bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of mouse urothelial cell lines in different phases of transitional‐cell carcinogenesis
Authors: De Boer W. I. , Rebel J. M. J. , Foekens J. A. , Vermey M. , Van Der Kwast T. H. 
Published: February 2007

AbstractAltered cellular responsiveness to growth factors is one of the factors involved in carcinogenesis. In order to study the role of growth factors in transitional‐cell carcinogenesis, we established 3 urothelial cell lines from normal mouse urothelium, designated g/G, NUC‐5 and NUC‐I. These cell lines were studied by light and transmission electron microscopy, karyotyp‐ing, grafting in syngeneic mice, growth‐factor response in vitro under serum‐free conditions, and EGF receptor expression. In the presence of insulin or insulin‐like growth factors I and II, proliferation of the non‐tumorigenic DNA‐tetraploid g/G and DNA aneuploid NUC‐5 cells is stimulated by EGF, TGFα, bFGF and aFGF. This stimulation can be abolished in g/G but not in NUC‐5 cells by simultaneous addition of TGFβ. Proliferation of g/G and NUC‐5 cells can also be stimulated by PDGF‐AA. The spindle‐cell‐like NUC‐I cells are DNA aneuploid and tumori‐genic in syngeneic mice; they express low levels of EGF receptors and their autonomous proliferation is only affected by insulin or insulin‐like growth factors. Each of these cell lines seems to reflect a different phase in transitional‐cell carcinogenesis: g/G cells have gained immortality, have become tetraploid, but are non‐tumorigenic and growth‐factor‐dependent. NUC‐5 cells have become aneuploid, have a growth‐factor responsiveness different from that of normal epithelial cells, but are still non‐tumorigenic. NUC‐1 cells are aneuploid, tumorigenic, and growth‐factor‐independent. These urothelial cell lines provide a suitable tool for further studies in transitional‐cell carcinogenesis.
Risk of kidney cancer among patients using analgesics and diuretics: A population‐based cohort study
Authors: Lindblad Per , McLaughlin Joseph K. , Mellemgaard Anders , Adami Hans‐Olov 
Published: February 2007

AbstractThe aim of this study was to determine the risk of kidney cancer in 2 cohorts defined on the basis of hospital discharge diagnoses associated with analgesic or diuretic use during the period 1965 to 1983. Patients were followed up through 1984 for cancer incidence. After excluding cancers in the first year of observation, 161 kidney cancers were observed vs. 138 expected among 54,662 patients in the analgesics cohort. The relative risk was higher for women than for men. When examined by sub‐site within the kidney, risk for cancer of the renal pelvis was similar in magnitude to that for the renal parenchyma. Among 115,616 patients in the diuretics cohort, 278 kidney cancers occurred vs. 209 expected. The risk for women was higher than for men. This elevation in risk was confined to cancer of the renal parenchyma, with no significantly increased risk seen for cancer of the renal pelvis. Although we observed little excess risk among members of the analgesics cohort, the significantly elevated risk among patients using diuretics supports a number of recent studies, but inability to adjust for confounding factors such as obesity preclude drawing any conclusion regarding diuretics. Further research is warranted to assess in detail the relationship between diuretic use and cancer of the renal parenchyma. © 1993 Wiley‐Liss, Inc.
Demonstration of a TGF‐α‐EGF‐receptor autocrine loop and c‐myc protein over‐expression in papillary thyroid carcinomas
Authors: Haugen D. R. F. , Akslen L. A. , Varhaug J. E. , Lillehaug J. R. 
Published: February 2007

