bluuebunny/crossref_metadata_2025_split huggingface dataset:
Two newly established cell lines derived from the same colonic adenocarcinoma exhibit differences in EGF‐receptor ligand and adhesion molecule expression
Authors: Solic Nicola , Collins Jane E. , Richter Audrey , Holt Susan J. , Campbell Ian , Alexander Peter , Davies Donna E. 
Published: February 2007

AbstractTwo morphologically distinct cell lines, GP2d and GP5d, derived from the same adenocarcinoma of the colon, have been established and characterised. Both clones have the same genetic changes, consistent with the usual pattern of tumour progression in colon cancer. The cells also have an inverted duplication of bands 10q11 to 10q21, but Southern blot analysis failed to identify any translocations involving the ret protooncogene, which maps to this region. GP2d grew by spreading from the edges of microcolonies to form a confluent layer of cells. GP5d grew in discrete islands of cells forming multilayered colonies. These differing patterns of growth correlated with variation in expression or cellular distribution of α2‐integrin, desmoplakin and e‐cadherin. Only GP2d responded to exogenously added epidermal growth factor (EGF), transforming growth factor‐alpha (TGFα) or insulin with an increase in cell numbers, even though both cell lines possessed similar numbers of EGF receptors. Analysis of EGF receptor ligand expression showed that GP5d cells expressed relatively more TGFα mRNA than did GP2d; in contrast, amphiregulin mRNA, which was abundant in GP2d, was virtually undetectable in GP5d. Even though GP5d failed to exhibit a growth response to EGF, it underwent a marked epithelial‐mesenchymal transition when treated with EGF, indicating separation of growth and morphological responses to EGF. © 1995 Wiley‐Liss Inc.
Radiation‐induced apoptosis in human sarcoma and glioma cell lines
Authors: Staffer Norbert J. , Stuschke Martin , Sak Ali , Stüben Georg 
Published: February 2007

AbstractSix human soft‐tissue sarcoma and 14 glioma cell lines, exhibiting considerable differences in radioresponsiveness and histological grade of differentiation of the parental tumour, were examined with respect to apoptosis development after irradiation with 60Co γ‐rays. After test doses of 6 and 25 Gy, significant changes characteristic of apoptosis occurring within 6 to 30 hr were exhibited by only 2 differentiated sarcoma cell lines, EL7 and ESS2. The characteristic intemucleosomal fragmentation of DNA was detected as early as 6 hr after exposure of subconfluent monolayer cultures to 6 Gy. It was limited to cells that had detached from the culture plate, whereas adherent cells showed random degradation of DNA, namely after higher doses (25Gy) or longer incubation times (30 hr). As assessed by fluorescence microscopy of unfixed cultures stained with Hoechst 33342 and propidium iodide, the proportion of cells showing apoptotic bodies in non‐irradiated controls was < 0.l% and 0.3% for EL7 and ESS2, respectively. The doseresponse relationship for apoptosis was determined at 9 hr post‐irradiation. After 2 Gy, the percentage of apoptotic cells was elevated to 3.4% in EL7 and 4.5% in ESS2 cultures. Saturation was obtained above 6 Gy, with 8.4% apoptosis in EL7 and 15% in ESS2 after 25 Gy. Taken together, rapid ionizing‐radiation‐induced apoptosis seems to be limited to a subgroup of sarcomas and is unlikely to occur in gliomas. © 1995 Wiley‐Liss Inc.
Microvessel density and vessel invasion in lymph‐node‐negative breast cancer: Effect on recurrence‐free survival
Authors: Obermair Andreas , Kurz Christine , Czerwenka Klaus , Thoma Martin , Kaider Alexandra , Wagner Theresa , Gitsch Gerald , Sevelda Paul 
Published: February 2007

