bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nucleolar protein B23 translocation after deferoxamine treatment in a human leukemia cell line
Authors: Yung Benjamin Y‐M. , Yang Y. H. , Bor Amy M‐S. 
Published: February 2007

AbstractLocalization of nucleolar protein B23 in HL‐60 cells under the treatment by iron chelator deferoxamine (DSF) was studied using indirect immunofluorescence. Bright nucleolar fluorescence was observed in exponentially growing control cells. The addition of DSF in the culture system resulted in time‐and dose‐dependent Induction of protein B23 translocation from nucleoli to nucleoplasm, inhibition of cell growth, DNA and RNA synthesis. The addition of FeCI3 at culture Initiation completely reversed the effects of DSF. Furthermore, significant numbers of HL‐60 cells could be rescued from the effects of DSF when iron was added back as late as 24 hr after exposure to DSF. Cells resumed their abilities to grow and to synthesize DNA and RNA upon the iron rescue. Protein B23, accordingly, relocated from nucleoplasm to nucleoli. These results indicate the importance of iron for proliferation of leukemfc cells and localization of protein B23 in nucleoli. Preribosomal ribonucleoprotein particles (pre‐rRNPs) were extracted from isolated nucleoli of HL‐60 cells and fractionated on sucrose density gradients. Protein B23 was found to be co‐localized with the pre‐rRNPs as determined by ELISA assays. No such B23‐associated pre‐rRNPs or other pre‐rRNP fractions were obtained from nucleoli of DSF‐treated cells. These results suggest that one of the effects of the anti‐proliferative action of DSF is the Inhibition of rRNA synthesis in nucleoli. Due to the lack of new synthesis of rRNA in nucleoli, protein B23 loses its binding target and translocates into the nucleoplasm. B23 translocation, as observed by immunofluorescence, may be a simple and rapid method for assessing inhibition of cell growth in response to anti‐proliferative drugs such as deferoxamine in cancer chemotherapy.
Enhancement by tyrosine methyl ester of 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 tyrosine methyl ester (TME) on the incidence, number, and histological types of gastric cancers induced by N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG) was investigated in male Wistar rats, Rats were subcutaneously given TME, 512 mg/kg body weight, every other day after 20 weeks of oral treatment with MNNG. Prolonged alternate‐day administration of TME caused a significant increase in the incidence and number of gastric cancers of the glandular stomach by week 52. However, it did not affect the histology of the cancers. TME also caused a significant increase in tissue norepinephrine concentrations in the antral portion of the gastric wall and in the labelling indices of the antral epithelial cells. However, TME had no influence on the serum gastrin level and antral pH. These findings indicate that TME enhances gastric carcinogenesis, and this may be related to its effects on increasing norepinephrine levels in the gastric wall and stimulating proliferation of the antral epithelial cells.
Differential expression of two lck transcripts directed from the distinct promoters in HTLV‐I+ and HTLV‐I− T‐cells
Authors: Nakamura Kazuhiko , Koga Yasuhiro , Yoshida Hiroki , Kimura Genki , Nomoto Kikuo 
Published: February 2007

AbstractThe lck gene encodes a lymphocyte‐specific tyrosine protein ktnase,p56lck, the expression of which is almost exclusive In T‐cells. The expression of lck in human T‐cell leukemia virus type I (HTLV‐1)‐transformed T‐cell lines is closely associated with interleukin‐2 (IL‐2) dependence for their growth. That is, IL‐2‐dependent HTLV‐1‐transformed cell lines contain the lck message abundantly as HTLV‐1‐negative T‐cell lines, whereas IL‐2‐Independent HTLV‐1‐transformed cell lines express either no or little lck mRNA, although they are derived from T‐cells. The lck gene contains 2 distinct promoters which direct 2 types of lck transcript with different S′ untranslated regions. In this study, we show that HTLV‐1‐transformed IL‐2‐dependent T‐cell lines contain the upstream promoter‐initiated lck transcript exclusively, in contrast to HTLV‐1‐negative transformed T‐cell lines which express the downstream promoter‐as well as the upstream promoter‐initiated lck transcript. In addition, lck mRNA disappears transiently in IL‐2‐dependent HTLV‐1‐transformed T‐cell lines after stimulation for T‐cell activation, which is also observed In peripheral blood T lymphocytes. These results indicate that the disappearance of lck mRNA in HTLV‐1‐transformed, IL‐2‐independent cell lines Is caused by a mechanism which down‐regulates the upstream promoter‐initiated lck transcript and this IL‐2‐independent state may represent a further “activated” condition of the IL‐2‐dependent state by the stimulation which mediates T‐cell activation.
The epstein‐barr‐virus‐encoded membrane protein LMP but not the nuclear antigen EBNA‐1 induces rejection of transfected murine mammary carcinoma cells
Authors: Trivedi Pankaj , Masucci Maria G. , Winberg Gösta , Klein George 
Published: February 2007