AbstractAutocrine growth stimulation has been identified in several types of human cancer. In the present study we wanted to establish whether autocrine stimulation of the epidermal‐growth‐factor receptor (EGF‐r) by its ligand, transforming growth factor alpha (TGF‐α) occurs in thyroid neoplasia. We examined 190 fresh, frozen thyroid tissue samples from 70 patients by immunohistochemistry with antibodies to EGF‐r, TGF‐α, c‐erbB‐2 and c‐myc. EGF‐r expression was detected in 17 out of 19 papillary carcinomas, TGF‐a expression in 10, and c‐erbB‐2 expression in IS. No papillary carcinoma expressed TGF‐a without also expressing EGF‐r. Concomitant expression of EGF‐r, TGF‐α and c‐erbB‐2 was seen in 7 papillary carcinomas. No EGF‐r, TGF‐α or c‐erbB‐2 immunopositivity was found in normal‐appearing thyroid tissue (25 cases), whereas a few of the non‐neoplastic lesions (colloid goitres and diffuse hyperplasias) expressed either EGF‐r or TGF‐α. c‐myc expression was detectable in all tissue samples, and expression was invariably nuclear. Increased expression was observed in 10 out of 19 papillary carcinomas, and 8 of these also co‐expressed EGF‐r and TGF‐α. In situ hybridization confirmed the presence of TGF‐α mRNA in tumour epithelium of TGF‐α‐immunopositive samples. The concomitant expression of EGF‐r, TGF‐α and TGF‐α mRNA gives evidence for a TGF‐α‐EGF‐r autocrine loop in thyroid papillary carcinomas. The increased c‐myc expression may reflect the proliferative advantage of these tumours. © 1993 Wiley‐Liss, Inc.
Cytogenetic findings in 33 osteosarcomas
Authors: Mertens F. , Mandahl N. , Örndal C. , Baldetorp B. , Bauer H. C. F. , Rydholm A. , Wiebe T. , Willén H. , Åkerman M. , Heim S. , Mitelman F. 
Published: February 2007

AbstractThirty‐three osteosarcomas (OS) were analyzed cytogenetically. Clonal chromosome changes were detected in 17 cases. Six tumors had chromosome numbers in the diploid range, 6 in the triploid range, 1 in the tetraploid range and 1 in the pentaploid range, while 3 tumors had multiple clones with different ploidy levels. Including the present 17 tumors, a total of 27 OS with clonal aberrations have been reported. The recognizable structural rearrangements in these 27 tumors clustered to chromosome arms 1p, 1q, 3p, 3q, 7q, 11p, 17p and 22q. Chromosome bands 1q11, 1q21, 1q42 and 7q11 were the most frequently rearranged, and the most common numerical rearrangements were ‐3, ‐ 10, ‐ 13 and ‐ 15. Supernumerary ring chromosomes, in 2 tumors as the sole change, were found in all 3 parosteal OS, which is in agreement with the findings in 1 previously reported parosteal OS. The association between ring formation and parosteal morphology represents the first cytogenetic‐morphologic entity among OS. © 1993 Wiley‐Liss, Inc.
p53 protein expression in breast cancer as related to histopathological characteristics and prognosis
Authors: Lipponen P. , Ji H. , Aaltomaa S. , Syrjänen S. , Syrjänen K. 
Published: February 2007

AbstractFormalin‐fixed, paraffin‐embedded biopsies of 193 women with primary breast cancer followed‐up for over 10 years were analysed immunohistochemically for the expression of p53 protein. Altogether, 58% (113/193) of the tumors were positive for p53 protein. Over‐expression of p53 was associated with the ductal type, high‐grade tumors, dense stromal inflammatory cell infiltrate, high S‐phase fraction, high mitotic frequency and high values of the nuclear factors. In univariate analysis, intense p53 over‐expression predicted a poor outcome, whereas a short recurrence‐free survival (RFS) was related to p53 negativity. In axillary lymph‐node‐negative (ANN) tumors, p53 negativity was related to short RFS, and in axillary lymph‐node‐positive (ANP) tumors this inverse relationship was statistically significant. In Cox's analysis, p53 protein over‐expression had no independent prognostic value comparable with the well‐established prognostic factors. However, p53 protein accumulation was an independent indicator of long RFS in the entire cohort, in ANP tumors and in rapidly proliferating tumors. The results indicate a dual role for p53 protein over‐expression in breast cancer prognosis. The low survival probability associated with intensively p53‐positive tumors is probably related to rapid cancer‐cell proliferation, whereas the long RFS of p53‐positive tumors might be explained by the development of circulating antibodies to p53 protein. The role of p53 protein in breast cancer is incompletely understood, and the p53 gene should be subjected to detailed analysis of specific mutations. © 1993 Wiley‐Liss, Inc.
Cancer among teenagers in Denmark, 1943‐1987
Authors: Martos M. Carmen , Winther Jeanette F. , Olsen Jørgen H. 
Published: February 2007

