bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cystatin C and cathepsin B in human colon carcinoma: Expression by cell lines and matrix degradation
Authors: Coriicchiato Olivier , Cajot Jean‐Franqois , Abrahamson Magnus , Chan Shu Jin , Keppler Daniel , Sordat Bernard 
Published: February 2007

AbstractExpression of the cysteine proteinase cathepsin B and its physiological inhibitor cystatin C was analyzed in vitro in I human fibrosarcoma and 4 human colon carcinoma cell lines. Cystatin C antigen as well as cathepsin B activity were detected in the conditioned media of the 5 cell lines. The corresponding cell extracts expressed high levels of cathepsin B activity, whereas only trace amounts of cystatin C antigen could be found. Northern‐blot analysis revealed the presence in the 5 cell lines of a 0.8‐kb cystatin C mRNA transcript and 2 cathepsin B transcripts of 2.3 and 4.3 kb. Pepsin treatment of tumor‐cell‐released cathepsin B induced an average 7.3‐fold increase in activity, indicating that the enzyme was mainly present as a latent form in conditioned medium. The pepsin‐activated cathepsin B from one colon carcinoma cell line was further characterized using the cysteine proteinase inhibitors E‐64, recombinant cystatin C, a cystatin‐C‐derived peptidyl inhibitor (Z‐LVG‐CHN2), and cathepsin‐B‐specific diazomethyl ketone inhibitors (Z‐FT(OBzl)‐CHN2, Z‐FS(OBzl)‐CHN2). This activity was totally neutralized by recombinant cystatin C, suggesting a potential for interaction between released extracellular cathepsin B and cystatin C. In vitro assays of degradation of extracellular matrix showed that cyrteine proteinase inhibitors could decrease matrix degradation induced by pepsin‐activated conditioned media. With colon cells, this inhibition was not observed, indicating a requirement for an extracellular activation of latent cathepsin B. Our data provide evidence that cystatin C and latent cathepsin B are both released extracellularly by colon carcinoma cells in vitro. They suggest that cystatin C and cathepsin B interactions may participate, in an as yet unelucidated way, in the modulation of the invasive phenotype of human colonic tumors. © 1992 Wiley‐Liss, Inc.
Phosphoprotein B23 translocation and modulation of actinomycin D and doxorubicin cytotoxicity by dipyridamole in hela cells
Authors: Bor Amy Meei‐Shuu , Chang Fu‐Jung , Yunc Benjamin Yat‐Ming 
Published: February 2007

AbstractDuring continuous exposure, cells were more responsive to doxorubicin (DOX) in the presence of dipyridamole (DPM). Translocation of nucleolar phosphoprotein 823 and inhibition cell growth occurred with a lower dose of DOX and in a shorter incubation time in the presence of DPM. DPM did not change translocation induced by actinomycin D (Act‐D). Short exposure of HeLa cells to Act‐D induced “reversible” translocation of protein 823 as well as “reversible” inhibition of cell growth. DPM included in the cell culture after removal of Act‐Dinhibited the recovery of cell growth as well as the corresponding relocalization of protein 823 from the nucleoplasm to nucleoli. DPM administered in the fresh medium after 30 min exposure to DOX had little effect on the potentiation of the induced translocation of protein 823 and inhibition of cell growth. Our results indicated that “B23 translocation” closely associated with states of cell growth. The potentiation the inhibition of cell growth by DPM is associated with the extent of enhanced protein 823 translocation. “B23 translocation” may therefore be a simple and rapid method for assessing the inhibition of cell growth and for determining the efficacy of combination cancer chemotherapy. © 1992 Wiley‐Liss, Inc.
Differences in expression of SPan‐1 and CA15‐3 antigens in blood and tissues
Authors: Ho Jenny J. L. , Chung Yong‐Suk , Yuan Mei , Henslee Jerry G. , Kim Young S. 
Published: February 2007

