bluuebunny/crossref_metadata_2025_split huggingface dataset:
Partial circumvention of multi‐drug resistance by annamycin is associated with comparable inhibition of DNA synthesis in the nuclear matrix of sensitive and resistant cells
Authors: Ling Yi‐He , Zou Yiyu , Priebe Waldemar , Perez‐Soler Roman 
Published: February 2007

AbstractWe studied the subcellular and subnuclear distributions of the partially cross‐resistant anthracycline Annamycin (Ann) in KB‐3‐1 and multi‐drug resistant KB‐V1 cells. Subcellular drug localization was assessed qualitatively by fluorescence microscopy and quantitatively by cell fractionation and fluorescence measurements. Doxorubicin (Dox) localized predominantly in the nucleus in KB‐3‐1 cells and in the membranes in KB‐V1 cells. In contrast, the subcellular distribution of Ann was identical in both cell lines, with preferential drug localization in the perinuclear region, Golgi apparatus, endoplasmic reticulum and endosomes. Dox rate of efflux from the nucleus was negligible in KB‐3‐1 cells but markedly enhanced in KB‐V1 cells, whereas Ann was lost at a similar rate from the nucleus in both cell lines. In KB‐3‐1 cells Dox levels in the nuclear non‐matrix were about 2‐fold higher than those of Ann, while in the matrix the inverse relationship was observed. In spite of these differences, Dox and Ann had a similar inhibitory effect on new DNA synthesis in the nuclear matrix and non‐matrix of KB‐3‐1 cells. Dox levels were reduced by 10‐fold in the nuclear non‐matrix and 2‐fold in the matrix in KB‐V1 cells compared with KB‐3‐1 cells, whereas Ann levels were reduced by about 2‐ to 3‐fold in the non‐matrix and were unchanged in the matrix. In correlation with these findings, Dox did not cause inhibition of new DNA synthesis in either nuclear fraction in KB‐V1 cells, whereas inhibition of new DNA synthesis in the matrix by Ann was similar in both cell lines. Our results indicate that Ann's partial circumvention of multi‐drug resistance is associated with its ability to cause comparable new DNA synthesis inhibition in the nuclear matrix of sensitive and resistant cells. © 1995 Wiley‐Liss, Inc.
Mechanism of cross‐resistance to cisplatin in a mitomycin C‐resistant human bladder cancer cell line
Authors: Singh Shivendra V. , Xu Bing H. , Jani Jitesh P. , Emerson Erling O. , Backes Mary G. , Rihn Christopher , Scalamogna Domenic , Stemmler Nancy , Specht Susan , Blanock Kurt , Katoh Arthur , Gupta Vicram 
Published: February 2007

AbstractThis study was undertaken to elucidate the mechanism(s) of cross‐resistance to cisplatin (CDDP) in a mitomycin C (MMC)‐resistant human bladder cancer cell line, J82/MMC. The J82/MMC celi line displayed 2‐ to 3‐fold cross‐resistance to CDDP and carboplatin when compared to the parental J82/WT cells. Drug uptake studies revealed that cross‐resistance to CDDP in the J82/MMC cell line was independent of reduced platinum accumulation. The J82/MMC cetl line exhibited approximately a 1.5‐fold resistance to cadmium chloride, an indicator for increased metallothionein (MT) content, when compared to the J82/WT cells. Northern blot analysis showed a 2.7‐fold higher level of MT‐IIA mRNA in the J82/MMC ceil line compared with J82/WT. We have reported previously that, whereas glutathi‐one (GSH) level is comparable in these cells, GSH transferase (GST) activity is significantly higher in the J82/MMC eell line compared with J82/WT. Results of the present study showed that the elevated GST activity in the J82/MMC cell line was due to an over‐expression of π‐type GST protein. Although buthio‐nine‐S,R‐sulfoximine (BSO)‐induced GSH depletion significantly enhanced CDDP cytotoxicrty in both cell lines, the magnitude of potentiation was markedly higher in J82/MMC cells (about 2.1‐fold) relative to J82/WT (about 1.6‐fold). Our results suggest that cross‐resistance to CDDP in the J82/MMC cell tine may be due to alterations in cellular thiols. © 1995 Wiley‐Liss, Inc.
Expression of E‐selectin on endothelial cells of small veins in human colorectal cancer
Authors: Ye Chunlin , Kiriyama Kozo , Mistuoka Chikako , Kannagi Reiji , Ito Katsuki , Watanabe Tadashi , Kondo Ken , Akiyama Seiji , Takagi Hiroshi 
Published: February 2007