AbstractA population‐based study was carried out on 3,988 tumours in teenagers (aged 10‐19 years) diagnosed during the period 1943‐87 in Denmark and abstracted from the files of the National Cancer Registry. In that Registry, codes for tumours were based solely on topography until the end of 1977. In order to obtain a uniform data set, coded by the system of the International Classification of Diseases for Oncology (ICD‐O) now used at the Cancer Registry, all cases of teenage cancer diagnosed prior to 1978 were re‐evaluated, and an ICD‐O code was applied. Tumours were further aggregated into diagnostic groups using an internationally agreed scheme. The average incidence rates for all histological types combined were 136 per million for boys and 108 per million for girls, which are close to those reported in Connecticut, USA. Central nervous system tumours, leukaemia and malignant lymphomas accounted for 60% of all cancers among teenagers. An overall excess of cancers among boys was mainly due to more frequent occurrence of leukaemias, malignant lymphomas, sarcomas and germ‐cell tumours. Increasing trends with time were seen for malignant lymphomas in both boys and girls and for subtypes of non‐seminoma germ‐cell tumour among boys aged 15‐19. For other diagnostic groups, including the main group of leukaemias, the rates have remained largely unchanged, suggesting that environmental factors associated with modern society play a minor role in the aetiology of cancer among teenagers. © 1993 Wiley‐Liss, Inc.
Reduced expression of nm23‐H1, but not of nm23‐H2, is concordant with the frequency of lymph‐node metastasis of human breast cancer
Authors: Tokunaga Yuji , Urano Takeshi , Furukawa Koichi , Kondo Hisayoshi , Kanematsu Takashi , Shiku Hiroshi 
Published: February 2007

AbstractThe nm23 gene is a potential metastasis‐suppressor gene originally identified in a murine melanoma line. Several investigators have reported the probable inverse association of nm23 expression with disease prognosis and/or metastasis. Since there are now 2 known isotypes of human nm23, namely nm23‐H1 and ‐H2, we immunohistochemically examined expression of these isotypes in human breast‐cancer tissues using monoclonal antibodies (MAbs) specific for each isotype protein. We also analyzed expression of c‐erbB‐2 in the same collection of cancer tissues, in order to examine the significance of nm23 expression in comparison with c‐erbB‐2 expression. Of 130 tumors from breast‐cancer patients, 73 (56%) and 69 (53%) positively expressed nm23‐H1 and ‐H2 respectively. Expression of c‐erbB‐2 was positive in 36 (28%). Expression of nm23‐H1, but not nm23‐H2, was inversely associated with lymph‐node metastasis (p < 0.01). Expression of c‐erbB‐2 was associated with Tnm stage, tumor size and lymph‐node metastasis (p < 0.01, p < 0.05 and p < 0.05 respectively). Overall survival was better (p = 0.014) in patients in whom expression of nm23‐H1 was positive than in those in whom it was negative. In multivariate analyses using a Cox's proportional‐hazards regression model with 9 variables, nm23‐H1 showed the fourth greatest contribution to patient survival following lymph‐node metastasis, Tnm stage and menopausal status. No significant contribution was shown for c‐erbB‐2 expression. nm23‐H1, but not nm23‐H2, may perform a role in disease prognosis in addition to its participation in cancer metastasis. It may have value for predicting long‐term survival of human breast‐cancer patients. © 1993 Wiley‐Liss, Inc.
Cytotoxicity, differentiating activity and metabolism of tiazofurin in human neuroblastoma cells
Authors: Pillwein Konrad , Schuchter Katharina , Ressmann Gabi , Gharehbaghi Kamran , Knoflach Andreas , Cermak Benedikt , Jayaram Hiremagalur N. , Szalay Stefan M. , Szekeres Thomas , Chiba Peter 
Published: February 2007