AbstractPancreatic and mammary cancer cells are reported to have different oligosaccharides on the same apomucin, the MUCI gene product. A better understanding of the tissue specificity of these sugar structures may help in identifying the source of mucins when they are found in the sera. Serum levels of 3 pancreatic‐cancer‐associated carbohydrate epitopes identified by monoclonal antibodies (MAbs) SPan‐1, 19‐9 and DU‐PAN‐2, were compared to those of CA15‐3 in a variety of malignant conditions. CA15‐3 identifies both carbohydrate and peptide determinants associated with the MUCI apomucin in breast tissues. SPan‐1 antigen was elevated in a high percentage of patients with pancreatic, gastric and colorectal cancer but in only a few of the patients with malignancies of non‐G1 origin such as breast, ovary and lung. The 19‐9 and DU‐PAN‐2 antigens had a similar pattern of much greater sensitivity for pancreatic cancer than for these non‐gastrointestinal cancers. The levels of these 3 markers showed significant correlations in pancreatic cancer. In contrast, CA15‐3 was elevated in a large number of patients with breast, lung, ovarian and pancreatic cancers. There was no correlation of CA15‐3 with the 3 other markers in pancreatic cancer. SPan‐1 and DF3/115D8 antigens in blood have different mobilities in SDS‐PAGE and buoyant densities. Moreover, SPan‐1 and DF3 antigenic determinants are localized in different regions of the same normal and malignant pancreas and breast tissues. Thus the SPan‐1 determinant can be dissociated from the breast peptide and/or carbohydrate determinants. © 1992 Wiley‐Liss, Inc.
Breast cancer and timing of surgery during menstrual cycle. A 5‐year analysis of 385 pre‐menopausal women
Authors: Gnant Michael F. X. , Seifert Michael , Jakesz Raimund , Adler Arthur , Mittlboeck Martina , Sevelda Paul 
Published: February 2007

AbstractIt has been proposed that the timing of breast‐cancer surgery in relation to menstrual phase has a prognostic impact on outcome. We carefully evaluated a combined 2‐center series of 385 pre‐menopausal women operated on for stage‐I and stage‐II breast cancer with a median follow‐up of 5 years for a possible impact on outcome of the date of their last menstrual period (LMP) before surgery. The distribution of risk factors of the study cohort as well as prognostic indicators corresponded to previously published results. Nodal status, grading, and (in part) hormone‐receptor status differentiate well between patient subgroups with high and low risk of relapse and death after breast‐cancer surgery. In neither univariate nor multivariate analysis was any impact of the so‐called “unopposed” estrogen secretion detected. We did not observe any effect of LMP on long‐term survival in any of several prognostic subgroups, in particular in hormone‐receptor‐positive patients. From our results and from the literature, we conclude that LMP does not provide any prognostic information for outcome after breast‐ cancer surgery and therefore the proposed modification of scheduling of breast‐cancer operations is not justified. © 1992 Wiley‐Liss, Inc.
Breast cancer is associated with loss of the c‐kit oncogene product
Authors: Natali P. G. , Nicotra M. R. , Sures I. , Mottolese M. , Botti C. , Ullrich A. 
Published: February 2007

AbstractThe proto‐oncogene c‐kit encodes a tyrosine kinase receptor related to the PDGF/CSF‐I receptors. Mutations of this gene result in impairment of hematopoiesis, melanogenesis and gametogenesis. Using monoclonal antibodies to the c‐kit gene product, we have analyzed its expression in normal and transformed human tissues. Unexpectedly, the receptor was found to be expressed in normal mammary epithelium. While in benign breast lesions, the c‐kit gene product was detected at variable levels in 82% of the instances, in primary tumors, no product could be identified in 87% of the cases. This phenotype is maintained in metastatic foci. These findings were confirmed by paired Northern blot analysis of RNA preparations from normal and tumor tissues. These results demonstrate that the c‐kit receptor may also be involved in the growth control of mammary epithelium and that this function may be impaired following malignant transformation and de‐differentiation. © 1992 Wiley‐Liss, Inc.
Expression of carcinoembryonic antigen and related genes in lung and gastrointestinal cancers
Authors: Kim Joohang , Kaye Frederic J. , Henslee Jerry G. , Shively John E. , Park Jae‐Gahb , Lai Shinn‐Liang , Linnoila R. Ilona , Mulshine James L. , Gazdar Adi F. 
Published: February 2007