AbstractThe EBV‐encoded membrane protein (LMP) and the nuclear antigen EBNA‐I were compared for their capacity to induce rejection of transfected murine mammary carcinoma cells in syngenelc hosts. The tumorigenic potential of stable LMP and EBNA‐I expressing sublines of the ACA (H‐2f)‐derived mammary carcinoma line S6C was tested in pre‐immunized syngeneic and semi‐syngeneic animals. LMP expressing S6C cells elicited a strong rejection response as demonstrated by the lower tumor take and slower growth in immunized vs. control mice. In contrast, EBNA‐I‐expressing cells were non‐immunogenic in syngeneic hosts and in one semi‐syngeneic F1‐hybrid. Rejection in 2 additional F1‐hybrids did not appear to be due to EBNA‐I‐specific immune responses. Our findings support the hypothesis that the escape of EBV carrying tumor cells from EBV‐specific immune surveillance may be facilitated by the fact that viral gene expression is limited to EBNA‐I.
Early‐age body size, adult weight gain and endometrial cancer risk
Authors: Marchand Loïc Le , Wilkens Lynne R. , Mi Ming‐Pi 
Published: February 2007

AbstractTo further characterize the association of obesity and endometrial cancer, in particular with regard to the role of early‐age obesity and adult weight gain, the authors assembled by computer linkage a population‐based historical cohort of 30,266 women born between 1913 and 1932, for whom weight and height had been recorded in 1942‐43 and 1972. Linkage of this cohort to the Hawaii Tumor Registry resulted in the Identification of 214 (mainly post‐menopausal) Incident cases of endometrial cancer for 1972‐1986. An average of 3.7 cancer‐free controls were matched to each case on month and year of birth and ethnicity. A case‐control analysis, conducted In each 5‐year birth cohort, revealed no clear association of endometrial cancer with weight, height or body mass at ages 10 to 29 years. However, positive associations with adult body weight and gain in body mass since 1942 were observed for women diagnosed at age 60 or older. This association with obesity was strongest in women whose body mass was below the median in 1942 and equal to or above the median in 1972. No association with body size was detected in women diagnosed before age 60. Parity, age at first birth and socio‐economic indicators for 1942 and 1972 did not confound the analysis. These findings suggest that obesity affects the late stages of endometrial carcinogenesis, and the possibility that one or more determinants of weight gain may be independently associated with endometrial cancer risk.
Alcohol consumption and risk of breast cancer
Authors: Sneyd M. J. , Paul Charlotte , Spears G. F. S. , Skegg D. C. G. 
Published: February 2007

AbstractIn a national case‐control study, 891 New Zealand women aged 25 to 54 with newly diagnosed breast cancer were compared With 1,864 control subjects selected at random from the electoral rolls. The relative risk of breast cancer for current drinkers of alcohol, compared with women who had never drunk alcohol, was 1.0 (95% confidence Interval 0.64 to 1.7). For ex‐drinkers the relative risk was 1.3 (95% confidence interval 0.74 to 2.5). Women drinking up to 14 drinks per week had no increase in risk, while the relative risk in those consuming more than 14 drinks per week was 1.8 (95% confidence interval 0.87 to 3.8). There was no evidence of effect modification by age at diagnosis, menopausal status, body mass index, or any of the other variables examined. While these results provide little support for the hypothesis that moderate alcohol consumption increases the risk of breast cancer, they are not inconsistent with the weak associations that have been found in many other studies. Possible explanations for such a relationship are considered.
opisthorchis viverrini infestation and endogenous nitrosamines as risk factors for cholangiocarcinoma in thailand
Authors: Srivatanakul P. , Sukaryodhin S. , Ohshima H. , Khlat M. , Parkin M. , Brouet I. , Bartsch H. 
Published: February 2007