AbstractThe IMP dehydrogenase inhibitor, tiazofurin (TR)‐2‐β‐D‐ribofuranosylthiazole‐4‐carboxamide, which exhibited oncolytic activity in patients with chronic myelogenous leukaemia (CML) in blast crisis was found to inhibit the growth of human neuroblastoma SK‐N‐SH cells with an IC50 of 4.2 μM. TR treatment of cells perturbed nucleic acid and catecholamine pathways. As biochemical markers of TR action decreased cellular GTP pools, increased inosine and hypoxanthine concentrations and depleted dopamine content were found. Incubation of tumour specimens obtained from paediatric patients with grade‐IV neuroblastoma with TR resulted in the formation of the active metabolite, thiazole‐4‐carboxamide adenine dinucleotide, in concentrations sufficient to inhibit tumour growth. Cytotoxic and biochemical effects of TR were enhanced by combining it with allopurinol (an inhibitor of xanthine dehydrogenase), and hypoxanthine (an alternate substrate for hypoxanthine‐guanine phosphoribosyltransferase). Induction of transdifferentiation of SK‐N‐SH cells from a neuroblast to an epitheloid, substrate‐adherent phenotype was more pronounced with TR than with all‐trans‐retinoic acid. Transdifferentiating treatment with TR resulted in a 2‐fold‐enhanced sensitivity towards adriamycin. However, differentiation with all‐trans‐retinoic acid rendered the cells more resistant to adriamycin. Our results suggest that TR might be a promising agent for the treatment of children suffering from neuroblastoma. © 1993 Wiley‐Liss, Inc.
Altered expression of basement‐membrane components and collagenases in ascitic xenografts of OVCAR‐3 ovarian cancer cells
Authors: Liebman Jeffrey M. , Burbelo Peter D. , Yamada Yoshihiko , Fridman Rafael , Kleinman Hynda K. 
Published: February 2007

AbstractAscitic ovarian cancer cells, which derive from solid tumors, complicate the treatment of ovarian cancer by spreading throughout the peritoneal cavity. Because basement‐membrane components may influence tumor‐cell proliferation and dissemination, the present studies examined the production of (a) basement‐membrane attachment and migration factors (laminin, fibronectin and type IV collagen); (b) a laminin receptor, the 32/67‐kDa laminin‐binding protein, the presence of which correlates with malignancy; and (c) metalloproteinases (types I and IV collagenase and stromelysin), by ascitic and cultured OVCAR‐3 cells and solid OVCAR‐3 tumors. The cultured cells and solid tumors produced high levels of mRNA encoding attachment factors and metalloproteinases, and low levels of mRNA for the 32/67‐kDa laminin receptor. In contrast, the ascitic ovarian cells had low or undetectable levels of mRNA encoding laminin, type IV collagen and metalloproteinases, but higher levels of transcripts for the laminin receptor. Our results suggest that the apparent inability of ascitic OVCAR‐3 cells to attach to host‐tissue surfaces may be a consequence, in part, of low levels of expression of laminin, type IV collagen and/or type IV collagenase. © 1993 Wiley‐Liss, Inc.
Correlation between the growth‐inhibitory effect of TGF‐β1 and phenotypic characteristics in a panel of B‐cell lines
Authors: Altiok Aysin , Ehlin‐Henriksson Barbro , Klein Eva 
Published: February 2007

