contribute to the regional variation of stomach cancer occurrence in Italy, and offer clues for further etiologic and prevention research.