bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trends in cervical and breast cancer in Iceland. A statistical evaluation of trends in incidence and mortality for the period 1955–1989, their relation to screening and prediction to the year 2000
Authors: Sigurdsson Kristjan , Adalsteinsson Stefan , Ragnarsson Jonas 
Published: February 2007

AbstractThe time trends in incidence and mortality from cervical cancer and breast cancer in Iceland, from 1955 to 1989, were analyzed by fitting curvilinear regressions to the age‐standardized rates. The effect of the screening was evaluated by comparing the curvature of the fitted regression lines and changes in screening activity. The incidence and mortality rates for both cancer types were predicted up to the year 2000. At the commencement of cervical cancer screening in 1964, both the incidence and mortality rates were on the increase. After 1970, both rates decreased significantly. Assuming that regular attendance at screening will be 85%, It is predicted that the incidence and mortality rates will level out at about 7.5 and 2 cases per 100,000 women per year, respectively, by the year 1995 and remain at that level. The incidence of breast cancer has increased steadily since 1955. A sharp rise has been observed since 1987, due to screening with mammography. The mortality rate has shown small but significant fluctuations with time. The incidence rate is predicted to increase at the same rate as before 1987 (i.e. at 1.1 cases per 100,000 women per year), but at a slightly higher level and is predicted to reach 84 cases per 100,000 women per year by the year 2000. Breast cancer mortality is predicted to decrease to about 17 cases per 100,000 women per year by 1995 and to remain at that level.
Establishment and characterization of Epstein‐Barr virus gp350‐expressing transfected human lymphoid (Raji) cell clones
Authors: Khyatti Menem , Patel Pravin C. , Menezes José 
Published: February 2007

AbstractGp350, a late Epstein‐Barr‐virus (EBV) glycoprotein expressed on both the envelope of viral particles and EBV‐producing cells, is also the candidate for the development of an anti‐EBV subunit vaccine. This glycoprotein is thought to play an important role in anti‐EBV immunity. However, studies on the role of this viral antigen in cellular cytotoxicity and other immune functions have been hampered by the lack of a suitable model expressing gp350. We describe here a study in which we successfully transfected a gp350‐negative cell line resistant to natural‐killer(NK)‐cell activity (i.e., Raji) with a recombinant plasmid (pZIP‐MA) containing the EBV‐gp350 and the neomycin resistance gene. Three clones with a stable and strong expression of gp350 on their surface membrane, as demonstrated using a gp350‐specific (i.e., 2L10) monoclonal antibody (MAb) were isolated, characterized and used as targets in an antibody‐dependent cellular cytotoxicity (ADCC) assay. However, gp350 expression on 2 of the 3 isolated clones was not recognized by an anti‐gp350 MAb (72AI) which is specific to a unique gp350 epitope with a dual function (i.e., involved in both EBV binding to its target cell receptors and in Inducing virus‐neutralizing antibody). We have also found that gp350 expression on our 3 selected clones does not affect EBV‐receptor (CR2) density. Our model of gp350‐expressing, NK‐cell‐activity‐resistant targets revealed very useful In determining that gp350 serves as a target antigen for EBV‐specific ADCC. These gp350‐expressing cell clones appear to represent a valuable tool for diagnostic purposes (i.e., for detecting and titrating gp350 antibodies in patients with EBV‐associated diseases). Our approach should also prove useful for studying the expression of other cell‐surface‐associated viral and tumor antigens and their role in specific cellular immunity and immunosurveillance.
Differential in vitro sensitivity of human tumor and normal cells to chemotherapeutic agents and resistance modulators
Authors: Nygren Peter , Larsson Rolf 
Published: February 2007