AbstractMicrovessel density (MVD) and blood and lymphatic vessel invasion (BLVI) were investigated with regard to their influence on the disease ‐ free survival (DFS) in node ‐ negative breast cancer patients. Paraffin embedded microsections of 230 patients with T1,2 NO breast cancer were immunohistochemically stained for factor Vlll ‐ related antigen. Every cluster consisting of more than highlighted endothelial cells was considered a countable microvessel. MVD was counted in 4 fields of 0.25 mm2each. All MVD values are given as value for the sum of 4 fields of 0.25 mm2each, that is, I mm2. BLVI was considered positive, when at least one tumor cell could be identified in a stained lumen. Out of 230 patients, 49 experienced local or distant recurrence and had a mean MVD of 72.4/mm2, whereas 181 patients who lived without recurrent disease had a mean MVD of 45.3/mm2. BLVI was negative in 6.2% of the cases with and in 93.8% of the cases without recurrent disease. BLVI was positive in 59.4% of the cases without and 40.6% of the cases with recurrent disease. MVD and BLVI remained the only significant prognostic factors of DFS in the Cox ‐ Model. Tumor size, histological grade, and hormonal ‐ receptor status were not prognosticallv relevant in the Cox ‐ model. 10 ‐ year ‐ DFS was 93.3% in BLVI ‐ negative/MVD ⩽ 40/mm2patients, 88.1% when MVD was high or BLVI was positive and 48.9% in BLVI positive/MVD ⩽ 40/mm2patients. Our present data indicate that MVD and BLVI identify a very ‐ low risk group among node ‐ negative breast cancer patients, who will not benefit from systemic adjuvant therapy. MVD and BLVI should be used as stratification criteria in clinical trails on node ‐ negative breast cancer patients. © 1995 Wiley‐Liss Inc.
Purine enzyme profile in human colon‐carcinoma cell lines and differential sensitivity to deoxycoformycin and 2′‐deoxyadenosine in combination
Authors: Camici Marcella , Turriani Maura , Tozzi Maria Grazia , Turchi Gino , Cos Joan , Alemany Cristina , Miralles Angela , Noe Veronique , Ciudad Carlos J. 
Published: February 2007

AbstractDifferent cell lines, 2 from human colon carcinoma (LoVo and HT29) and 1 from Chinese hamster ovary (CHO K‐1), were examined to assess the effect of deoxycoformycin (dCF), an inhibitor of adenosine deaminase (ADA), and 2′‐deoxyadeno‐sine (dAdo) on their growth. When used alone, neither dCF or dAdo were cytotoxic for the 3 cell lines, while their combination caused inhibition of cell growth, with the following sensitivity: CHO K‐1 > LoVo > HT29. We studied the pattern of enzymatic activities involved in the metabolism of dAdo in the 3 cell lines. The phosphorylation of dAdo by adenosine kinase appears to play a central role in the toxicity of the deoxynucleoside in combination with dCF. In fact, CHO K‐1 cells, which are the most sensitive, possess the highest level of this enzyme. Moreover, the cytotoxic effect was almost completely reversed in the 3 cell lines when inhibitors of adenosine kinase, such as 5′‐amino‐5′‐deoxyadenosine and iodotubercidine, were added to the culture medium together with dCF and dAdo. In addition, baby hamster kidney (BHK) adenosine‐kinase‐deficient (AK−) cells were highly resistant to this treatment. Uptake inhibition of dAdo using dipyridamole also caused reversal of the toxicity. The AMP and deoxyAMP dephosphorylating activities, much lower in the CHO K‐1 cells, also appear to play a central role in the toxicity of dAdo when adenosine deaminase is inhibited. However, our data suggest that other factors may modulate the toxic effect, such as S‐adenosyl‐homocysteine‐hydrolase inhibition by dAdo at high concentrations. © 1995 Wiley‐Liss, Inc.
Induction of 2,5 oas gene expression and activity is not sufficient for IFN‐γ‐induced neuroblastoma cell differentiation
Authors: Corrias Maria Valeria , Gribaudo Giorgio , Guarnaccia Francesco , Ponzoni Mirco 
Published: February 2007

