bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cancer mortality trends in Uruguay 1953–1991
Authors: De Stefani Eduardo , Fierro Luis , Barrios Enrique , Ronco Alvaro 
Published: February 2007

AbstractCancer mortality trends from 1953 to 1991 were assessed by means of data supplied by the Department of Vital Statistics of the Ministry of Public Health. The population at risk was obtained from the Bureau of Statistics and Censuses. Age specific and age‐adjusted mortality rates were calculated, using the world standard population, for a number of sites or groups of sites. In order to obtain relative risks of death for each period, Poisson regression models were fitted to the data using the GLIM program. The main model included age and period as explanatory variables. Among males, the principal increase was observed for lung cancer, followed by prostatic cancer. The rates were mainly stable in colon cancer and leukaemias, whereas gastric cancer showed a marked decline. Also, a recent decline was seen for oesophageal cancer. In females a steady decline in mortality was observed for all sites combined. Major decreases were seen for oesophageal, gastric, cervical and total uterine cancers. The only cancers showing significant increases were breast cancer, and lung cancer for the most recent period. Providing that there were no changes in death registration or in survival rates, changes in prevalence of risk factors might be responsible for the observed trends.
Detection of tumor‐specific cytotoxic drug activity IN VITRO using the fluorometric microculture cytotoxicity assay and primary cultures of tumor cells from patients
Authors: Nygren Peter , Fridborg Helena , Csoka Katalin , Sundström Christer , De La Torre Manuel , Kristensen Jörgen , Bergh Jonas , Hagberg Hans , Glimelius Bengt , Rastad Jonas , Tholander Bengt , Larsson Rolf 
Published: February 2007

AbstractThe semi‐automated fluorometric microculture cytotoxicity assay (FMCA), based on the measurement of fluorescence generated from cellular hydrolysis of fluorescein diacetate (FDA) by viable cells, was employed for cytotoxic drug sensitivity testing of tumor cells from patients with hematological or solid tumors. In total, 390 samples from 20 diagnoses were tested‐with up to 12 standard cytotoxic drugs. The technical success rate for different tumor types ranged from 67 to 95%. Fluorescence was linearly related to cell number but variably steep depending on tumor type. Samples from most solid tumors thus showed higher signal‐to‐noise ratios than hematological samples. A wide spectrum of in vitro drug activity was obtained, with acute leukemias and non‐Hodgkin's lymphomas being sensitive to almost all tested drugs, whereas renal and adrenocortical carcinomas were essentially totally resistant. Between these extremes were samples of breast and ovarian carcinomas and sarcomas. When in vitro response was compared with known clinical response patterns, a good correspondence was observed. The results indicate that the FMCA is a rapid and efficient method for in vrtro measurement of tumor‐specific drug activity both in hematological and in solid tumors. The assay may be suitable for new drug development and direction of phase‐2 trials to suitable patients.
Response of normal and oncogene‐transformed human mammary epithelial cells to transforming growth factor β1 (TGF‐β1): Lack of growth‐inhibitory effect on cells expressing the simian virus 40 large‐t antigen
Authors: Basolo Fulvio , Fiore Lisa , Ciardiello Fortunato , Calvo Simonetta , Fontanini Gabriella , Conaldi Pier Giulio , Toniolo Antonio 
Published: February 2007