AbstractThe intrinsically Vincristine(Ver)‐resistant human kidney adenocarcinoma cell line ACHN, the human acute lympho‐blastic leukemia cell line L0, Its more‐than‐100‐fold Ver‐resistant subline L100, normal human fibroblasts and lymphocytes, also tumor cells from patients with chronic lymphocytic leukemia (CLL), acute myeloblastic leukemia (AML) and solid tumors, were compared for sensitivity to cytotoxic drugs and resistance modulators (RMs). The L100 cells showed pronounced sensitivity to the RMs verapamil (Ver), cyclosporin A (CsA) and buthionine sulfoximine (BSO) alone as well as to clsplatinum, whereas the L0 and ACHN cells, also slowly growing fibroblasts and non‐proliferating lymphocytes, were considerably less sensitive. Compared with AML cells and lymphocytes, CLL cells were more sensitive to Ver and CsA alone. The cytotoxlcity of Vcr was significantly increased in the Vcr‐resistant ACHN and L100, but also in sensitive L0 cells by Ver and CsA, with smaller effects on Dox and Vp‐16 toxicity. Fibroblasts and lymphocytes were generally resistant to the cytotoxic agents and RM addition had only minor effects. CLL cells were more sensitive to Dox and Ver as compared with normal lymphocytes, with potentiation of the Ver effect by Ver and CsA. The Ver effect in non‐proliferating Vcr‐resistant cells from a malignant schwannoma was potentiated by Ver and CsA, which had no effect in cells from a kidney adenocarcinoma. We conclude that cytotoxlcity of RMs alone is not dependent on the proliferation rate of tumor cells and that potentiation of cytotoxic drugs by RMs may be selective for tumor cells irrespective of their initial level and mode of drug resistance.
Attenuating effect of the monoamine oxidase inhibitor furazolidone on the anti‐carcinogenetic effect of cysteamine on gastric carcinogenesis induced by N‐methyl‐N′‐nitro‐N‐nitrosoguanidine in Wistar rats
Authors: Tatsuta Masaharu , Iishi Hiroyasu , Baba Miyako , Taniguchi Haruo 
Published: February 2007

AbstractThe effect of furazolidone on inhibition by cysteamine of gastric carcinogenesis induced by N‐methyl‐N′‐nitro‐N‐nltrosoguanidine (MNNG) was investigated in inbred Wistar rats. After oral treatment with MNNG for 25 weeks, rats received cysteamine, furazolidone, or both compounds. In week 52, rats treated with cysteamine had a significantly decreased incidence of gastric cancers. Concomitant treatment with furazolidone significantly attenuated the inhibitory effect of cysteamine on gastric carcinogenesis. Administration of furazolidone alone significantly increased the number, but not the incidence, of gastric cancers. The norepinephrine concentration of the antral portion of the gastric wall and the labelling index of the antral mucosa were significantly reduced in rats treated with cysteamine, and significantly higher in rats treated with both compounds than in those treated with cysteamine alone. These findings indicate that the cysteamine‐induced inhibition of gastric carcinogenesis is mediated by catecholamlnes.
Production of a recombinant human T‐cell leukemia virus type‐I trans‐activator (tax1) antigen and its utilization for generation of monoclonal antibodies against various epitopes on the tax1 antigen
Authors: Tanaka Yuetsu , Yoshida Atsushi , Tozawa Hideki , Shida Hisatoshi , Nyunoya Hiroshi , Shimotohno Kunitada 
Published: February 2007