AbstractCarcinoembryonic antigen (CEA), a tumor marker for lung cancers of small cell (SCLC) and non‐small cell (NSCLC) types, belongs in a multigene family which includes non‐specific cross‐reacting antigen (NCA) and biliary glycoprotein 1 (BGP). We used specific cDNA probes and a CEA immunoassay to determine the pattern of expression in normal and malignant lung and gastrointestinal (GI) tissues. Normal lung contained high amounts of NCA and a low concentration of CEA. All 3 genes were expressed discordantly in lung tumors and cell lines. In contrast, all three genes were expressed in most GI tumor cell lines. In both king and colorectal cell lines expression of NCA RNA was relatively high, while BGP RNA was relatively low, and the median concentrations of CEA were greater than in corresponding non‐malignant tissues. While CEA protein concentrations in lung cell lines were similar to those present in GI cell lines, the ratio Of NCA:CEA RNA was significantly higher in lung cancer lines than in colorectal lines. Thus, NCA constitutes most of the “CEA‐like” immunoreactivity previously described in lung cancers. There was excellent concordance between expression of CEA RNA and CEA protein, as well as between concentrations of CEA protein in cell line pellets and supernatant fluids. Of interest, significantly higher rates of CEA expression were present in lung cancers expressing neuroendocrine (NE) markers. The association between CEA expression and NE cell properties is intriguing and may prove to be of clinical interest. © 1992 Wiley‐Liss, Inc.
Specific cytogenetic abnormalities and k‐ras mutation in two new human colorectal‐adenoma‐derived cell lines
Authors: Williams Ann C. , Harper Sara J. , Marshall Christopher J. , Gill Robert W. , Mountford Richard A. , Paraskeva Christos 
Published: February 2007

AbstractTwo new human epithelial cell lines from sporadic colorectal adenomas designated S/RR and S/BR are reported. Both cell lines have extended growth capacities in vitro, reaching passages 38 and 40 respectively and show no sign of senescence. S/RR and S/BR cell lines have retained the ability to differentiate in vitro, as shown by mucin production from goblet‐like cells. S/BR was derived from a large colonic tubular villous adenoma (3 to 4 cm), whereas S/RR was derived from a small rectal adenoma (< 1 cm), and may represent a relatively early‐stage adenoma. The parent S/RR cell line has given rise to a clonogenic variant, designated S/RR/Cl, which also has shown no sign of senescence and has currently reached passage 43. Both the S/BR and the S/RR cell lines had mutations in codon 12 of the K‐ras gene, while retaining one normal allele. The presence of this mutation, particularly in the cell line S/RR derived from a small adenoma, is consistent with ras mutation being a relatively early event in colorectal carcinogenesis and is perhaps involved in the ability of the adenoma cells to progress and to give rise to an immortal cell line in vitro. The clonal derivatives of the S/RR cells have an isochromosome Iq and abnormalities Of chromosome 13 which include an isochromosome 13q. The S/BR cells have a deletion on the short arm of chromosome 1 and trisomy 7. The common abnormality for S/RR and S/BR cells involves chromosome 1. The involvement of different chromosomes in the 2 cell lines also suggests different pathways for malignant progression of the premalignant adenoma cells. © 1992 Wiley‐Liss, Inc.
Enhancement of cisplatin activity by lonidamine in human ovarian cancer cells
Authors: Silvestrini Rosella , Zaffaroni Nadia , Villa Raffaella , Orlandi Linda , Costa Aurora 
Published: February 2007

AbstractThe ability of lonidamine, an energolytic derivative of indazole‐carboxylic acid, to modulate the cytotoxicity of cisplatin was investigated in human ovarian‐cancer cell lines sensitive (A2780) or with experimentally induced resistance (A2780/cp8) to the alkylating agent. A 24‐hr post‐incubation with 300 μM lonidamine significantly potentiated the activity of a 1‐hr cisplatin treatment in both cell lines. In particular, the cisplatin IC50 value was reduced 4‐fold in the sensitive line and 5‐fold in the resistant line. Flow cytometric analysis showed that, in the resistant cell line, lonidamine alone did not affect cell kinetics, but when given after cisplatin it was able to transform the temporary G2 + M cell accumulation induced by the alkylating agent to a persistent block in S/G2 + M. In the A2780/cp8 cell line, lonidamine was also able to significantly enhance the accumulation of cisplatin‐induced DNA interstrand cross‐links. Our results suggest that lonidamine can positively modulate the anti‐tumor activity of cisplatin in ovarian cancer cells and also indicate that the drug is potentially useful in combination therapy including the alkylating agent for ovarian cancer patients. © 1992 Wiley‐Liss, Inc.
Secretion of cell‐adhesion‐promoting factors, fibronectin, fibronectin fragments and A 53‐kDa protein, by human rectal adenocarcinoma cells
Authors: Suzukl Katsuo , Ono Tetsuo , Umeda Makoto , Itoh Hajime 
Published: February 2007