AbstractCholanglocarcinoma (CCA) is one of the most common cancers In north‐east Thailand and has been associated with infestation by the liver fluke Opisthorchis viverrini (OV). Two samples of 12‐hr overnight urine (after dosing with proline and ascorbic acid or proline alone) were collected from 20 Inhabitants from each of 5 contrasting incidence areas for CCA. The incidence of CCA was not correlated with either the amount of NPRO or other nitrosamino acids, endogenous nitrosation potential (difference in NPRO levels between proline dose and proline and ascorbic dose), or nitrate level. However, when urinary levels of nitrosamino acids were compared in subjects living in high‐risk areas, subjects who were positive for OV antibody excreted significantly more (P < 0.01) NPRO (12.3 ± 18.7 μg/12 hr) after proline ingestion than those who were negative (3.5 ± 3.2 μg/12 hr). After ingestion of ascorbic acid, the NPRO levels in the positive subjects were significantly reduced (p < 0.01) to 2.4 ± 2.0 μg/12 hr, suggesting that endogenous nitrosation of proline was inhibited. Thus, endogenous nitrosation potential estimated from the difference between NPRO and the sum of nitrosamino acids excreted in the 2 urine samples was significantly higher in subjects positive for the OV antibody. Small amounts of pre‐formed nitrosamines were found in fermented fish and pork food items, which are consumed frequently in the high‐risk area for CCA. These results suggest that the interaction between chemical carcinogens, especially nitrosamines, and OV infestation may play a role in the development of cholangiocarcinoma in Thailand.
Tumor IGF‐II content in a patient with a colon adenocarcinoma correlates with abnormal expression of the gene
Authors: Lambert Sylvie , Gol‐Winkler Rosita , Collette Julien , Gillis Jacqueline , Franchimont Paul , Desaive Claude 
Published: February 2007

AbstractWe have recently reported abnormal insulin‐like growth factor‐II (IGF‐II) mRNA levels in a number of human colorectal adenocarcinomas. Using an IGF‐II radioimmunoassay, we have now detected high levels of both 10‐kDa and 7.5‐kDa IGF‐II species (2,370 ng/g) in a right colon tumor showing a 800‐fold IGF‐II gene over‐expression in comparison to the normal adjacent tissue. The higher‐molecular‐mass form represents 74% of the total immunoreactive IGF‐II detected in the tumor. This form appears to be less reactive in the radioreceptor assay than in the radioimmunoassay. The insulin‐like growth factor‐I (IGF‐I) concentration in the tumor is low. The patient's pre‐operative serum IGF‐II level is not increased and the proportion of the 10‐kDa species Is normal. In addition, the IGF‐II/IGF‐I ratio is 3 in the serum and 308 in the tumor. Our results show that the very high IGF‐II level produced by the tumor does not Influence the seric concentration of the growth factor.
The eortc melanoma group exchange program: Evaluation of a multicenter monoclonal antibody study
Authors: Carrel Stefan , Doré Jean‐François , Ruiter Dirk J. , Prade Michel , Lejeune Ferdy J. , Kleeberg Ulrich R. , Rümke Philip , Bröcker Eva B. 
Published: February 2007

AbstractIn the framework of the European Organisation for Research and Treatment of Cancer (EORTC), the Immunology and Pathology Subgroups of the Malignant Melanoma Cooperative Group undertook a large multicenter monoclonal antibody (MAb) study. Fourteen laboratories from 7 European countries tested a panel of 23 MAbs for immunohistological staining reactivity for malignant and non‐malignant lesions involving the melanocytic lineage. A standardized im‐munoperoxidase procedure was used and the results were evaluated using a standard protocol and data evaluation form developed in collaboration with the EORTC Data Center. According to this analysis, the antibodies in the panel could be classified into 3 main groups. The first group of MAbs includes those antibodies which stained the majority (>80%) of all primary tumors, irrespective of their Breslow thickness and the majority of metastatic lesions. In addition, these MAbs stained a high percentage of cells within a given lesion. Several antibodies of Group I were likewise reactive with the majority of naevoblasts and with normal melanocytes. The second group of MAbs included antibodies reacting only with a limited number of primary melanomas and metastatic lesions. Antibodies of Group II reacted only weakly, if at all, with normal melanocytes or naevocytes. The percentage of cells within a malignant lesion stained by these MAbs was always rather tow. The MAb group III detected surface structures whose expression appeared to be related to tumor progression; they did not react or reacted only weakly with naevi, and they all reacted with a small number of early primary melanomas (<0.75 mm). The number of lesions stained increased with increasing Breslow thickness. Our study suggests that the application of a panel of well defined MAbs might be of diagnostic and prognostic value in evaluating malignant melanoma.
Modulation of cis‐diamminedichloroplatinum(II) accumulation and sensitivity by forskolin and 3‐isobutyl‐1‐methylxanthine in sensitive and resistant human ovarian carcinoma cells
Authors: Mann Stephen C. , Andrews Paul A. , Howell Stephen B. 
Published: February 2007