AbstractE‐selectin is an adhesion molecule of endothelial cells that binds to cancer cells mediated by sialyl Lewis A (sLea) or sialyl Lewis X (sLex). It is suspected to be involved in hematogenous metastasis of tumors. Therefore, it is worth examining E‐selectin expression in human colorectal cancer and its hepatic metastasis. In the present study, E‐selectin was clearly revealed on the endothelial cells of small vessels adjacent to cancer nests both in primary and in metastatic nests in immunohistochemistry. In these tissues, E‐selectin was observed on the endothelial cells lining the lumen of small vessels. Its expression adjacent to cancer nests appears to be induced through some stimuli by cancer cells, since its degree of expression is inversely correlated to the distance of the blood vessels from the cancer nests (p < 0.001). Endothelial cells adjacent to the metastatic lesion expressed E‐selectin more extensively than those adjacent to the primary foci. This is also in line with the finding on serum E‐selectin levels which were significantly elevated in the metastatic group as compared with the non‐metastatic group. The serum E‐selectin level may provide useful information in the diagnosis for hepatic metastasis of colorectal cancer, although the results are still tentative. © 1995 Wiley‐Liss, Inc.
Reduction in risk of mortality from colorectal cancer by fecal occult blood screening with immunochemical hemagglutination test. A case‐control study
Authors: Saito Hiroshi , Soma Yasushi , Koeda Junichi , Wada Toyohito , Kawaguchi Hitoshi , Sobue Tomotaka , Aisawa Tadashi , Yoshida Yutaka 
Published: February 2007

AbstractFecal occult blood testing by immunochemical hemagglutination has been shown to be superior to the Hemoccult test, both in sensitivity and in specificity. The test has been widely used as a tool for population screening in Japan, but there has been no study to evaluate the efficacy of screening using this test. A case‐control study to evaluate the screening was conducted in study areas where no previous and no other concomitant colorectal cancer screening had been performed. Case series in the study were 193 cases who died of colorectal cancer. Three controls were selected randomly from the list of individuals who were alive at the time of diagnosis of the corresponding case and had been living in the same area as the case, matched by gender and by age. Odds ratios (OR) of dying of colorectal cancer for those screened within 1, 2 and 3 years of case diagnosis vs. those not screened were 0.40 [95% confidence interval (CI) 0.17‐0.92], 0.41 (95% CI 0.20‐0.82), and 0.48 (95% CI 0.25‐0.92), respectively. OR increased towards 1.0 as the duration during which screening histories were compared was extended, and showed similar tendencies when analyzed by number of years since the most recent screening history. These results suggest that colorectal cancer screening by the immunochemical fecal occult blood test would reduce mortality from colorectal cancer.
Variations in the expression of cell‐adhesion molecules on liver‐associated lymphocytes and peripheral‐blood lymphocytes in patients with and without liver metastasis
Authors: García‐Barcina María , Bidaurrazaga Ioseba , Neaud Véronique , Bioulac‐Sage Paulette , Balabaud Charles , Vidal‐Vanaclocha Fernando , Winnock María 
Published: February 2007

AbstractWe evaluated the expression of the cell‐adhesion molecules (CAM) that might be involved in liver‐associated lymphocyte (LAL) contacts with other sinusoidal cells and/or be responsible for natural‐killer(NK)‐ and lymphokine‐activated killer(LAK) activity in patients with liver metastasis. The LAL population was isolated by sinusoidal high‐pressure lavage from partial hepatectomies obtained from patients operated for metastases (n = 13) and benign liver tumors (n = 9). Surface expression of the beta‐2‐integrin chains (CD11a, CD11b, CD11c and CD 18), and the beta‐1‐integrin chains (CD49b, CD49d, CD49f and CD29), as well as that of members of the immunoglobulin superfamily (CD2, CD54, CD56 and CD58), were analyzed by one‐ or two‐color flow cytometry. Quantitative and qualitative differences were observed in both groups of patients in the expression of CAM between LAL and peripheral blood lymphocytes (PBL). LAL were characterized by an increase in the percentage of CD11b‐, CD49b‐, CD49d‐, CD54‐, CD56‐ and CD58‐positive cells in comparison with PBL. Fluorescence values for CD2, CD11a, CD18 and CD56 were higher in LAL than in PBL. Moreover, the population expressing these antigens of differentiation presented a bimodal distribution (dim and bright): in LAL, as opposed to PBL, the percentage of cells with a bright phenotype was greater than of those with a dim one. The increase in CAM expression on LAL could be due to the influence of the liver sinusoidal micro‐environment. Results were more unexpected for the comparison between benign and malignant tumors. No difference was found in CAM expression on LAL between these 2 categories. Consequently, it cannot be this factor that explains the decrease in LAK activity of LAL in patients with metastasis. © 1995 Wiley‐Liss, Inc.
Establishment and characterization of cachexia‐inducing and ‐non‐inducing clones of murine colon 26 carcinoma
Authors: Fujimoto‐Ouchi Kaori , Tamura Sumie , Mori Kazushige , Tanaka Yutaka , Ishitsuka Hideo 
Published: February 2007