AbstractA 42‐kDa recombinant protein, PX141, consisting of the trans‐activator protein encoded by human T‐cell leukemia virus (HTLV‐I) (tax, antigen) and the amino‐terminal fusion peptide of 12 amino acid residues of the a‐peptide encoded by the plasmid pUC19 was produced. In order to investigate the immunogenicity of the tax, antigen, mice were immunized with the purified PX141 and 4 anti‐tax, monoclonal antibodies (MAbs) designated TAXY‐I, TAXY‐6, TAXY‐7 and TAXY‐8 were generated, and their reactivity was characterized along with another anti‐tax, MAb, Lt‐4. Immunoblot assays showed that all the MAbs reacted with the PX141, the native tax, antigen expressed in various HTLV‐I‐infected cell lines and the gp68 of MT‐2 cells expressing the tax, amino acids 94–353. Immunoblot assays using recombinant, truncated tax, antigens, XD59 (expressing amino acids 180–338) and XD128 (expressing amino acids 1–47 and 286–353) showed that: (I) TAXY‐I and Lt‐4 did not react with either antigen; (2) TAXY‐6 and TAXY‐8 reacted with only XD128; and (3) TAXY‐7 reacted with both. In addition, TAXY‐I, but not the other MAbs, reacted with a putative tax antigen of an STLV‐I‐infected cell line, designated RfM26‐I. Competitive binding assays showed that TAXY‐6 and TAXY‐8 did not compete against each other. Sera from HTLV‐I‐infected humans interfered with the binding of all of these anti‐tax, MAbs. These results indicate that the tax1 antigen and the PX141 express at least 5 distinct epitopes recognized by human and mouse antibodies.
Epidemiological and clinical correlations with genetic characteristics of Wilms' tumor: Results of the Brazilian Wilms' tumor study group
Authors: Franco Eduardo L. , de Camargo Beatriz , Saba Leda , Marques Lourdes A. ,   Brazilian Wilms' Tumor Study Group
Published: February 2007

AbstractThe epidemiological and clinical features of Wllms' tumor (WT) were analyzed in 176 patients admitted to the Brazilian WT Study Group. The occurrence of congenital anomalies (9.1%) and the M:F ratio (0.83) were comparable to those observed by the US National WT Study and the International Society of Pediatric Oncology trials. Bilateral cases were younger on average than unilateral cases (37.2 vs. 45.0 months). Ethnic group and gender were also associated with age, with non‐white children being generally older (46.1 months) than whites (39.5 months), and boys being younger than girls (37.0 vs. 44.1 months). However, the most important factor in association with age at diagnosis was disease stage. No early disease patients were diagnosed after 8 years of age (mean: 37.S months), whereas 10% of those with advanced disease were diagnosed between the ages of 8 and 10 years (mean: 56.3 months). There were no clear distinctions in age distributions on the basis of the presence of tumor multicentrlcity, intra‐or perilobar nephroblastomatosis, and of a combination of putative genetic determinants. The mean age at diagnosis for cases with congenital defects was higher than that for the remaining patients. Some of the study results are in support of the recessive oncogene model for WT. However, the possible confounding effect of disease stage and the strong Interdependence of the remaining factors may be masking important relations in regard to mutational events occurring during embryogenesis.
Detection of anti‐epstein‐barr‐virus transactivator (ZEBRA) antibodies in sera from patients with nasopharyngeal carcinoma
Authors: Joab Irène , Nicolas Jean‐Claude , Schwaab Guy , de‐Thé Guy , Clausse Bernard , Perricaudet Michel , Zeng Yi 
Published: February 2007

AbstractThe Epstein‐Barr virus (EBV) is a ubiquitous Herpes virus which causes infectious mononucleosis and is associated with such different neoplasms as Burkitt's lymphoma and nasopharyngeal carcinoma. EBV latently infects its target cells; nevertheless, evidence of viral replication in NPC tumours has been uncovered. Among the EBV transactivators, the ZEBRA protein plays a crucial role in switching the virus from a latent to a productive mode. ZEBRA protein was produced using a eukaryotlc expression vector: the open reading frame containing the BZFLI cDNA has previously been inserted downstream from the adenovirus major late promoter leading to expression of a 38‐kDa nuclear protein. We performed serological studies by employing ZEBRA protein expressed in human cells for immunofluorescence and Western‐blot assays. We were able to detect IgG anti‐ZEBRA antibodies (IgG/ZEBRA) in 87% of NPC patients. These antibodies were absent in control sera; IgG/ZEBRA antibodies can be proposed as a useful marker for diagnosis of NPC tumors.
A cell line (LIM 2463) derived from a tubulovillous adenoma of the rectum
Authors: Whitehead Robert H. , van Eeden Pauline , Lukeis Robyn E. 
Published: February 2007