AbstractWe have determined the effect of forskolin, an adenyl cyclase agonist, and 3‐isobutyl‐1‐methylxanthine (IBMX), a phosphodiesterase inhibitor, on the accumulation and cyto‐toxicity of cisplatin (DDP) In 2008 human ovarian carcinoma cells. In DDP‐sensitive 2008 cells, forskolin and IBMX caused 2.1‐fold and 2.3‐fold Increases, respectively, in the short‐term accumulation of DDP relative to untreated cells. The inactive analogue, 1,9‐dideoxyforskolin, decreased DDP accumulation. Forskolin and IBMX also increased accumulation in A2780 cells. Neither forskolin nor IBMX had any effect on DDP accumulation in DDP‐resistant 2008 cells, the effects were detectable as early as I min and persisted at 60 min. The concentrations for half‐maximal stimulation of DDP accumulation were approximately 0.2 μM for forskolin and 0.2 mM for IBMX. Forskolin caused marked increases in cAMP levels in both sensitive and resistant 2008 cells within I min, although there were differences in the subsequent time‐courses of the response. Both 2008 cell types had identical cAMP‐dependent protein kinase (PKA) activity. These results suggest that there is a target downstream of PKA that is an Important participant in DDP accumulation, and that this target is defective of missing in DDP‐resistant cells. Following a 1‐hr exposure to drugs, forskolin and IBMX at concentrations that were by themselves completely non‐toxic increased the slopes of the clonogenic survival vs. DDP concentration curves in 2008 cells 1.9‐fold and 3.3‐fold, respectively. In DDP‐resistant 2008 cells, however, forskolin and IBMX increased the slopes only 1.2 and 2.6‐fold, respectively. These effects of forskolin and IBMX on DDP cytotoxicity did not directly correlate with the effects on the 1‐hr DDP accumulation which suggested that, in addition to modulating DDP accumulation, these agents increase the cytotoxicity of the intracellular platinum. The results indicate that modulation of cAMP levels can have important effects on DDP accumulation and cytotoxicity in 2008 cells and that these effects are significantly diminished in DDP‐resistant cells.
Induction of mouse mammary tumours in a transplantation system by the sequential introduction of the myc and ras oncogenes
Authors: Bradbury Jane M. , Sykes Helen , Edwards Paul A. W. 
Published: February 2007

AbstractA novel helper‐free defective retrovirus containing the v‐Ha‐ras oncogene has been constructed and used to introduce the gene into primary mouse mammary epithelial cells already containing the v‐myc oncogene. Transplantation of such doubly altered cells into cleared mammary fat pads led to the formation of mammary tumors within 6 to 8 weeks of transplantation. In a separate experiment, both oncogenes were simultaneously introduced to normal epithelium and once again tumours were formed. Neither oncogene alone gave a significant rate of tumour formation, although myc alone gave a reproducible hyperplasia as previously reported and ras alone gave occasional dysplastic or alveolar lesions. The results presented here demonstrate the progression of a normal cell through a hyperplastic intermediate to a tumour‐forming cell in a versatile in vivo transplantation model.
Establishment of a human leukemia subline resistant to the growth‐inhibitory effect of 12‐o‐tetradecanoylphorbol 13‐acetate (TPA) and showing non‐P‐glycoprotein‐mediated multi‐drug resistance
Authors: Takeda Yuichiro , Nishio Kazuto , Sugimoto Yoshikazu , Kasahara Kazuo , Kubo Sachiyo , Fujiwara Yasuhiro , Saijo Nagahiro , Niitani Hisanobu 
Published: February 2007

