bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cancer registration in the European Community
Authors: Coleman Michel P. , Démaret Eva 
Published: February 2007

AbstractA survey of population‐based cancer registries in the European Community (EC) is reported: 82 (92%) of 89 registries replied. In 3 of the 12 EC countries (Denmark, Netherlands, UK), general cancer registration applies to the entire population; national registration for childhood neoplasms also applies in 3 countries (FRG, Ireland, UK). About 350,000 new cancers were recorded each year during 1982–1985 in the 32% of the EC population which is covered by general registration. It is estimated that during this period about 988,000 new cancers (excluding non‐melanoma skin cancer) occurred each year in the 10 EC countries for which incidence data are available. Most registries report 90–95% completeness of cancer registration, but there is evidence of imprecision in these estimates. Risk factors for cancer are recorded in 43 registries, in particular occupation (38), but recording of occupation is often incomplete. The use of international or compatible systems of coding occupation would facilitate screening of cancer registration data for occupational hazards in the European Community. The quality of cancer information in the Community would be greatly improved by the systematic and widespread use of simple methods to estimate completeness of registration and by allowing registries confidential access to death certificates.
Epidemiology of Kaposi's sarcoma in Sweden prior to the acquired immunodeficiency syndrome
Authors: Dictor Michael , Attwell Robyn 
Published: February 2007

AbstractWe studied retrospectively 529 cases of Kaposi's sarcoma (KS) reported to the Swedish Cancer Registry between 1958 and 1982 to determine incidence rates, survival and rate ratios, together with the frequency and types of associated malignancies. The age‐standardized (Swedish population 1970) incidence rate generally increased over the time period, with a mean of 0.27 cases per 100,000 population per year (males 0.40, females 0.14). The incidence rate ratio (based on 5‐year intervals and relative to the earliest period) reached 2.06 for males and 3.76 for females in the 1968–1972 interval, while the actual peak occurred between 1971 and 1974 for both sexes. Poisson regression modelling suggested a transient shift in the age‐specific male incidence rate pattern with a relative increase of the disease in younger age groups (p = 0.05) up to 1968–1972. The age‐adjusted male: female ratio did not change significantly from 2.9 during the period of study. In relation to the general population, 18% fewer men and 24% fewer women were alive 10 years after the diagnosis had been made. Ninety‐nine (19%) cases had other primaries, of which 17 were neoplasms of lymphocytic origin. Lymphoproliferative malignancy was 2.5 times (95% CI 1.38, 4.37) more common than expected in patients with KS (in particular in females) but a definite increase in other malignancies was not apparent. It is questionable whether immune dysfunction due to other malignant disease or drug therapy can account for the epidemiologic changes in KS, which began almost 2 decades prior to the AIDS epidemic in Sweden.
T‐cell‐mediated inhibition of EBV‐induced B‐cell transformation: Recognition of virus particles
Authors: Bejarano Maria Teresa , Masucci Maria Grazia , Klein George , Klein Eva 
Published: February 2007

AbstractIn order to analyze the components of EBV‐specific immunological memory that contribute to the T‐cell‐mediated inhibition of EBV‐induced B‐cell transformation, we have investigated the growth inhibitory potential of T cells cultured for 3 days with B cells exposed to transforming and nontransforming EBV preparations. T cells cultured for 3 days with EBV‐infected autologous B cells inhibited the transformation of newly infected B lymphocytes. T cells cultured with the virus, with autologous uninfected B cells, or in the presence of 10, ughl Con‐A had a significantly weaker inhibitory capacity. The inhibitory capacity was induced by co‐cultivation with B cells infected with the transforming 895–8 virus strain, with the non‐transforming P3HRI virus strain, and also with UV‐inactivated B95‐8 virus. B‐cells infected with transforming B95‐8 virus induced the strongest growth inhibitory activity. Activation of the T cells was shown by their IL‐2 production, proliferation, and generation of non‐specific cytotoxicity. These results suggest that the initial event of the cell response in EBV‐infected cultures is induced by antigens associated with the viral particles presented by B lymphocytes.
Gastric cancer after gastrectomy
Authors: Arnthorsson Gauti , Tulinius Hrafn , Egilsson Valgardur , Sigvaldason Helgi , Magnusson Bjarki , Thorarinsson Hjalti 
Published: February 2007