AbstractWe describe a new epithelial cell line (LIM 2463) derived from tubulovillous adenoma of the rectum. The cells grow as organoids and secrete large amounts of mucus. The cells are polarized, with a microvillar brush border, and express dipeptidyl peptidase IV in a polarized manner. No staining was seen with 3 other antibodies directed against other brush‐border hydrolases or disaccharidases. Focal polarized staining was obtained with 2 antibodies directed against other brush‐border‐associated peptides. The cells are aneuploid with a distinctive karyotype (48, XX, +9, +13). All attempts to clone the cells in semi‐solid agar or to grow them as xenografts in nude athymic mice have failed.
Establishment from a human chondrosarcoma of a new immortal cell line with high tumorigenicity in vivo, which is able to form proteoglycan‐rich cartilage‐like nodules and to respond to insulin in vitro
Authors: Takigawa Masaharu , Pan Hai‐Ou , Kinoshita Akihiro , Tajima Koji , Takano Yoshiro 
Published: February 2007

AbstractThe human chondrosarcoma cell line (HCS‐2/8) established by our group expresses cartilage phenotypes such as production of cartilage‐type proteoglycans and collagen type II, but its tumorigenicity is low. To develop an in vitro experimental system for studies of human chondrosarcomas, a new immortal cell line of human chondrosarcoma, named HCS‐2/A, was established from the same tumor. HCS‐2/A cells proliferated with a doubling time of 3° days in a medium containing 20% fetal bovine serum (FBS). This growth rate was comparable to that of HCS‐2/8 cells. However, HCS‐2/A cells proliferated more rapidly than HCS‐2/8 cells in the presence of 2–10% FBS. Like HCS‐2/8 cells, HCS‐2/A cells had a polygonal shape in sparse cultures and became spherical as they reached confluence, after which they formed nodules composed of multi‐layered cells and a large quantity of extracellular matrix showing strong metachromasia. The nodules formed by HCS‐2/A cells were thicker and also larger in diameter than those formed by HCS‐2/8 cells. Electron microscopically, the cells in the nodules resembled chondrocytes in vivo, but each cell had an irregular‐shaped nucleus which is a characteristic of tumor cells. The cells actively synthesized “cartilage‐specific” large proteoglycans and their level of proteoglycan synthesis was comparable to that of HCS‐2/8 cells. Insulin, which stimulates proteoglycan and DNA syntheses in cultured chondrocytes, markedly Increased proteoglycan synthesis in HCS‐2/A cells. On the other hand, the hormone only slightly increased proteoglycan synthesis in HCS‐2/8 cells. Insulin also stimulated DNA synthesis in cultured HCS‐2/A cells, but not in HCS‐2/8 cells. Immunostaining revealed that HCS‐2/A cells produced type‐11 collagen but not type‐1 collagen. However, the level of collagen synthesis of HCS‐2/A cells was lower than that of HCS‐2/8 cells. Inoculation of HCS‐2/A cells into athymic mice resulted in the formation of chondrosarcomas that grew faster than those arising from HCS‐2/8 cells.
Localization of monoclonal antibody G250 and bispecific monoclonal antibody CD3/G250 in human renal‐cell carcinoma xenografts: Relative effects of size and affinity
Authors: van Dijk J. , Zegveld S. Th. , Fleuren G. J. , Warnaar S. O. 
Published: February 2007