AbstractWe have previously reported that K562/ADM, a typical P‐glycoprotein‐mediated multi‐drug‐resistant cell line, is cross‐resistant to the growth‐inhibitory effect of 12‐O‐tetradecanoylphorbol 13‐acetate (TPA) and non‐TPA type tumor promoters. To elucidate the mechanism of cross‐resistance to tumor promoters in K562/ADM, we have established a K562 subline resistant to TPA‐induced growth inhibition by exposing K562 cells to N‐methyl‐N'‐nitro‐N‐nitrosoguanidine for 24 hr followed by continuous exposure to TPA. A K562 subline resistant to the TPA‐induced growth inhibition, termed K562/TPA, was selected by a limiting dilution technique. K562/TPA was more than 500‐fold resistant to TPA compared with parental K562 cells. K562/TPA showed cross‐resistance to etoposide, tenlposide, adriamycin (ADM), vincristine, vindesine and 3‐[(4‐amino‐2‐methyl‐5‐pyrimidinyl)] methyl‐1‐(2‐chloroethyl)‐l‐nitrosourea, but showed collateral sensitivity to cisplatin. Although K562/ADM was not cross‐resistant to 3′‐deamino‐3′‐morpholino‐13‐deoxo‐10‐hydroxycarminomycin (MX2), an anthracycline derivative, K562/TPA was cross‐resistant to MX2. By Northern blot analysis, K562/TPA did not express MDR‐1. Accumulation of ADM by K562/TPA was no lower than that of K562 although that of K562/ADM was 5‐fold lower than K562. We examined the subcellular distribution of ADM by fluorescence microscopy. The fluorescence of ADM was located in the nucleus of K562 and mainly in the cytoplasm of K562/TPA and K562/ADM. The distribution of ADM in K562/TPA, however, was different from that in K562/ADM. These results suggested that K562/TPA had a non‐P‐glycoprotein‐mediated multi‐drug‐resistance phenotype and that the mechanism of drug‐resistance in this cell line might be explained by an alteration in the intracellular drug distribution.
Induction of autologous tumor‐specific cytotoxic T cells in patients with liver cancer. Characterizations and clinical utilization
Authors: Aruga Atsushi , Yamauchi Katsumi , Takasaki Ken , Furukawa Takaji , Hanyu Fujio 
Published: February 2007

AbstractTo generate autologous‐tumor‐specific cytotoxic T cells (CTL), peripheral blood mononuclear cells (PBMC) obtained from cancer patients were cultivated with autologous tumor cells for 5 days, and restimulated with interleukin‐2 for another 5 days. Subsequently, their cytotoxic activity was examined by an in vitro cytotoxic test as well as by Winn's assay utilizing nude mouse transplanted autologous tumors. The present results demonstrated that these in vitro‐stimulated cells were able to kill autologous tumor cells but not allogeneic tumors, and that they also inhibited the growth of transplanted autologous tumors in the nude mouse. Their cytotoxic activity was completely abrogated by pre‐treatment with either anti‐CD3 or anti‐CD8, but not with anti‐CD4, plus complement. Based on these studies, we injected these CTL via the hepatic artery into patients having either non‐resected tumors or recurrent tumors in the liver. Among 15 treated patients (13 with hepatocellular carcinoma and 2 with metastatic liver cancer) 2 complete responses, 3 partial responses and 4 minor responses were observed. During the 6 to 25 months following injection of CTL, no definite signs of tumor recurrence or regrowth were demonstrated in these 5 responding patients (complete plus partial).
Prognostic significance of her‐2/neu expression in breast cancer and its relationship to other prognostic factors
Authors: Rilke Franco , Colnaghi Maria Ines , Cascinelli Natale , Andreola Salvatore , Baldini Maria Teresa , Bufalino Rosaria , Porta Giuseppe Della , Ménard Sylvie , Pierotti Marco A. , Testori Alessandro 
Published: February 2007

AbstractArchival surgical specimens from 1,210 female breast cancer patients treated between 1968 and 1971 and with a 19‐year follow‐up were reanalyzed with special reference to several parameters, such as size of the primary tumor, axillary nodal involvement, histologic grade, degree of inflammatory infiltrate (LPI) of the tumor and expression of the neu onco‐protein (p185) as detected by immunohistochemistry. In a multifactorial analysis the 4 former factors were found to be independent prognostic parameters. Over‐expression of p 185 was found to be related to tumor size and grade and to LPI but not to pathologic nodal status. Over‐expression of p185 showed a negative impact upon survival in node‐positive but not in node‐negative patients. However, in the subset of node‐negative patients without LPI, p185 over‐expression showed the same correlation with a poor prognosis as in node‐positive patients. In contrast, in node‐negative and LPI‐positive patients, p185 over‐expression correlated with a good prognosis. Also, the prognosis of patients with positive nodes, presence of LPI and no p185 over‐expression was similar to that of patients with negative nodes, absence of LPI and p185 over‐expression.