AbstractHuman B‐cell lines established from Burkitt lymphoma (BL) and normal B cells immortalized in vitro by EBV (LCLs) differ in phenotype. While the BL correspond to resting B cells, the LCLs resemble activated B cells. When BLs which have the EBV genome are carried in vitro, they acquire some of the features of LCLs, such as expression of B‐cell activation markers and the tendency to form aggregates. Comparison of several B‐cell lines for sensitivity to TGF‐β showed that the growth of BLs (with few exceptions), but not of the LCLs, was inhibited. The results suggested that the sensitivity to TGF‐β correlates with the cellular phenotype. In the present work, this assumption is even more critically substantiated by studying 2 sublines of an EBV‐genome carrying BL line, Mutu, which were selected for single cells and aggregates. The former (with resting phenotype) was inhibited, while the subline of aggregated cells, which also expressed B‐cell activation markers, was not inhibited. Somatic‐cell hybrids between BLs, LCLs and non‐B cells provided lines with phenotypic differences. Results with a panel of such hybrid lines also showed that those which express the activated B‐cell phenotype are not inhibited by TGF‐β. Differences in the levels of expression of activation markers did not influence the response to TGF‐β. © 1993 Wiley‐Liss, Inc.
Cytokines as adjuvants: Effect on the immunogenicity of NeuAcα2‐6GalNAcα‐O‐Ser/Thr (sialyl‐Tn)
Authors: Piera Mercé , de Bolós Carme , Castro Rosa , Real Francisco X. 
Published: February 2007

AbstractSialyl‐Tn, defined by monoclonal antibody (MAb) B72.3, shows restricted normal‐tissue distribution but is expressed in a wide variety of carcinomas. To analyze the immunogenicity of sialyl‐Tn, mice were immunized with ovine submaxillary mucin (OSM) in combination with monophosphoryl lipid A (MPLA), liposomes, or adjuvants that activate macrophages (rIL‐1, rlFN‐gamma, rM‐CSF, IL‐1‐derived peptides) or T cells (HL‐2). The level and specificity of the immune response were analyzed by ELISA. rIL‐l and rIFN‐gamma induced a very high and specific antibody response, whereas the effect of rM‐CSF was dose‐dependent: at a low dose it induced a high‐level specific antibody response and at the high dose level it induced a polyclonal non‐specific response. These results indicate that cytokines are powerful adjuvants which modulate both the magnitude and specificity of the immune response. More studies are necessary to determine the optimal doses in animal models and in active specific immunotherapy of patients with cancer. © 1993 Wiley‐Liss, Inc.
Human melanoma cells express a functional interleukin‐2 receptor
Authors: Plaisance S. , Rubinstein E. , Alileche A. , Han D. S. , Sahraoui Y. , Mingari M. C. , Bellomo R. , Rimoldi D. , Colombo M. P. , Jasmin C. , Carrel S. , Azzarone B. 
Published: February 2007