AbstractInhabitants of Iceland who had undergone gastric resection for non‐malignant diseases between 1930 and 1974 were identified and followed up at the Icelandic Cancer Registry in order to evaluate the risk of gastric cancer subsequent to gastric resection. There were 1,214 males and 581 females, contributing 30,792 person/years. The results show an overall 1.16‐fold, not significant, increase in the relative risk for gastric cancer. In the first 15 years after operation the risk was decreased, 0.49, 95% confidence interval (CI) 0.24–0.90, but from 15 years or more following operation, the risk was 2.17, 95% CI 1.46–3.10. We conclude that for these subjects the risk is not significantly increased. Patients surviving 15 years or more after operation have an increased risk (p < 0.001), but they do not contribute substantially to the number of gastric cancer patients in Iceland.
Localization of radiolabelled F(ab′)2 fragments of monoclonal antibodies in nude mice bearing intraperitoneally growing human ovarian cancer xenografts
Authors: Moseley Karan R. , Battaile Anne , Knapp Robert C. , Haisma Hidde J. 
Published: February 2007

AbstractThe biodistribution and pharmacokinetics of 2 monoclonal antibodies (MAbs) specific for ovarian carcinoma, OC125 and OV‐TL3, were studied in nude mice bearing intraperitoneally (i. p.) growing human ovarian carcinoma xenografts of NIH:OVCAR‐3. The ovarian carcinoma xenografts grew as non‐adherent cells in ascites and as solid implants in the peritoneal cavity of injected mice. The biodistribution and pharmacokinetics were determined by measurement of radioactivity in tumor masses, ascites, blood and other tissues after intravenous (i. v.) and i. p. injection of radioiodinated F(ab′)2 fragments of MAbs. The specificity of the observed tumor localization was then evaluated by comparing the uptake of the anti‐ovarian carcinoma antibodies OCI25 and OV‐TL3 with the uptake of a radioiodinated non‐ovarian carcinomaspecific MAb A2C6. The results of the study indicate that uptake of the anti‐ovarian carcinoma antibodies was highest in the non‐adherent tumor cells in the ascites after i. p. injection. The observed uptake was 85% Injected dose/g for OV‐TL3 and 22% injected dose/g for OCI25. This compares to the observed antibody uptake of 9% injected dose/g for OV‐TL3 and less than I% injected dose/g for OCI25 in solid tumor masses after i. p. injection. After i. v. injection, uptake of OCI25 and OV‐TL3 was less than 3% injected dose/g, both for nonadherent tumor cells and for solid tumor masses. The data support the conclusion that OV‐TL3 is superior to OC125 and that i. p. administration of radiolabelled MAb F(ab′)2 fragments is superior to their i. v. administration for immunotherapy of ovarian carcinoma.
Differential patterns of anti‐tumour drug responses and mechanisms of resistance in a series of independently‐derived VP‐16‐resistant human tumour cell lines
Authors: Lock Richard B. , Hill Bridget T. 
Published: February 2007

AbstractResistance to etoposide, which was expressed following exposure of a human tumour cell line (HN‐1) to fractionated X‐irradiation (II fractions to a total dose of 50Gy), was found to be exhibited after delivery of only 5 fractions (total dose of 22.5Gy). In addition, 2 new etoposide‐resistant sublines of these HN‐I cells have been developed by continuous exposure in vitro to sublethal drug concentrations. No significant differences in growth characteristics were shown between all these resistant sublines and the parental line. The drug‐treated line, HN‐1 VP‐2, expressed cross resistance to vincristine, adriamycin and daunomycin, and marginal cross resistance to vinblastine and cisplatin. The X‐irradiation‐treated subline (HN‐I/DXR‐II) also proved cross‐resistant to vincristine and marginally cross‐resistant to vinblastine, but showed unaltered responses to adriamycin and daunomycin, and expressed marginal collateral sensitivity to cisplatin. Comparisons of druguptake characteristics showed that only the HN‐1/VP2 cells and not the HN‐1/DXR‐II cells had reduced uptake of vincristine, vinblastine and daunomycin. However, etoposide uptake was not altered in either resistant subline. Further investigations have shown that the approximately 4‐fold level of resistance to etoposide in these HN‐1/VP‐2 and HN‐I/DXR‐II cells was associated with a reduction in etoposide‐induced DNA single‐strand breakage. However, repair of these lesions, after drug removal, was rapid and similar in the parental and drugresistant sublines, with 50% having resealed within 20–26 min. Resistance to etoposide was also associated with significantly elevated p < 0.01) glutathione peroxidase activity in both sublines, whilst glutathione S‐transferase activity was marginally elevated (117%) only in the HN‐I/DXR‐II cells. There were no significant alterations in total glutathione levels. These results suggest that not only do patterns of response to anti‐tumour drugs differ depending upon the agent employed to “induce” resistance, but that multiple mechanisms appear to be associated with these altered responses.
Monoclonal antibody JSB‐1 detects a highly conserved epitope on the P‐glycoprotein associated with multi‐drug‐resistance
Authors: Scheper R. J. , Bulte J. W. M. , Brakkee J. G. P. , Quak J. J. , van der Schoot E. , Balm A. J. M. , Melier C. J. L. M. , Broxteman H. J. , Kuiper C. M. , Lankelma J. , Pinedo H. M. 
Published: February 2007