AbstractProduction of cell‐adhesion proteins was examined in 10 cell lines and 5 cultured human cancer cells at an early passage. Two‐thirds of the tested cells produced and secreted into their culture medium variable amounts of material active in promoting cell attachment. One of the rectal carcinoma cell lines, CaR‐1, grew well in serum‐free medium and secreted a large amount of the active principle. The active principles produced by CaR‐1 cells were characterized after partial purification, and were found to be fibronectin and its fragments. The presence of fibronectin and its fragments was proved by the following facts: (I) reactivity to the monoclonal antibodies which recognize different epitopes of fibronectin, and (2) reactivity to RGD peptide which is the attachment sequence of fibronectin. In addition to fibronectin and its fragments, CaR‐1 cells were also shown to produce a 53‐kDa attachment factor. Unexpectedly, the protein was proved to be most probably the p53 suppressor gene product. © 1992 Wiley‐Liss, Inc.
Decreased expression of E‐cadherin and increased invasive capacity in EBV‐LMP‐transfected human epithelial and murine adenocarcinoma cells
Authors: Fahraeus Robin , Chen Welching , Trivedi Pankaj , Klein George , Obrink Björn 
Published: February 2007

AbstractThe EBV‐encoded membrane protein LMP is one of 9 viral proteins regularly expressed in virally immortalized B lymphocytes. It is expressed in EBV‐carrying lymphoblastoid cell lines of normal origin and in the majority of the poorly differentiated nasopharyngeal carcinomas, but not in Burkitt lymphomas. LMP has been reported to transform rodent fibroblasts, to inhibit epithelial differentiation and to alter morphology and cytokeratin expression in an in vitro immortalized human keratinocyte cell‐line, RHEK‐1. We now report that an LMP‐transfected mouse mammary carcinoma line, SHG, exhibits a similar morphological change to that previously described in the LMP‐transfected RHEK‐1. In the LMP‐transfected RHEK‐1 and SHG cells, we observed a decreased expression of the calcium‐dependent adhesion molecule E‐cadherin. The LMP‐transfected RHEK‐1 cells were capable of invading type‐1 collagen gels while the control cells were not. The LMP‐transfected SHG cells showed a significantly higher invasive capacity than the original cell line. © 1992 Wiley‐Liss, Inc.
Smoking‐related dna adducts in human gastric cancers
Authors: Dyke G. W. , Craven J. L. , Hall R. , Garner R. C. 
Published: February 2007

AbstractDNA was extracted from the tumour tissue of 26 patients (18 smokers, 8 non‐smokers) undergoing surgery for gastric cancer, and analyzed for the presence of DNA adducts by the 32P‐post‐labelling method. Adducts were detected in all samples tested, and adduct levels ranged from 2 adducts/108 nucleotides to 60 adducts/108 nucleotides. In male subjects, adduct levels were significantly greater in the DNA of smokers than in that of non‐smokers. These results support epidemiological data suggesting that smoking is a risk factor for gastric cancer. © 1992 Wiley‐Liss, Inc.
Quantitation of biological tumor markers (p53, c‐myc, Ki‐67 and DNA ploidy) by multiparameter flow cytometry in non‐small‐cell lung cancer
Authors: Mørkve Odd , Halvorsen Ole Johan , Stangeland Lodve , Gulsvik Amund , Laerum Ole Didrik 
Published: February 2007

AbstractFifteen primary non‐small‐cell lung carcinomas (8 adenocarcinomas and 7 squamous‐cell carcinomas) were analyzed by multiparameter flow cytometry for their expression of p53 and c‐myc proteins. In addition, the fraction of cells staining with the proliferation‐associated antibody Ki‐67 and DNA ploidy was determined. These 4 biological markers were analyzed in parallel samples from a single‐cell suspension made from fresh, frozen biopsies. Thus, the internal relationship between these markers within each tumor‐cell population was established. Three different anti‐pS3 antibodies were used: PAb 421, PAb 1801 and PAb 240. All 15 tumors were p53‐positive with the antibodies PAb 1801 and PAb 240, whereas only 9 were positive as judged by the antibody PAb 421. This indicates that the choice of p53 antibody is not irrelevant. Ten tumors were c‐myc‐positive; 7 of these were adenocarcinomas. The c‐myc‐positive tumors had a significantly higher level of p53 expression, judged by PAb 1801 and PAb 240, than c‐myc‐negative tumors. For PAb 421, there was no difference. We did not find any correlation between Ki‐67 staining and expression of p53 and c‐myc proteins, either with DNA ploidy, S‐phase fraction or histological type. Our study indicates that there might be an association between accumulation of p53 protein and c‐myc over‐expression in non‐small‐cell lung cancer, and that this in particular might apply to adenocarcinomas. Furthermore, we show that multiparameter flow cytometry is a powerful tool in the study of the relationship between different markers in a cell population. © 1992 Wiley‐Liss, Inc.
EGF receptor expression in primary laryngeal cancer: Correlation with clinico‐pathological features and prognostic significance
Authors: Maurizi Maurizio , Scambia Giovanni , Panici Pierluigi Benedetti , Ferrandina Gabriella , Almadori Giovanni , Paludetti Gaetano , De Vincenzo Rosa , Distefano Mariagrazia , Brinchi Domenico , Cadoni Gabriella , Mancuso Salvatore 
Published: February 2007