AbstractThe relationship between the expression of selected oncogenes having different modes of action and the loss of the capacity to respond in vitro to transforming growth factor‐β1 (TGF‐β1) was analyzed in human mammary epithelial cells (MEC). Primary MEC cultures from healthy donors and the spontaneously immortalized MCF‐10A cell line were used as normal controls. Various assays (employing both complete and chemically defined media) were used: short‐term DNA synthesis, long‐term cell proliferation under anchorage‐dependent and ‐independent conditions, expression of surface‐differentiation molecules. Whereas primary MEC and the MCF‐10A cell line were fully responsive to the growth‐inhibitory activity of TGF‐β1 under different test conditions, MEC transformed by c‐Ha‐ras, c‐erbB2, int‐2, or SV40‐large‐T antigen were not inhibited by TGF‐pl in a short‐term DNA‐synthesis assay. However, in anchorage‐dependent conditions TGF‐β1 inhibited the proliferation of all lines investigated, with the exception of SV40‐T‐antigen‐transformed MEC. The colony‐formation assay in soft agar revealed that all lines, but not those expressing the int‐2 or the SV40‐T‐antigen genes, were inhibited by TGF‐β1. Neutralizing antibody to TGF‐β had no significant effects on oncogene‐transformed lines, suggesting that the endogenous production of an active form of this growth factor is not a major determinant in MEC transformation by the oncogenes investigated. The only observed effect of TGF‐β1 on selected surface‐differentiation molecules was that normal MEC produced increased levels of the human milk fat globule antigen‐1. Thus it appears that the response of MEC to TGF‐β1 is consistently attenuated by the insertion of a variety of oncogenes and that it is abolished only by the expression of the SV40‐large‐T antigen. Whereas no single in vitro assay was capable of accurately reflecting the actual responsiveness of different lines, the growth‐curve assay in anchorage‐dependent conditions was the best single predictive test.
Polymorphism of T‐cell receptor genes in nasopharyngeal carcinoma
Authors: Chen Yan , Chan Soh Ha 
Published: February 2007

AbstractGerm‐line TCR genes from 41 Singaporean Chinese patients with nasopharyngeal carcinoma and 54 Singapore Chinese normal subjects were investigated by restriction fragment length polymorphism (RFLP) analysis. Genomic DNA from BLCLs of patients and normal subjects was digested with the restriction end nucleases BamHI, EcoRI, HindIII, Taql, transferred to nylon membrane by the Southern‐blot technique and hybridized with radioactively labelled TCR cDNA probes. When the combination of BamHI/VβII was used, NPC patients had a lower frequency of the 25/25‐kb allelic pattern and a higher frequency of the 20‐kb fragment compared to controls. With the combination of Taql/Vβ8, the 4.3/3.2‐kb fragment allelic frequency was lower in total NPC but particularly in patients with HLA B46. The result suggested that TCR restriction may be important in the pathogenesis of NPC.
The genotypes and prognostic significance of human papillomaviruses in cervical cancer
Authors: Chen Tzer‐Ming , Chen Chi‐An , Wu Chih‐Cheng , Huang Su‐Cheng , Chang Chin‐Feng , Hsieh Chang‐Yao 
Published: February 2007

AbstractAn integrated study on the role of human papillomaviruses (HPV) in cervical cancer has been conducted. Out of a total of 433 cases of cervical cancer, HPV‐DNA was detected in 342 (79%) using the polymerase chain reaction (PCR). The incidence of HPV infection was not significantly related to histological types, although a lower incidence was noted in adenocarcinonu cases. The incidence of lymph node (LN) metastasis in adenosquamous carcinoma (55.6%) was significantly higher than in squamous cell carcinoma (SCC) and adenocarcinoma. HPV 16 was detected significantly more often in SCC than in adenocarcinoma. In contrast, HPV 18 was detected more often in adenocarcinoma than in SCC. As a whole, pelvic LN metastases were found in 24.3% of HPV+ cases, significantly higher than 11% of HPV− cases. However, the significant association of HPV‐DNA with LN metastasis was only noted in stage I but not stage II. As far as histological types were concerned, the incidence of positive LN was; HPV+ SCC >HPV‐ SCC (p < 0.01), whereas HPV− adenocarcinoma > HPV+ adenocarcinoma (p = 0.12). Genotypes of HPV did not have any effect on nodal status. The presence and types of HPV were not associated with tumor size and distribution of clinical stage. Our results suggest that the prognostic significance of HPV‐DNA on nodal status is dependent on histological types while the genotypes of HPV cannot account for prognostic significance in cervical cancer. © 1994 Wiley‐Liss, Inc.
Autocrine growth stimulation of human renal Wilms' tumour G401 cells by a gastrin‐like peptide
Authors: Blackmore Melanie , Doherty Elaine , Manning Janet E. , Hirst Barry H. 
Published: February 2007