AbstractFlow cytometric analysis reveals that 5 human melanoma cell lines (M14, IGR3, MEI 477, JUSO, GLL 19) express both α and β chain of the interleukin 2 receptor (IL‐2Rα and IL‐2Rβ). These chains are able to specifically bind IL‐2 and to form high‐affinity heterodimers (IL‐2Rαβ). Analysis of poly A+ RNAs by Northern blot reveals the presence of typical transcripts for both the IL‐2Rα gene (3.6 kb) and the IL‐2Rβ gene (4 kb). Reverse transcription/polymerase chain reaction analysis allowed transcripts for the IL.2Rγ (p64) gene to be detected in 3 of these melanoma cell lines (M 14, IGR3, ME 1477). Incubation with human recombinant IL‐2 modifies in IL‐2Rα+β+γ+ (M14) the expression of several surface molecules: down‐regulation of ICAM‐1, HLA class I and HLA‐DR and up‐regulation of CD44. IL‐2 is also active on IL‐2α+β+γ− cell lines since it decreases ICAM‐1 and HLA class‐II expression at the surface of JUSO cells. Down‐regulation of ICAM‐1, whose expression in melanoma cells is a marker of tumor progression, is detectable within 3 hr in MI4 cells and is maximal after 48 hr incubation, at IL‐2 concentrations corresponding to the high‐affinity heterodimers. This feature is specific since it is partially inhibited by MAbs directed against the IL‐2 binding site of the IL‐2Rα (MAR93, 10TI4) and IL‐2Rβ (MiKβ1, TU27) chains. Our data support the notion of a direct effect of IL‐2 on human melanoma cells. Modulation of the expression of surface molecules which is important for the interaction with immunocompetent cells or for tumor progression, could have a role to play during in vivo IL‐2 treatment of human melanomas. © 1993 Wiley‐Liss, Inc.
Diet and risk of gastric cancer. A population‐based case‐control study in Sweden
Authors: Hansson Lars‐Erik , Nyrén Olof , Bergström Reinhold , Wolk Alicja , Lindgren Anders , Baron John , Adami Hans‐Olov 
Published: February 2007

AbstractA case‐control study to evaluate risk factors of gastric cancer was carried out in areas with contrasting incidence rates in Sweden. Face‐to‐face interviews were conducted with 338 of 456 eligible histologically confirmed gastric‐cancer cases and 669 of 880 eligible control subjects, sampled from population registers and frequency‐matched by age and gender. We focused on 2 periods, adolescence and 20 years prior to interview. The association of gastric‐cancer risk with dietary habits during adolescence were similar to that found for the period 20 years before interview; high consumption of wholemeal bread, fruit and vegetables was associated with reduced gastric‐cancer risk. In addition, cheese, fish and tea had a protective effect during adolescence. Increased gastric‐cancer risk was related to whole‐milk consumption, but this association decreased substantially in a multivariate analysis including vegetables. There was a positive relationship between gastric‐cancer risk and the age at which the interviewees started using refrigerators. This population‐based study confirmed the protective effect of a high consumption of vegetables and fruit in the development of gastric cancer, but failed to find any association between intake of meat, sausage, cold cuts, liver, salt, coffee, the habit of frying, smoking or grilling foods, and risk of gastric cancer.
Cancer incidence in estonian migrants to Sweden
Authors: Nilsson Bo , Gustavson‐Kadaka Evi , Rotstein Samuel , Hakulinen Timo , Rahu Mati , Aareleid Tiiu 
Published: February 2007

AbstractCancer incidence in Estonians who took refuge in Sweden in 1944‐1945 has been compared with that in the total Swedish population and that among Estonians in Estonia in 1974‐1985 using data from the Swedish and the Estonian countrywide population‐based cancer registries. The vast majority of the Estonian immigrants studied had been living in Sweden for 30 years when the follow‐up with respect to cancer incidence started in this investigation. In spite of the long residence in Sweden, differences in cancer incidence could be observed between these immigrants and the total Swedish population. The age‐standardized incidence of stomach cancer was higher in the Estonian migrants than in the total Swedish population (SIR = 1.6 and 2.1 for males and females, respectively). Breast cancer incidence was lower in the migrant women (SIR = 0.75) and lung cancer incidence higher in migrant men (SIR = 1.5). An increased incidence of colorectal cancer was also found for both sexes in the migrant population (SIR = 1.4 for both males and females). A comparison between Estonians in Estonia and the total Swedish population revealed that the cancer incidence for the Estonians was lower than expected at age 70 and over. Male lung cancer and stomach cancer showed a higher incidence in the Estonian population than in the Swedish and in the migrant populations. The migrant population showed an intermediate incidence relative to Estonians in Estonia and the entire Swedish population. The colon‐cancer risk in Estonian migrants to Sweden was higher than the risk for Estonians in Estonia and for the Swedish population. This contrasts with most findings in the present and other studies on intermediate risks of migrants compared to the risks in the country of origin and in the new country of residence.