AbstractTo investigate the mechanism causing cachexia and its association with shorter patient survival, we cloned weight‐loss‐inducing and ‐non‐inducing sublines of murine colon 26 carcinoma (colon 26). One clone, clone 20, induced substantial weight loss, wasting of adipose tissue and muscle, and hypogly‐cemia in mice with a minimum tumor burden of 0.3 g (2 g per 100 g body weight). Clone‐20‐bearing mice had a median survival of 24.5 days with average tumor weight of 0.4 g. In contrast, clone 5 induced neither severe weight loss, wasting of adipose tissue and muscle, nor hypoglycemia; clone‐5‐bearing mice survived for a median of 70 days with average tumor weight of 12 g. These results clearly indicate that shorter survival is associated with the degree of cachexia and is independent of tumor size. Using this pair of colon 26 clones, we examined mediators of cachexia. Neither TNFα, IL‐1α nor IFNγ was detected in the serum of mice bearing either clone, while IL‐6 was detected in mice bearing both clones by ELISA and a bioassay. Administration of anti‐IL‐6 monoclonal antibody (MAb) partially but significantly suppressed cachexia induction in clone‐20‐bearing mice. These results point to the involvement of IL‐6 in experimental cachexia. However, our finding of the presence of IL‐6 in the serum of mice bearing clone 5, which does not induce weight loss, clearly indicates that IL‐6 is not solely responsible for the induction of cachexia. © 1995 Wiley‐Liss, Inc.
Urokinase plasminogen activator and urokinase plasminogen activator receptor in breast cancer
Authors: Duggan C. , Maguire T. , McDermott E. , O'Higgins N. , Fennelly J. J. , Duffy M. J. 
Published: February 2007

AbstractUrokinase plasminogen activator (uPA) is a serine protease involved in cancer invasion and metastasis. uPA mediates its action while attached to a membrane‐bound receptor (uPAR). In this investigation we show that uPAR levels correlate with uPA levels in human breast cancers. uPAR levels, however, do not correlate with other components of the plasminogen activator system such as tissue‐type plasminogen activator (t‐PA), PAI‐1 or PAI‐2. In addition, uPAR levels showed no correlation with tumor size, axillary‐node status or estrogen‐receptor status. On the basis of an optimum cut‐off point, patients with breast cancers containing high levels of uPAR had a worse prognosis than patients with low levels of the receptor. However, as a prognostic marker in breast cancer, uPAR was not as strong as uPA. Our results are consistent with data from model systems suggesting that both uPA and uPAR are necessary for metastasis. © 1995 Wiley‐Liss, Inc.
p53 mutations in esophageal tumors from high‐incidence areas of China
Authors: Liang Yuan‐Yuan , Estève Asuncion , Martel‐Planche Ghyslaine , Takahashi Satoru , Lu Shih‐Hsin , Montesano Ruggero , Hollstein Monica 
Published: February 2007

AbstractCarcinomas of the upper digestive tract (squamous‐cell carcinoma of the esophagus, adenocarcinoma of the cardia) from 24 patients residing in Linxian (China) and near‐by high‐incidence areas were analyzed for mutations in exons 5–8 of the p53 tumor‐suppressor gene. Mutations were identified by polymerase chain reaction amplification and direct sequencing in 50% of the specimens. Eleven tumors harbored a single base‐pair substitution leading to either an amino‐acid substitution (8 tumors) or a chain‐termination signal (3 tumors), and one tumor revealed a 15‐bp deletion in exon 7 with a silent base substitution adjacent to the deletion site. Mutations occurred in all 4 exons examined, with a preponderance in exon 5. Of the 6 mutations identified among the 14 adenocarcinomas examined, 3 were G to T transversions, a mutation that has thus far been absent from reported mutations in Barrett's esophageal adenocarcinomas and dysplasias from patients residing in Europe and North America. © 1995 Wiley‐Liss, Inc.
Synergistic effects of co‐expression of the Th1 cytokines il‐2 and IFNγ on generation of murine tumor‐reactive cytotoxic cells
Authors: McAdam Alexander J. , Pulaski Beth A. , Harkins Stephanie S. , Hutter Elizabeth K. , Lord Edith M. , Frelinger John G. 
Published: February 2007