AbstractThe role of gastrin in the control of growth of renal G401 cells isolated from a human nephroblastoma (Wilms' tumour) was investigated. G401 cell growth was enhanced in the presence of exogenous gastrin. Addition of anti‐gastrin antibodies to serum‐free medium significantly inhibited the growth of G401 cells. G401 cells contained the equivalent of 4.3 pg/106 cells of gastrin, and serum‐free medium collected over 48 hr from G401 cells contained the equivalent of 38 ng/106 cells of gastrin, as determined by radioimmunoassay. Growth of G401 cells was inhibited in a concentration‐related way by a variety of gastrin/CCK receptor antagonists. Devazepide and proglumide were, respectively, the most and the least potent inhibitors of G401 cell growth (potency order devazepide > L‐365,260 = lorglumide > loxiglumide > benzotript > proglumide). These gastrin/CCK receptor antagonists had similar growth‐inhibitory activities in human colonic adenocarcinoma HCT‐116 cells. Growth of HCT‐116 cells was stimulated to a lesser extent, as compared with G401 cells, by exogenous gastrin, and endogenous gastrin was not detectable in HCT‐116 cells. The results are consistent with a role for a gastrin‐like peptide in the control of growth of a renal cell line. The data suggest that gastrin/CCK receptor antagonists warrant further investigation as therapeutic agents for the control of gastrin‐responsive tumours derived from outside, as well as inside, the gastrointestinal tract, including tumours derived from the kidney. © 1994 Wiley‐Liss, Inc.
Homozygous deletion, rearrangement and hypermethylation implicate chromosome region 3p14.3‐3p21.3 in sporadic breast‐cancer development
Authors: Buchhagen Dorothy L. , Qiu Luping , Etkind Polly 
Published: February 2007

AbstractDNAs from 19 malignant human breast tumors and 2 benign fibroadenomas were analyzed for heterozygosity at 5 polymorphic loci on the short arm of chromosome 3. One homozygous deletion and one rearrangement were identified using probe D3S2 which maps to 3p14.3‐3p21.1. This probe also detected novel hybridizing fragments of 2.0 kb and/or 3.4 kb in 6/18 (33%) of the malignant tumor samples that hybridized with the D3S2 probe following digestion with the 5′‐methylcytosine‐insensitive enzyme Mspl. Comparisons of Hpall and Mspl digestion showed that all but one of the tumor DNAs analyzed were hypermethylated. The two fibroadenoma DNAs were not as highly methylated and had hybridizing fragments of 3.4 kb after Hpall digestion. These malignant breast‐tumor DNAs exhibit 3 mechanisms by which a tumor‐suppressor gene hypothesized to reside at 3p 14‐3p21 could be inactivated: homozygous deletion, rearrangement and hypermethylation, and strongly implicate this 3p chromosome region in breast‐tumor development. © 1994 Wiley‐Liss, Inc.
Identification of functional domains of adenovirus tumor‐specific transplantation antigen in types 5 and 12 by viable viruses carrying chimeric E1A genes
Authors: Sawada Yukiharu , Rašková Jana , Fujinaga Kei , Raška Karel 
Published: February 2007