AbstractA study was made of the relative effects of size and binding strength of various forms of the monoclonal antibody (MAb) G250, reacting with primary and metastatic human renal‐cell carcinoma (RCC), on the localization in human RCC xenografts in nude mice. Preferential tumor localization was demonstrated after injection of 1251‐labelled intact IgG, with increasing tumor/non‐tumor ratios in time. Approximately 27.4% of the injected dose/gram (%ID/g) was localized in the xenograft 24 hr post‐injection. A control MAb did not preferentially localize in xenografts. With F(ab′), fragments, higher tumor/blood ratios were obtained, although a lower percentage of injected dose per gram was bound to the tumor, 24 and 48 hr post‐injection. Using a bispecific MAb CD3/G250 F(ab′)2 fragment, which reacts with CD3 on human T lymphocytes and binds monovalently to RCC, an enhanced accumulation in tumor tissue was also observed. The %ID/g tumor obtained with bispecific CD3/G250 F(ab′)2 was comparable with %ID/g tumor found with G250 F(ab′)2. The 10‐fold lower binding affinity to RCC compared with intact IgG or F(ab′)2 had only marginal effects on %ID/g tumor. These results show that MAb G250 preferentially localizes to RCC xenografts. Because injection of F(ab′)2 fragments resulted in higher tumor/non‐tumor ratios, G250 F(ab′)2 may therefore be more suitable for diagnostic evaluation of RCC in patients. The tumor uptake is more dependent on size than on affinity. Furthermore, the data obtained with bispecific MAb CD3/G250 F(ab′)2 support the hypothesis that this bispecific MAb may be able to target cytotoxic T lymphocytes to RCC in humans to mediate destruction of RCC.
A novel recombinant tumor necrosis factor‐alpha mutant with increased anti‐tumor activity and lower toxicity
Authors: Nakamura Satoshi , Kato Arata , Masegi Tsukio , Fukuoka Masami , Kitai Kazuo , Ogawa Hiroko , Ichikawa Yataro , Maeda Masahiro , Watanabe Naoki , Kohgo Yutaka , Niitsu Yoshiro 
Published: February 2007

AbstractWe prepared a novel recombinant tumor necrosis factor‐α (TNF) mutant (mutant 471), in which 7 N‐terminal aminoacids were deleted and Pro8Ser9Asp10 was replaced by ArgLysArg, and compared its biological activity with that of wild‐type recombinant TNF. Mutant 471 had a 7‐fold higher anti‐tumor activity against murine L‐M cells in vitro, and a higher binding activity to TNF receptors on L‐M cells, than wild‐type TNF. Furthermore, mutant 471 showed a higher anti‐tumor effect on murine Meth A‐HM tumors transplanted Into BALB/c mice, with complete regression of the tumors being observed in the animals. The possible cachectin activity of mutant 471 was almost the same as that of wild‐type TNF. The acute lethal toxicity of mutant 471 in β‐D‐galactos‐amine‐sensitized C3H/HeJ mice was 18 times lower than that of wild‐type TNF. These results suggest that mutant 471 might be a more promising anti‐cancer agent than wild‐type TNF.
The effects of γ‐interferon combined with 5‐fluorouracil or 5‐fluoro‐2′‐deoxyuridine on proliferation and antigen expression in a panel of human colorectal cancer cell lines
Authors: Maas Ingrid W. H. M. , Boven Epie , Pinedo Herbert M. , Schlüper Hennie M. M. , Haisma Hidde J. 
Published: February 2007