AbstractWe showed earlier that interferon‐γ is a powerful inducer of differentiation of human neuroblastoma (NB) cells. Although 2′,5′oligo‐adenylate synthetase (2,5 OAS) may play a role in mediating the anti‐proliferative and/or differentiative effects of interferons (IFNs), direct evidence is lacking. We have investigated gene and protein expression of the 4 different 2,5 OAS isoforms and their cumulative enzymatic activity in a previously characterized IFN‐γ‐sensitive human NB cell line, LAN‐5. Analysis of total and poly(A)+ RNA by Northern Mot and RT‐PCR indicated that expression of the mRNA coding for the 40‐, 46‐and 69‐kDa Isoforms was induced in a time‐ and dose‐dependent manner, reaching a maximum after a 36‐hr treatment with 1000 IU/ml of IFN‐γ. In the absence of treatment, only the mRNA for the 69‐kDa isoform was detectable by RT‐PCR. Inhibition of transcription with actinomycin D showed that 2,5 OAS mRNA was quite stable, with a half‐life of about 4 hr. With respect to the protein content, no 2,5 OAS isoform was present in proliferating LAN‐5 cells; following IFN‐γ treatment, the 100‐, 69‐ and 46‐kDa isoforms became detectable. Accordingly, 2,5 OAS enzymatic activity, virtually undetectable in untreated LAN‐5 cells, increased up to 132 pmol oligoadenylate/μg protein/hr after 48 hr of treatment, then slowly decreased, remaining detectable up to 96 hr. However, the 2,5 OAS proteins required an exogenous activation by synthetic dsRNA to exert enzymatic activity. It is therefore conceivable that they do not play a biological role in NB cell functions. Moreover, an increase in 2,5 OAS enzymatic activity was also observed in NB cells resistant to the differentiation‐promoting activity of IFN‐γ, further suggesting that 2,5 OAS induction was not sufficient to trigger IFN‐γ‐dependent neuronal maturation. Furthermore, other differentiation‐inducing agents, such as retinoic acid and cytosine arabinoside, or complete proliferative arrest produced by serum deprivation, failed to enhance 2,5 OAS activity, thus indicating that the 2,5 OAS system is not directly involved in mediating other differentiative pathways of NB cells. © 1995 Wiley‐Liss, Inc.
The prognostic influence of neuroendocrine cells in prostate cancer: Results of a long‐term follow‐up study with patients treated by radical prostatectomy
Authors: Noordzij Marinus A. , Van Der Kwast Theodorus H. , Van Steenbrugge Gert Jan , Hop Wim J. C. , Schröder Fritz H. 
Published: February 2007

AbstractThe distribution of immunohistochemically defined neuroen‐docrine (NE) cells in benign, pre‐cancerous and neoplastic prostatic tissues and the prognostic value of these cells in prostate cancer were studied in the radical prostatectomy specimens of 90 patients from whom complete long‐term follow‐up data were available. The tissue blocks containing all the different Gleason patterns observed in a particular tumor were selected and immunostained. Since chromogranin B stained only a few cells compared to chromogranin A (CgA), NE cells were only defined by their reactivity with CgA. A semiquantificative CgA score was assessed for all distinct pathological areas. Cox's regression model was used to analyze the influence of final TNM classification (TNM, 1992), Gleason sum score (GSS), age and CgA score on the probability of progression and tumor‐specific death. NE cells were demonstrated in all normal prostatic tissues and in most hyperplastic and intra‐epithelial neoplastic lesions. CgA staining was seen in 78% of the tumors. CgA scores were not related with Gleason growth patterns, GSS or TNM classification and had no prognostic value. The independent prognostic variables in Cox's regression model were: GSS and pT stage for progression and GSS for tumor‐specific survival. Theoretically, NE cells could influence tumor behavior and this discrepancy suggests the need for experimental studies to investigate the role of NE cells in the normal and neoplastic prostate. © 1995 Wiley‐Liss Inc.
Effect of different platelet agonists on intracellular free CA++ concentrations in human tumor cells: Possible role in tumor growth
Authors: Saporiti Anna , Brocchieri Alessandra , Porta Camillo , Moroni Mauro , Grignani Guido 
Published: February 2007

AbstractModulation of cytoplasmic Ca++ concentration is a mechanism common to signal transduction pathways regulating many cellular phenomena, including the interactions of tumors with the hemostatic system. We have investigated the pro‐aggregating and pro‐coagulant activities of human tumor cell lines cultured in vitro and the ability of different platelet agonists to induce Ca++ transients in these cells. Cells of a malignant mesothelioma line activated platelets by a thrombin‐dependent mechanism; on the contrary, HeLa cells, derived from a uterine cervical cancer, possessed ADP‐dependent pro‐aggregating activity, and DND‐1A melanoma cells did not stimulate platelet aggregation. All cell lines showed a tissue‐factor‐like procoagulant property, more pronounced in mesothelioma cells. Furthermore, ADP was able to induce a transient increase in cytoplasmic Ca++ concentration in tumor cells from all lines; collagen showed this effect in mesothelioma cells and in HeLa cells, and thrombin was effective only in mesothelioma cells. PAF never induced Ca++ fluxes in any of the cell lines investigated. Finally, the calcium‐channel blocker verapamil inhibited agonist‐induced Ca++ transients in tumor cells and in vitro tumor‐cell growth. These data may help to identify new possible mechanisms of the 2‐way interaction of tumors with the hemostatic system. © 1995 Wiley‐Liss Inc.
Treatment of wistar rats with a renal carcinogen, ferric nitrilotriacetate, causes dna‐protein cross‐linking between thymine and tyrosine in their renal chromatin
Authors: Toyokuni Shinya , Mori Toshiaki , Hiai Hiroshi , Dizdaroglu Miral 
Published: February 2007