AbstractWhile the effect of cytokines on the generation of tumor‐reactive cytotoxic cells has been a topic of active investigation, the effect of physiological cytokine combinations has not been determined. We have investigated the effect of co‐expression of IL‐2 and IFN‐γ on the generation of cytotoxic cells against the murine line 1 tumor in vivo. These cytokines were selected because they are normally produced in concert by a subset of T‐helper cells called T‐helper 1 (Th1). We transfected the line 1 murine carcinoma with cDNA for IL‐2 and IFN‐γ, alone or combined. IFN‐γ alone does not elicit rejection of the transfectant, but IL‐2 increases the tumorigenic dose by 10,000‐fold above the parental cells. Co‐expression of IFN‐γ and IL‐2 increases this rejection to at least 100,000‐fold above parental line 1. Unlike IL‐2 transfectants, tumor cells expressing both IFN‐γ and IL‐2 can also elicit rejection of admixed parental tumor cells. Finally, the IFN‐γ/IL‐2 transfectants are more effective at generating memory cells that are cytolytic for the parental tumor. Our results show that synergistic interactions of Th1 cytokines can remarkably enhance the cytotoxic response to tumors. © 1995 Wiley‐Liss, Inc.
Human skin fibroblasts induce anchorage‐independent growth of HPV‐16‐DNA‐immortalized cervical epithelial cells
Authors: Zheng Jie , Vaheri Antti 
Published: February 2007

AbstractImmortalized non‐malignant cells do not grow in soft agarose. We found, however, that HPV‐16‐DNA‐immortalized human uterine exocervical epithelial cells (HCE 16/3 cell line) formed colonies when co‐cultured with human embryonic skin fibroblasts. This appeared to be mediated by diffusible growth factors, and direct cell‐cell contacts were not required. HCE 16/3 cells from colonies remained unable to grow alone in soft agarose like the parental HCE 16/3 cells, indicating that only transient phenotypic changes without genetic alterations had occurred in the co‐cultures. In a modified soft‐agarose assay, HCE 16/3 cells grown as an underlying monolayer did not produce enough (transforming) growth factors which could confer an anchorage‐independent phenotype to non‐transformed fibroblasts. Lethally irradiated fibroblasts were able to stimulate DNA synthesis and proliferation of HCE 16/3 cells. Northern‐blot analysis showed that HPV‐16‐DNA expression of the immortalized cells was not altered in the presence of fibroblasts. The expression of the IL‐I gene in the immortalized cells, however, was augmented by the co‐cultured fibroblasts compared with immortalized cells alone. In organotypic collagen raft co‐cultures, in which epithelial cells were grown on top of a collagen gel containing fibroblasts, HCE 16/3 cells appeared to be chemotactic to fibroblasts and fibroblasts stimulated the growth of the immortalized epithelial cells. Our results suggest that fibroblasts may contribute to human epithelial carcinogenesis in vivo. © 1995 Wiley‐Liss, Inc.
Mediation of glucocorticoid receptor function by the activation of latent transforming growth factor beta 1 in MG‐63 human osteosarcoma cells
Authors: Boulanger Jocelyn , Reyes‐Moreno Carlos , Koutsilieris Michael 
Published: February 2007

AbstractWe analyzed glucocortcoid receptor function using ligand binding assays, DNA band‐shift analysis and trans‐activation of the murine mammary tumor virus‐thymidine kinase‐chloramphenicol acetyltransferase reporter gene in transiently transfected MG‐63 human osteosarcoma cells. Dexamethasone increased the distribution of MG‐63 cells in the G1/G0 phase of the cell cycle, thus decreasing the rate of DNA synthesis and cell growth. Its effect on MG‐63 cell growth was neutralized by RU486 and anti‐transforming growth factor beta 1 (TGFβ1) antibody. In addition, (i) dexamethasone increased the levels of active TGFβ1 in MG‐63‐conditioned media without significantly altering the expression of TGFβ1 mRNA in MG‐63 cells and (ii) TGFβ1 inhibited proliferation of MG‐63 cells. Therefore, we conclude that glucocorticoid receptor function is mediated by the activation of latent‐TGFβ1 in MG‐63 osteosarcoma cells. © 1995 Wiley‐Liss, Inc.
Melanoma and use of sunscreens: An EORTC case‐control study in germany, belgium and france
Authors: Autier Philippe , Doré Jean‐François , Schifflers Eugène , Cesarini Jean‐Pierre , Bollaerts Anne , Koelmel Klaus F. , Gefeller Olaf , Liabeuf André , Lejeune Ferdy , Lienard Danièle , Joarlette Marie , Chemaly Philippe , Kleeberg Ulrich R. 
Published: February 2007