AbstractThe adenovirus (Ad) EIA gene induces in immunized animals a strong tumor transplantation (TSTA) immunity against Ad tumors. Such immunity with group‐A and group‐C viruses is highly group‐specific and no cross‐protection is detected between se retypes 5 and 12. This fact was used to map the domains of the Ad 5 and Ad12 EIA gene products, respectively, which control the TSTA. We constructed a library of 8 recombinant viruses (H5sub1101 through H5sub1108) which carry chimeric Ad5/Ad12 EIA genes in the background of Ad5. The chimeric genes are functional and these viruses are viable. Some of these constructs induce strong and highly specific tumor syngraft immunity in immunized rats. The viruses carrying the 5′ terminus of the first EIA exon derived from Ad12 (viruses H5sub1101, H5sub1102 and H5sub1103) induce strong protection against Ad12 tumors irrespective of the rest of their EIA sequence. The viruses which carry the second exon of the AdS EIA gene (viruses H5sub1101, H5sub1102 and H5sub1106) protect against group‐C tumors, regardless of the origin of the rest of their EIA gene. The 2 viruses that carry the 5′ EIA terminus of the first exon of Ad12 and the second exon of AdS (H5sub1101 and H5sub1102) are thus effective in inducing immunity against Ad12 tumors as well as against Ad2 tumors. The viruses which carry the 5′ terminus of the first exon derived from Ad5 and the second exon of Ad12 (H5sub1107 and H5sub1108) fail to induce immunity against either tumor. Expression of only the truncated 5′ terminus of the Ad12 EIA gene (viruses H5sub1104 and H5sub 1105) is sufficient for induction of Ad12 TSTA. Our results provide direct and unequivocal in vivo evidence that TSTA activities of adenovirus groups A and C are controlled by different domains of their respective EIA genes. The Ad12 TSTA is a function of the 5′ terminus of the first EIA exon, while the Ad5 TSTA is coded for by the 3′ exon of its EIA gene. © 1994 Wiley‐Liss, Inc.
Interaction of IFN α/β with host cells essential to the early inhibition of friend erythroleukemia visceral metastases in mice
Authors: Gresser Ion , Kaido Thomas , Maury Chantal , Woodrow David , Moss Jill , Belardelli Filippo 
Published: February 2007

AbstractWe have previously shown that an intact immune system was essential to the increase in survival time of IFN‐α/β‐treated mice injected i.v. with an IFN‐α/β‐resistant line of Friend erythroleukemia cells (FLC) highly metastatic to the liver and spleen. Here, we have investigated the early interactions of IFN α/β with host cells prior to the development of the immune response. IFN α/β treatment resulted in 50‐ to 100‐fold inhibition of FLC multiplication in the liver and spleen of normal DBA/2 mice shortly after tumor inoculation, as evaluated by colony formation in agarose. IFN treatment was far less effective in inhibiting the multiplication of FLC in the livers of NK‐cell‐deficient DBA/2 beige mice, or in immunocompetent DBA/2 mice treated with antibody to asialo GMI, or silica, or in mice subjected to sub‐lethal irradiation. Injection of antibody to CD4 or CD5 did not affect the early inhibitory action of IFN α/β on FLC multiplication but did decrease survival time. Light‐ and electron‐microscope examination of the livers of IFN‐treated, FLC‐injected mice confirmed the early inhibition of FLC multiplication in the liver and spleen. Our results indicate that IFN α/β inhibits the development of FLC visceral metastases by acting first on host cells, such as NK cells and macrophages, and then continues to act in consort with the developing immune response. © 1994 Wiley‐Liss, Inc.
Identification and potential use of a soluble tumor antigen for the detection of liver‐fluke‐associated cholangiocarcinoma induced in a hamster model
Authors: Prempracha N. , Tengchaisri T. , Chawengkirttikul R. , Boonpucknavig S. , Thamavit W. , Duongchawee G. , Sirisinha S. 
Published: February 2007