AbstractFerric nitrilotriacetate (Fe‐NTA) induces renal proximal tubular damage associated with lipid peroxidation and oxidative DNA base modifications that finally leads to a high incidence of renal adenocarcinoma in rodents. In the present study, we report on the in vivo formation of DNA‐protein cross‐links (DPCs) involving thymine and tyrosine in the renal chromatin of Wistar rats treated with single or repeated i.p. administration of Fe‐NTA. Analyses of chromatin samples by gas chromatography/mass spectrometry revealed a significant increase in the amount of 3‐[(1, 3‐dihydro‐2, 4‐dioxopyrimidin‐5‐yl)‐methyl]‐L‐tyrosine (Thy‐Tyr cross‐link) 24 and 48 hr after the administration of Fe‐NTA. At 19th day of Fe‐NTA treatment, the amount of Thy‐Tyr cross‐link decreased to the control level, indicating the presence of cellular repair activity. Thy‐Tyr cross‐link may play a role in the genetic alteration of this renal carcinogenesis model, since mitoses for regeneration of renal proximal tubules were closely associated with the increase in DPCs. © 1995 Wiley‐Liss Inc.
Manifestations of cancer cachexia induced by colon 26 adenocarcinoma are not fully ascribable to interleukin‐6
Authors: Soda Kuniyasu , Kawakami Masanobu , Kashii Akiyoshi , Miyata Michio 
Published: February 2007

AbstractIn order to further clarify the role of interleukin 6 (IL‐6) in the pathogenesis of cachexia, recombinant human IL‐6 (hIL‐6) was administered s.c. by osmotic pump for 9 days at a dose of 1 or 10 μg/day into CDFI mice inoculated with a non‐cachexia‐inducing subclone of colon 26 adenocarcinoma (clone 5), or with a cachexia‐inducing subclone (clone 20) of this malignancy. The serum level of IL‐6 in non‐cachectic mice with clone‐5 tumors was 35% lower than in cachectic mice bearing clone 20 of colon 26 adenocarcinoma on the 19th day after tumor inoculation. IL‐6 administration induced anemia, thrombocytosis and visceral organ hypertrophy not only in mice with clone‐5 tumors but also in control mice with no tumor burden. Lipolysis and proteolysis became conspicuous when a large dose (10 μg/day) of IL‐6 was infused into mice with clone‐5 tumors. However, IL‐6 supplementation did not induce loss of body weight, a decline in food intake or lymphocytopenia, which were characteristically observed in cachectic mice with clone‐20 tumors. In conclusion, IL‐6 appears to be a permissive factor for the development of cachexia but, while it can induce some of the symptoms typical of cachexia, it cannot in itself induce the full cachectic syndrome. © 1995 Wiley‐Liss Inc.
Translocation t(9;22)(q22;q12) is a primary cytogenetic abnormality in extraskeletal myxoid chondrosarcoma
Authors: Stenman Göran , Andersson Helene , Mandahl Nils , Meis‐Kindblom Jeanne M. , Kindblom Lars‐Gunnar 
Published: February 2007

AbstractThe cytogenetic and in vitro growth characteristics of 3 cases of extraskeletal myxoid chondrosarcoma (EMC) are described. In cell culture, the tumor cells retained the immunocytochemical and ultrastructural characteristics of EMC. Cytogenetically, 2 of the cases showed an apparently identical t(9;22)(q22;q12). In one case, the t(9;22) was found together with a dup(1)(q12q44), and in the other case it was found together with several other aberrations. The third case had an inv(10)(p11.2q22) as the sole karyotypic abnormality. Of 4 cases of EMC previously analyzed, 2 showed a t(9;22)(q22;q11–12) and one case a t(9;22;15)(q31;q12.2;q25). Thus, 5 out of 7 cases of EMC showed recombination between 9q22–31 and 22q11–12, indicating that this represents a tumor specific abnormality. The breakpoints on 22q were in all 5 cases Cytogenetically indistinguishable from those seen in Ewing's sarcoma with t(11;22), clear‐cell sarcoma with t(12;22), and desmoplastic small round cell tumors with t(11;22). Molecular cloning of these translocation breakpoints revealed involvement of the EWS gene (located at 22q12) in all 3 tumor types. These observations raise the intriguing question of whether the EWS gene might also be involved in the t(9;22) in EMC. © 1995 Wiley‐Liss, Inc.
Breast‐cancer risk and oral contraceptive use in slovenian women aged 25 to 54
Authors: Primic‐Žakelj Maja , Evstifeeva Tatiana , Ravnihar Božena , Boyle Peter 
Published: February 2007