AbstractResistance to multiple chemotherapeutic agents is a common clinical problem in the treatment of cancer. This resistance may occur before primary therapy or be acquired during treatment. We have generated a monoclonal antibody (MAb) (JSB‐I), specific for a conserved epitope on the plasma membrane 170‐ to 180‐kDa glycoprotein, the expression of which is strongly correlated with the degree of multi‐drug resistance (MDR). JSB‐1 strongly binds to both Chinese‐hamster‐derived MDR cell lines and human MDR cell lines, including cell lines derived from lung and ovary. A drug‐sensitive revertant line, and the corresponding drug‐sensitive parent lines, showed only weak reactivity or none at all. JSS‐l reacts strongly to air‐dried or acetone‐fixed cells and therefore has potential value for diagnostic detection of MDR cells in human tumor samples.
Kinetics of uptake and degradation of an abrin immijnotoxin by melanoma cells and studies of the rates of cellular intoxication
Authors: Godal Aslak , Fodstad Øystein , Pihl Alexander 
Published: February 2007

AbstractThe mechanism of action of an abrin 9.2.27 antimelanoma antibody conjugate has been studied in 2 human melanoma cell lines, FEMX and LOX, which differ in sensitivity to the immunotoxin (IT) and to native abrin. The IT, which had been affinity purified before use to remove molecules with exposed gal‐binding sites on the toxin B‐chain, inhibited cellular protein synthesis at a faster rate in the LOX than in the FEMX cells despite the fact that the LOX cells express less specific antigen and bind less IT to the cell surface. Surface‐bound abrin‐IT, as well as surface‐bound specific antibody, disappeared at equal rates from the cell surface of the 2 cell lines. After binding of labelled IT the disappearance of total cell associated radioactivity, as well as the appearance of TCA precipitable and TCA‐soluble radioactivity in the incubation medium, occurred at faster rates in the LOX than in the FEMX cells. No free abrin or antibody B‐chain complex could be detected in the medium or inside the cells. The results indicate that the different sensitivities of the melanoma cell lines reflect different abilities to process endocytosed IT and to translocate the active A‐chain to the cytosol. Experiments carried out in the presence of lactose are interpreted to mean that the A‐chain may be translocated to the cytosol by two mechanisms, one involving antigen‐antibody interaction and one involving the 8‐chain, and that the lectin binding site contributes to the B‐chain‐facilitated mechanism.
Co‐operation in cell transformation between BK virus and the human C‐harvey‐ras oncogene
Authors: Pagnani M. , Corallini A. , Caputo A. , Altavilla G. , Selvatici R. , Catozzi L. , Possati L. , Barbanti‐Brodano G. 
Published: February 2007

AbstractEarly‐passage hamster embryo cells were transformed by recombinant DNA molecules containing BK virus (BKV) earlyregion gene and either the activated c‐Ha‐ras oncogene (pBK/c‐rasA) or the normal c‐Ha‐ras proto‐oncogene (pBK/c‐rasN). The recombinant DNAs had a greater transforming ability and converted hamster cells to a more malignant phenotype than the single genes transfected separately. pBK/c‐rasA was significantly more powerful than pBK/c‐rasN in conferring to cells all the characteristics of transformation. Transfected DNA sequences were integrated mostly as single insertions into cellular DNA. Specific c‐Ha‐ras p21 and BKV T antigen were detected in transformed cells. Although stimulation of c‐Ha‐ras expression by BKV enhancers cannot be excluded in recombinants, super‐transfection and co‐transfection experiments in hamster embryo cells and pre‐neoplastic cell lines showed that BKV early‐region and c‐Ha‐ras co‐operate in transformation by contributing separate and independent functions.
Effect of retinoids on the proliferation, morphology and expression of glial fibrillary acidic protein of an anaplastic astrocytoma cell line
Authors: Rutka James T. , De Armond Stephen J. , Giblin Jane , McCulloch John R. , Wilson Charles B. , Rosenblum Mark L. 
Published: February 2007