AbstractUse of sunscreens is widely advocated as a preventive measure against sun‐induced skin cancers. However, to date, no epidemiologic study has reported a decreased melanoma risk associated with sunscreen use. We have conducted a case‐control study aimed at evaluating the influence of sunscreen use on the occurrence of cutaneous malignant melanoma. In 1991 and 1992, 418 melanoma cases and 438 healthy controls were interviewed in Germany, France and Belgium. The questionnaire used differentiated between regular sunscreens, psoralen sunscreen (prepared with 5‐methoxypsoralen, a tanning activator and photocarcinogen), and self‐tanning cosmetics (which produce a tan without ultraviolet radiation). After adjusting for age, sex, hair colour and holiday weeks spent each year in sunny resorts, the melanoma risk was of 1.50 (95% CI:1.09–2.06) for regular sunscreens, and of 2.28 (95% CI: 1.28–4.04) for psoralen sunscreens. No melanoma risk was associated with use of self‐tanning cosmetics. Among subjects with a poor ability to tan, psoralen sunscreen users displayed a melanoma risk of 4.45 (95% CI: 1.25–15.8) when compared with regular sunscreen users. There was a significant negative interaction between regular sunscreen use and sunburns experienced in adulthood. Use of sunscreens, especially psoralen sunscreen, was associated with higher density of pigmented lesions of the skin. Although we cannot exclude the presence of an unknown confounding factor, our results support the hypothesis that sunscreens do not protect against melanoma, probably because of their ability to delay or avoid sunburn episodes, which may allow prolonged exposure to unfiltered ultraviolet radiation. Serious doubts are raised regarding the safety of sunscreens containing psoralens. © 1995 Wiley‐Liss, Inc.
Trends in incidence of testicular cancer in boys and adolescent men
Authors: Møller Henrik , Jørgensen Niels , Forman David 
Published: February 2007

AbstractSeveral epidemiological studies have described increasing trends over time in the incidence of testicular cancer in adult men. Less attention has been given to the trends in young boys, adolescents and old men. This paper describes the incidence of testicular cancer in young boys (0–4 years) and adolescents (15–19 years) in Denmark, Norway and Sweden, and compares these trends with the corresponding data on adults. Although only small numbers were available, the data suggest that the incidence of testicular cancer in young boys has been constant, at a level around 0.5 per 100,000. This observation lends support to the idea that testicular cancer in young boys is aetiologically distinct from testicular cancer in adults. In all three populations we found a particularly high average annual increase in the incidence of testicular cancer in adolescents (around 6% per year). It is proposed that this increase is mainly caused by a secular trend towards earlier age at puberty. © 1995 Wiley‐Liss, Inc.
Cytogenetic findings in malignant peripheral nerve sheath tumors
Authors: Mertens Fredrik , Rydholm Anders , Bauer Henrik F. C. , Limon Janusz , Nedoszytko Boguslaw , Szadowska Anna , Willén Helena , Heim Sverre , Mitelman Felix , Mandahl Nils 
Published: February 2007

AbstractClonal chromosome aberrations were detected in 8 short‐term cultured malignant peripheral nerve sheath tumors (MPNST). Seven had a near‐triploid chromosome number and I was in the hyperhaploid‐hypodiploid range. No recurrent structural rearrangements were found; the bands most frequently involved (3 tumors) were 7p11, 12p13 and 14q11. The most common numerical changes were loss of a sex chromosome (all tumors) and loss of at least 1 copy of chromosomes 8, 16 and 22 (4 tumors). Pooling our data with those on the 20 previously published MPNST with abnormal karyotypes, we found that the chromosome number has often been in the triploid range (12 tumors), with stem line variation between 34 and 270. All chromosome arms, except 22p and the Y chromosome, were involved in recombinations. The most frequently rearranged bands were 7p22 (6 tumors) and 1p21, 7p11 and 14q11 (5 tumors each). Most numerical and unbalanced structural aberrations have led to loss of genetic material, in particular from Xq26‐qter (13 tumors); 11q22‐qter and 13p (12 tumors); 9p22‐pter, 11p13‐pter, 17p and 17q11‐21 (11 tumors); 1p22‐32 and 1p34‐pter (10 tumors) and 6q25‐qter and chromosome 16 (9 tumors). © 1995 Wiley‐Liss, Inc.