AbstractResults of a previous case‐control study in Slovenia showed a significantly elevated risk of breast cancer for ever‐OC users aged 25 to 54 years. A further study was conducted in 1988–1990 in the whole of Slovenia, employing more rigorous epidemiological methodology. Cases were 624 women with breast cancer, aged 25 to 54 years, diagnosed at the Institute of Oncology in Ljubljana and other Slovenian hospitals. Controls were 624 women identified through the Population Registry, randomly selected and matched with cases by date of birth and commune of residence. Data were collected by personal interview, using coloured photographs of packages of all OC on the Slovenian market since 1964. A calendar of reproductive life events was constructed with participants to improve estimation of exposure. The adjusted odds ratio (OR) for ever‐users was 1.09. There was no increase in risk with total duration of use, interval since first use, age at starting OC, according to use before or after first delivery and time between menarche and age at first use. Increased risk (OR = 2.92) was found for OC users at the time of diagnosis and for those stopping them less than 6 months before (current users). The risk was not increased for those who stopped OC more than 6 months before diagnosis. The results of this study are consistent with most studies showing no overall effect of OC in women aged till 55 years ever using them. Increased risk of breast cancer in current OC users suggests a possible promoting effect of the pill in susceptible women, and indicates the need for careful breast surveillance of these women while they are using OC and in the period immediately following cessation. © 1995 Wiley‐Liss, Inc.
Studies of in vivo recruitment and activation of cytotoxic lymphocytes using a gelatin‐sponge model of concomitant tumor immunity
Authors: Park Julie A. , Brown Rebecca A. , Kurt Robert A. , Akporiaye Emmanuel T. 
Published: February 2007

AbstractWe have earlier described a sponge model of concomitant tumor immunity that permits the capture and isolation of effector T lymphocytes that mediate the rejection of a secondary EMT6 tumor implant In this study, we have employed the sponge model to study lymphocyte homing and in situ activation during the development of concomitant tumor immunity. Our results demonstrate that EMT6‐specific CTL in animals bearing primary EMT6 tumors home preferentially to sponges implanted with EMT6 tumor cells, as compared with contralateral sponges lacking tumor cells or sponges injected with antigenically distinct 168 tumor cells. We further show that recruitment is selective and is not in response to a foreign‐body reaction to the sponge. In addition, we show that EMT6‐specific CTL were recovered from sponges injected either with intact EMT6 tumor cells or with a mixture of EMT6‐derived membranes and supernatant. In contrast, cells accumulating in sponges injected with membranes or supernatant alone were not cytolytic. Thus, maximal recruitment, retention, and activation of CTL precursors require putative chemo‐attractive factors secreted by tumor cells as well as interaction with tumor antigen. © 1995 Wiley‐Liss, Inc.
The epithelial/carcinoma antigen EGP‐1, recognized by monoclonal antibody RS7–3G11, is phosphorylated on serine 303
Authors: Basu Amartya , Goldenberg David M. , Stein Rhona 
Published: February 2007

AbstractRS7–3G11 is a murine monoclonal antibody (MAb) raised against human non‐small‐cell lung carcinoma, and is under clinical evaluation. The epithelial/carcinoma antigen EGP‐1, defined by RS7–3G11, was isolated and purified to homogeneity from a cervical carcinoma cell line, ME 180. EGP‐I is a glycoprotein with an average molecular mass of 47.8 kDa. Metabolic labeling of the antigen with 32P‐orthophosphate and subsequent immunoprecipitation with RS7–3G11 showed that it is a phospho‐protein. Phosphoamino acid analysis of the in vivo phosphorylated EGP‐1 revealed that the phosphorylation is on serine. In vitro analysis with purified antigen demonstrated that protein kinase C, and not protein kinase A, is involved in phosphorylating the antigen in vitro. In vitro analysis indicated a stoichiometry of phosphorylation of 0.54 mole of phosphate per mole of EGP‐1. Phosphoamino acid analysis and phosphopeptide mapping of the antigen phosphorylated in vitro by protein kinase C showed that phosphorylation occurred on a serine residue, specifically on serine 303, located in the cytoplasmic domain of EGP‐1. Treatment of ME 180 cells with phorbol ester increased the phosphorylation of EGP‐1. The biological function of EGP‐1 remains to be elucidated. In this report we elucidate an involvement of protein kinase C in phosphorylating EGP‐1, which may signify a role for this antigen in signal transduction across the cell membrane. © 1995 Wiley‐Liss, Inc.