AbstractA liver‐fluke‐associated cholangiocarcinoma (CCA), comparable to that occurring in humans, was induced by exposing Opisthorchis viverrini‐infected hamsters to dimethylnitrosamine (DMN). Tumor masses were removed and histopathologically identified, then one portion was extracted for antigens used in the production of monoclonal antibodies (MAbs). The remaining portions were used to establish CCA cell lines. The antigens produced and secreted by these cell lines, as well as those originally present in the tissue extracts, possessed a 200‐kDa glycoprotein that appeared to be immunologically distinct from other tumor markers. A specific MAb called 6E5 was used to set up a sandwich ELISA for the quantification of this antigen in the serum and bile of tumor‐bearing animals. The assay system was sensitive enough to detect the antigen at concentrations below 10 ng/ml. The serum and biliary levels of this antigen were markedly elevated in animals with progressive tumors when compared with untreated controls. The serum taken serially from each animal that subsequently developed CCA showed a gradual but significant elevation of the antigen as carcinogenesis progressed. A few isolated animals exhibited a slight elevation of the antigen at a time as early as the end of DMN treatment, when the CCA should not yet have developed, judging from microscopic examination. The data from this animal model suggested that the CCA‐associated soluble antigen defined by MAb 6E5 was a useful marker for the detection of tumors at an early stage of development.
Scatter factor modulates the metastatic phenotype of the EMT6 mouse mammary tumor
Authors: Rosen Eliot M. , Knesel Jaromir , Goldberg Itzhak D. , Jin Liang , Bhargava Madhu , Joseph Ansamma , Zitnik Ralph , Wines James , Kelley Marianne , Rockwell Sara 
Published: February 2007

AbstractEMT6 is a transplantede mouse mammary tumor cell line Chat has been utilized widely as a model system to study the effects of various treatments on local tumor growth and pulmonary metastasis. In this study, we examined the cellular mechanisms by which scatter factor (SF), a fibroblast‐derived cytokine that stimulates epithelial cell motility, may contribute to tumor‐cell dissemination, using the EMT6 model system. In vitro, SF stimulated EMT6 cell motility, invasiveness and cell‐surface expression of urokinase (an enzyme required for cell migration through tissue). SF differentially stimulated EHT6 cell adhesion to and migration onto surfaces coated with collagen I and laminin. EMT6 cells treated in vitro with SF and injected i.v. into isogeneic BALB/c‐Rw mice showed a small but significant increase (1.7‐fold) in lung colony formation as compared with control cells. For EMT6 cells in vitro, SF had no effect on DNA synthesis, cell proliferation, cell size distribution, or in vitro colony‐forming ability. Thus, the increase in lung colonization may be due to enhanced ability of SF‐treated cells to adhere to subendothelial basement membrane or to invade through tissue. Studies of the tissue distribution of SF in BALB/c‐Rw mice demonstrated high levels of active factor in the lung. Thus, the presence of endogenous pulmonary SF may have reduced the degree to which SF treatment stimulated EMT6 lung colonization. Significant SF activity was also found in extracts of EMT6 tumors. Cultured EMT6 cells did not produce SF, but did produce high titers of a soluble low‐molecular‐weight protein activity that is capable of stimulating SF production in human fibroblasts 3‐ to 5‐fold. EMT6 tumor extracts contained high titers of a similar SF‐inducing activity. These observations suggest that SF may contribute to the invasive and metastatic phenotype of EMT6 cells via a paracrine mechanism in which tumor cells induce the production of SF in stromal fibroblasts.
Chromosome aberrations in adenomas of the colon. Proof of trisomy 7 in tumor cells by combined interphase cytogenetics and immunocytochemistry
Authors: Herbergs J. , de Bruïne A. P. , Marx P. T. J. , Vallinga M. I. J. , Stockbrügger R. W. , Ramaekers F. C. S. , Arends J. W. , Hopman A. H. N. 
Published: February 2007