AbstractWe studied the effect of retinoids on the growth and differentiation of a cell line (U 343 MG‐A) derived from a human malignant astrocytoma. Cultures treated with all‐trans or 13‐cis retinoic acid showed a dose‐dependent inhibition of proliferation and a marked reduction in the mean cell number at the plateau phase of growth (3.5 × 106 vs. 1 × 107 cells/25 cm<2>) compared with untreated cultures. At confluence, cells treated with all‐trans or 13‐cis retinoic acid were contactinhibited, whereas control cultures showed crowding, piling, and overgrowth. All‐trans retinol or retinyl acetate did not inhibit growth. Astrocytoma cultures treated with all‐trans retinoic acid (10−6 M) for 5 days were modestly growth‐inhibited but by day 16 had the same numbers of cells as controls; cultures that received all‐trans retinoic acid for 9 days were markedly growth‐inhibited for 7 days after the drug was removed. All‐trans and 13‐cis retinoic acid (10−6 M) prevented the EDTA‐induced cell detachment seen in control cultures. Strongly adherent all‐trans retinoic‐acid‐treated astrocytoma cells grew at a slower rate than did readily detached all‐trans retinoic‐acid‐treated or control cells. Cell spreading, an increased cytoplasmic:nuclear ratio, and greater numbers of broadly bipolar cells, some bearing thin cytoplasmic processes, were seen in cultures treated with 10−6 M all‐trans or 13‐cis retinoic acid. Small tightly packed cuboidal cells and large broadly bipolar cells were seen in astrocytoma cultures from which all‐trans retinoic acid was removed on days 5 and 9. Indirect immunofluorescence revealed more intense staining with antiserum to glial fibrillary acidic protein in cultures treated with 10−6 M all‐trans retinoic acid than in control cultures; electron‐microscope examination of similarly treated cultures revealed more abundant 8–10 nm intermediate filaments than in control cultures. An enzyme‐linked immunosorbent assay showed that all‐trans or 13‐cis retinoic acid caused a dose‐dependent increase in the quantity of glial fibrillary acidic protein in the astrocytoma cells.
Activation of mononuclear cells to be used for hybrid monoclonal antibody‐induced lysis of human ovarian carcinoma cells
Authors: Pupa S. M. , Canevari S. , Fontanelli R. , Ménard S. , Mezzanzanica D. , Lanzavecchia A. , Colnaghi M. I. 
Published: February 2007

AbstractRecently we reported that cytotoxic T‐cell clones can be retargeted to unrelated tumor cells by bispecific monoclonal antbodies (MAbs), anti‐CD3 and anti‐ovarian carcinoma (αOC/TR) (Mezzanzanica et al., 1988). In the perspective of in vivo tumor immunotherapy, as an alternative to cytotoxic T lymphocytes (CTL) from T‐cell clones, since human peripheral blood mononuclear cells (PBMCs) without stimulation were quite ineffective, a suitable in vitro activation method was developed to render PBMCs lytic for relevant targets in the presence of the bispecific hybrid MAb αOC/TR. This activation protocol was applied to PBMCs from 9 healthy donors (HD) and 6 ovarian carcinoma patients (P) and to tumorassociated lymphocytes (TAL) from 4 ovarian carcinoma P. The method consisted of in vitro stimulation with phytohemagglutinin (PHA) for 2 days, followed by culture with a low dose of recombinant human interleukin‐2 (rIL‐2) for 6 to 10 days. The antibody‐mediated lysis of CTL from HD PBMCs was found to be specifically directed against cells expressing the relevant ovarian tumor antigen when different tumor cell lines and short‐term cultures of tumor and normal cells were tested. The antibody‐mediated lysis of CTL from P PBMCs or TAL was efficient both on autologous and allogeneic ovarian tumor cells, whereas no reactivity with autologous normal cells was observed and LAK activity was only evident in I out of 4 cases. The hybrid antibody induced cytotoxic activity of CTL from P was, however, lower than that of CTL from HD.
RNA polymerase activity and protein synthesis in mouse tumor‐host liver compared to benign para‐neoplastic reactions
Authors: Ternell Marie , Zachrisson Helen , Lundholm Kent 
Published: February 2007