AbstractEpidermal‐growth‐factor‐receptor (EGFR) expression was evaluated in 103 primary laryngeal tumors and in 42 normal laryngeal tissue specimens. Significantly higher EGFR levels were found in cancer specimens than in normal mucosa (p = 0.0053). EGFR expression did not correlate with age, tumor localization, T classification, cervical‐lymph‐node involvement or type of surgery, whereas it was higher in poorly differentiated tumors (G3) than in well/moderately differentiated (G1‐G2) tumors (p < 0.05). Follow‐up data were available for 74 patients. When EGFR status and the most important clinico‐pathological characteristics were submitted to univariate analysis, tumor localization, type of surgery and EGFR status were found to be significantly correlated with disease‐free survival. The 24‐month disease‐free survival rate was 58% for EGFR+ cancer patients and 82% for EGFR‐ ones. With multivariate analysis, only EGFR status and tumor localization were identified as significant independent prognostic parameters. Data reported here suggest that high EGFR levels may identify a sub‐set of laryngeal‐cancer patients with a particularly unfavorable prognosis. © 1992 Wiley‐Liss, Inc.
Prognostic relevance of serum hyaluronan levels in patients with breast cancer
Authors: Ponting J. , Howell A. , Pye D. , Kumar S. 
Published: February 2007

AbstractThe serum hyaluronan (HA) level of 238 women with breast cancer was measured by means of a specific radiometric assay. The results show no significant increase in serum HA when compared to levels in 120 control sera. A number of prognostic factors were evaluated including stage of disease, lymph‐node involvement, tumour size, histology and presence of oestrogen and progesterone receptors in the tumour. No correlation was found with serum HA concentration and we conclude that serum HA level is of no prognostic significance in breast cancer. © 1992 Wiley‐Liss, Inc.
Growth of hodgkin cell lines in severely combined immunodeficient mice
Authors: von Kalle Christof , Wolf Jürgen , Becker Andreas , Sckaer Andrea , Munck Martina , Engert Andreas , Kapp Ursula , Fonatsch Christa , Komitowski Dymitr , de Lacroix Wolfgang Féaux , Diehl Volker 
Published: February 2007

AbstractNo animal model exists for the in vivo growth of Hodgkin's‐lymphoma‐derived cells. Neither unmanipulated Hodgkin's‐disease(HD)‐derived cell lines nor primary biopsy tissue could be grown in nude mice. Since the severe combined immunodeficient (SCID) mouse has been reported to be a better recipient for transplanted human lymphatic tissue than the nude mouse, we tested whether SCID mice provide suitable conditions for the in vivo growth of HD cell lines. Tumorigenicity of HD cells was tested in untreated and pre‐treated SCID mice and in another combined immunodeficient mouse strain, beige/nude/X‐linked immunodeficient (BNX) mouse. SCID mice supported in vivo growth of the 6 HD cell lines tested (L428, L540, L591, DEV, HD‐LM2, KM‐H2). Only one of the 6 lines (DEV) was tumorigenic in BNX mice. No HD cell line proliferated in T‐cell‐deficient nude mice. Thus, in vivo growth of HD cell lines appeared to be related to the degree of host immunodeficiency. Additional growth supportive treatments such as fibrosarcoma co‐transplantation, intraperitoneal mineral oil injection or immunosuppressive pre‐treatment (anti‐asialo‐GMI ‐antibody injection) permitted growth of 3 additional HD cell lines in BNX mice. The immunophenotype and karyotype of explanted graft cells were identical to the original cell lines. Our experiments describe an effective and reproducible xenograft model for growth of Hodgkin's‐disease‐derived cell lines. This may be of value for elucidating the growth characteristics of Hodgkin's‐lymphoma‐derived cells as well as for testing new therapeutic regimens. © 1992 Wiley‐Liss, Inc.