AbstractThirty‐five colon adenomas from 26 patients were analyzed with centromeric probes for chromosomes 1,7, 17, X and Y in order to study numerical aberrations, chromosome imbalances, aneuploidy and tetraploidization. The fluorescent in situ hybridization (FISH) technique was applied to single‐cell suspensions and a combination of FISH and immunocytochemistry (ICC) was employed to identify the cell type under study. Trisomy of chromosome 7 was detected in 37% of the cases. In 7 out of 13 cases this aberration was combined with abnormalities of one or 2 of the other investigated chromosomes. No correlation could be demonstrated between any of the detected chromosomal aberrations and size, localization or degree of epithelial dysplasia. With the combined FISH/ICC procedure, the abnormal cells were shown to be of epithelial rather than of stromal origin. Our data indicate that trisomy 7 is a common chromosome aberration in the epithelial component of colon adenomas. © 1994 Wiley‐Liss, Inc.
Cytotoxicity of the anticancer agents cisplatin and taxol during cell proliferation and the cell cycle
Authors: Donaldson Karen L. , Goolsby Gay Lynn , Wahl Alan F. 
Published: February 2007

AbstractThe overt effects of the anti‐cancer drugs cisplatin (cis‐DDP) and taxol appear to be DNA modification and microtubule stabilization respectively, yet the mechanisms by which these drugs elicit tumor cell death are not well understood. In this report cell sensitivities to cis‐DDP and taxol were accurately determined as a function of cell proliferation and cell cycle stage. Quiescent fibroblasts restimulated to synchronously enter the cell cycle become maximally sensitive to cis‐DDP immediately preceding DNA synthesis, and resistance increases with onset of DNA synthesis. Mid‐log proliferating cells were separated into progressive stages of the cell cycle by centrifugal elutriation or by double thymidine (dThd) block. Cells staged by either method are maximally sensitive to cis‐DDP in G1, just prior to the onset of DNA synthesis and minimally sensitive in peak DNA synthesis, with entry into S phase resulting in a 2‐fold decrease in sensitivity. Cells that remained blocked at the G1/S phase boundary during cis‐DDP treatment remain maximally sensitive after release. Sensitivity to taxol increases at 2 points: transiently during transition of normal cells from quiescence to proliferation and steadily as proliferating cells progress from early G1 to late G2. This 3‐fold increase in taxol sensitivity through the cell cycle is rapidly reversed upon cell division. Synchronous cells treated with either drug at points of maximum sensitivity initiate apoptotic DNA fragmentation 12‐14 hr post‐exposure to drug. © 1994 Wiley‐Liss, Inc.
Residential radon exposure and lung cancer—an epidemiological study of Norwegian municipalities
Authors: Magnus Knut , Engeland Anders , Green B. Martyn R. , Haldorsen Tor , Muirhead Colin R. , Strand Terje 
Published: February 2007

AbstractThe study is based on a collaboration between the Cancer Registry of Norway, the Norwegian Radiation Protection Authority, and National Radiological Protection Board (NRPB, UK). The association between indoor radon exposure and lung cancer was studied in 427 municipalities. NRPB detectors were sent to 10,000 householders, and 7,500 of the detectors were returned. Data from a nation‐wide survey of smoking habits in 1964‐1965 were available. Data on asbestos exposure were also used in a regression analysis. The reporting to the Cancer Registry of all new cases of cancer is fairly complete, as hospital departments and institutes of pathology are obliged to report all cancer cases. The histologically confirmed lung cancer cases were grouped into squamous‐cell carcinoma, small‐cell carcinoma, adenocarcinoma and other or non‐specified histological types. The age‐adjusted rate of lung cancer by histological type was the dependent variable in the regression analysis. A consistent increase in incidence of lung cancer was seen with increasing tobacco consumption, but no positive trend could be shown with increasing radon exposure in the descriptive presentation of the data. In the regression analysis, however, the incidence of small‐cell anaplastic lung tumors in females increased significantly with increasing radon exposure. When based on the regression coefficients, the fraction of lung cancers attributable to radon is about 2‐4%. However, systematic errors cannot be excluded in an ecological study such as presented here. © 1994 Wiley‐Liss, Inc.