AbstractElevated protein synthesis in mouse tumor‐host liver is the net result of both stimulatory and inhibitory responses. This study compares the directional change in transcription and synthesis of liver and plasma proteins in tumor‐host liver as compared with para‐neoplastic conditions, such as malnutrition, inflammation, benign cell proliferation and protein deficiency. A methylcholanthrene‐induced sarcoma was used in weight stable mice (C57B1/6J). Inflammation was induced by s. c. turpentine injection, and benign cell proliferation by injection of heat‐killed Corynebacterium parvum. DNA‐dependent RNA‐polymerase activity (I, II and III) (EC2.7. 7.6) was measured in isolated hepatic nuclei. Protein synthesis was measured by labelling of hepatic and plasma proteins following the injection of a “flooding dose” of the labelled amino acid. Benign hepatic cell proliferation and sterile inflammation caused increased rates of transcription, while malnourished and healthy control animals had lower hepatic transcription than animals bearing a malignant tumor. Inflammation was associated with increased activities of free (nonchromatin engaged) RNA polymerase, which was not found in any other para‐neoplastic condition or in the tumor‐host liver. A protein‐ and calorie‐deficient state was associated with depressed hepatic and plasma protein synthesis compared with the tumor condition. Tumor‐host livers had a nonsecretory protein synthesis rate equal to that of normal livers, but 45% higher plasma protein synthesis. Animals with inflammation and benign cell growth had liver protein synthesis rates which were approximately 50% higher than in tumorbearing animals, but plasma protein synthesis in tumor‐bearing animals was comparable with that of animals which had inflammation. Benign cell growth was not associated with an overall elevated plasma protein synthesis. The translation rate per transcription activity was highest in normal animals and decreased in animals suffering from either tumor, protein deficiency or benign cell proliferation. Hepatic protein synthesis in tumor‐host livers is high considering the degree of anorexia and malnutrition, although not as high as in livers from animals with pronounced inflammation. This counter‐regulation in tumor‐host livers may indicate a compensatory state to maintain protein synthesis against attenuating factors such as the declining food intake. Protein metabolism in tumorhost livers represents an unusual combination of findings.
Urokinase‐type plasminogen activator in colorectal carcinomas and adenomatous polyps: Quantitative expression of active and proenzyme
Authors: Sim Pheng‐Siew , Stephens Ross W. , Fayle David R. H. , Doe William F. 
Published: February 2007

AbstractTotal urokinase‐type plasminogen activator (u‐PA) content (proenzyme plus active enzyme) was significantly higher in 20 colorectal carcinomas and in 27 adenomatous polyps than in metaplastic polyps and autologous normal mucosa. u‐PA content was also markedly increased in adenomatous polyps and autologous colonic mucosa removed from familial polyporis coli patients. Using a new monoclonal antibody technique to distinguish the proenzyme of u‐PA from the active enzyme, we found that 70% of the u‐PA in polyp and cancer tissue was present in the proenzyme form compared to 47% in normal colonic mucosa. For colon cancers, there was a significant correlation between their stage of invasiveness and the levels of proenzyme. No correlation was observed between the u‐PA content of adenomatous polyps and their size or degree of dysplasia. Study of the u‐PA content of the colonic mucosa may offer a useful biochemical correlate of epithelial cell transformation in the colon.
Risk factors for breast cancer in chinese women of Beijing
Authors: Tao Su‐Chang , Yu Mimi C. , Ross Ronald K. , Xiu Kuang‐Wei 
Published: February 2007

AbstractA self‐administered questionnaire was completed by 497 Chinese women in Beijing with histologically confirmed breast cancer and by an equal number of age‐ and neighborhood matched control women. High body weight (71 + kg) was a risk factor for breast cancer in women aged 50 + (RR = 1.90), but this effect did not quite reach statistical significance. Nulliparity and late age at first birth were associated with an elevated risk of breast cancer. In comparison to parous women who had their first child before age 20, those who delayed this event until after age 29 had an RR of 1.65. The comparable RR for nulliparous women was 3.72. Late age at menopause was a risk factor for breast cancer. The RR for menopause after age 50 compared to menopause before age 45 was 2.16. High parity and long duration of lactation were protective factors against breast cancer. These 2 factors were highly correlated with each other and also with age at first birth. The effect of each on breast cancer risk was somewhat reduced after adjustment for the other two. A personal history of benign breast disease (RR = 3.21) and a family history of breast cancer (RR = 2.17) were also associated with an increased risk of breast cancer.