AbstractGamma‐lnterferon (IFN‐γ) and the antimetabolites 5‐fluorouracil (5‐FU) and 5‐fluoro‐2′‐deoxyuridine (FUdR) were investigated as individual agents and in combination for their In vitro antiproliferative capacity and for their effect on the expression of HLA class‐1 antigen, carcinoembryonic antigen (CEA) and the intracellular tumor‐associated antigen CTA‐I In 7 human colorectal cancer cell lines: WiDr, HT29, Colo 205, SW1116, LS174T, SW1398, and LoVo. Growth inhibition by IFN‐γ at clinically relevant concentrations (50–100 U/ml) was found in 4/7 cell lines. The cell lines were equally sensitive to 5‐FU (IC50, in a range of 2–10 μM), while sensitivity to FUdR varied considerably (IC50 in a range of 0.01–90 μM). When 50 U/ml IFN‐γ were combined with 5‐FU or FUdR, the antiproliferative effects were synergistic in those cell lines with sensitivity to IFN‐γ as a single agent, but not in the IFN‐γ‐insensitive cell lines. IFN‐γ was able to enhance the expression of HLA Class I and CEA in 4/7 and 3/7 cell lines, respectively, as measured by flow cytometry. CTA‐1 expression could not be enhanced with IFN‐γ. The expression of the 3 antigens tested was also increased by 5‐FU and FUdR. This effect was concentration‐dependent in most instances and varied between the individual cell lines. The combination of 50 U/ml IFN‐γ with 25% growth‐inhibitory concentration of 5‐FU or FUdR for each cell line resulted in an additional increase in antigen expression in 4/7 cell lines. No relation was found between the enhancement of antigen expression and the sensitivity to IFN‐γ or the anti‐metabolites. The enhancement in antigen expression also did not show a relationship with changes in cell‐cycle distribution upon exposure to IFN‐γ or the anti‐metabolites. These results suggest independent mechanisms for the antiproliferative and antigen‐enhancing effects of IFN‐γ, 5‐FU and FUdR.
Comparison of serological expression of different epitopes on the CA50‐carrying antigen CanAg
Authors: Johansson Christina , Nilsson Olle , Lindholm Leif 
Published: February 2007

AbstractC203 and C242 are mouse monoclonal antibodies (MAbs) generated using a human colon carcinoma cell line. They recognize novel tumour‐associated epitopes present in elevated levels in sera from patients with colon and pancreatic cancer. These epitopes were found to be co‐expressed with sialylated Lewis2 on the CanAg molecule. To study the association and distribution of the epitopes of CanAg in sera, these new antibodies, together with C50, were used in different combinations in time‐resolved fluoroimmunoassays. Relative serum concentrations were examined in patients with various types of carcinoma and in patients with ulcerative colitis and benign pancreatic, and hepatobiliary diseases. A double‐determinant assay using C50 and C242 was shown to distinguish carcinoma from benign biliary and hepatocellular diseases better than a single‐determinant assay based on C50 as both catching and tracing antibody. The number of sera with elevated CanAg levels from patients with benign obstructive biliary disease was 17 out of 29 using the single‐determinant CASO assay. This was reduced to 4 out of 29 in the double‐determinant assay. When sera from patients with liver cirrhosis were analyzed, 16 of 23 patients showed elevated CanAg levels with the C50‐C50 combination, but only 4 of 23 patients had elevated antigen values using the C50‐C242 assay. The increased specificity was obtained without loss of sensitivity. MAb C203 was evaluated both in a double‐determinant combination with C50 and in an homologous assay, but did not contribute either Increased sensitivity or specificity as compared with C50‐C50.
A human bronchial epithelial cell strain with unusual in vitro growth potential which undergoes neoplastic transformation after SV40 T antigen gene transfection
Authors: Reddel Roger R. , Hsu Ih‐Chang , Mass Marc J. , Hukku Bharati , Gerwin Brenda I. , Salghetti Simone E. , Somers Angela N. A. , Galati Anthony J. , Gunning William T. , Harris Curtis C. , Stoner Gary D. 
Published: February 2007

AbstractBronchial epithelial cells were cultured from an individual with no evidence of malignant disease. These cells, designated HB56B, had a greatly extended In vitro life‐span, being able to undergo 50 passages and 200 population doublings in contrast to the usual 3 to 4 passages and 20 to 30 population doublings characteristic of normal human bronchial epithelial cells. HB56B cells had karyotypic evidence of an amplified region on the short arm of chromosome 11. Unlike normal bronchial epithelial cells, which undergo terminal squamous differentiation In vitro in response to fetal bovine serum, HB56B cells were only minimally affected by serum. These cells were readily established as an immortalized cell line, HB56B/5T, following transfection with a plasmld containing SV40 early region DNA. HB56B cells were non‐tumorigenic in athymic nude mice, but HB56B/5T cells within a few passages of transfection with the SV40 plasmid formed tumors of which 28/37 regressed. HB56B cells may offer an experimental system for the study of proliferation, differentiation, and senescence control in human bronchial epithelial cells.