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  • 1
    Electronic Resource
    Electronic Resource
    Expression of the cyclin dependent kinase inhibitor p21WAF1/CIP1 in oesophageal squamous cell carcinomas (1997)
    Springer
    Virchows Archiv 430 (1997), S. 389-395 
    Details
    ISSN: 1432-2307
    Keywords: Key words Oesophageal neoplasms ; Cyclin-dependent kinase inhibitor ; p21 ; p53 ; Apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  To elucidate the role of CDK inhibitor p21WAF1/CIP1 in human oesophageal squamous cell carcinomas, we examined its expression immunohistochemically using surgically resected tissues from 25 patients, and have analyzed the relationship with alteration of p53 gene (F-SSCP analysis), proliferative activity (Ki-67 labelling index), frequency of apoptosis (in situ DNA nick end labelling), and degree of differentiation. P21 expression was observed in 11 cases (44%) with a percentage of positive cells ranging between 1% and 10%. Of the 25 cases, 4 cases showed 〉5% of positive cells. As for the relationship with p53 gene, all 7 p53-mutation positive cases were negative for p21 expression, whereas 11 out of 18 mutation negative cases showed positive for p21 expression. As for the relationship with degree of tumour differentiation, 6 out of 8 well differentiated type cases showed positive for p21 expression. By contrast, all 8 cases of poorly differentiated type were negative for p21 expression. Frequency of apoptotic cells was significantly higher in p21 positive cases than negative cases although Ki-67 labelling index was almost the same regardless of the expression of p21. P21 expressing cells were distributed mainly in the middle layers of the invading nests, especially around the keratinization, which was almost similar to the distribution of apoptotic cells. Our results suggest that expression of p21 in human oesophageal squamous cell carcinomas is induced by a p53-dependent pathway and affects apoptosis and differentiation of carcinoma cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004280050048
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  • 2
    Electronic Resource
    Electronic Resource
    Proliferative activity and p53 protein accumulation correlate with early invasive trend, and apoptosis correlates with differentiation grade in oesophageal squamous cell carcinomas (1997)
    Springer
    Virchows Archiv 430 (1997), S. 107-115 
    Details
    ISSN: 1432-2307
    Keywords: Oesophageal neoplasms ; Squamous cell carcinoma ; Proliferative activity ; Ki-67 ; p53 ; Apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using oesophageal squamous cell carcinoma samples of both intramucosal and advanced types, proliferative activity (Ki-67 labelling index), p53 protein accumulation and apoptosis (in situ DNA nick end labelling) were assessed, and the relation of these values to progression or differentiation grade of tumours was analysed. In terms of proliferative activity and the proportion of positive cases with p53 accumulation, a statistically significant difference was demonstrated between intraepithelial carcinomas and intramucosal carcinomas with stromal invasion (17.2% vs 31.7% for the Ki-67 labelling index, and 23.5% vs 67.4% for the proportion of positive cases of p53 accumulation). Values for the latter were almost comparable to those of advanced carcinomas. Immunohistologically, Ki-67 positive, proliferating cells were distributed preferentially in the peripheral fronts of invading nests. Apoptotic cells were observed in the inner areas of the invading nests of the intramucosal carcinomas with stromal invasion and in more advanced lesions, but were rarely observed in the normal epithelium or intraepithelial carcinomas. Apoptotic cells were seen mainly around areas of keratinization, and the apoptotic cell index was higher in well and moderately differentiated types of advanced carcinomas than in the poorly differentiated type (2.59% vs 1.09%). An increase in proliferative activity and an accumulation of p53 protein are associated with the onset of early carcinomatous invasion, while apoptosis is closely linked with the differentiation grade of carcinoma cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01008031
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  • 3
    Electronic Resource
    Electronic Resource
    Enhanced antitumor activity of a combination treatment with a mouse/human chimeric anti-MK-1 antibody and lymphokine-activated killer cells in vitro and in a severe combined immunodeficient mouse xenograft model (1999)
    Springer
    Cancer immunology immunotherapy 48 (1999), S. 165-171 
    Details
    ISSN: 1432-0851
    Keywords: Key words Immunotherapy ; MK-1 antigen ; Chimeric antibody ; ADCC ; Apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mouse monoclonal antibody FU-MK-1, raised against a human gastric adenocarcinoma, recognizes a glycoprotein antigen (termed MK-1 antigen) present on most carcinomas and seems to be valuable in immunodiagnosis and immunotherapy of various cancers. In a recent study, we constructed a mouse/human chimeric antibody, designated Ch FU-MK-1, by fusing the FU-MK-1 VH and Vκ genes to the human Cγ1 and Cκ genes, respectively. In the present study, we tested combination immunotherapy of Ch FU-MK-1 with human lymphokine-activated killer (LAK) cells in vitro and in mice with severe combined immunodeficiency (SCID) bearing human MK-1-expressing tumors. In in vitro experiments, Ch FU-MK-1 effectively mediated antibody-dependent cell-mediated cytotoxicity (ADCC) against MK-1-expressing MKN-74 cells, which was completely blocked by an anti-FcR antibody. Since the apoptotic pathway as well as the necrotic pathway have been shown to be utilized in various cytotoxic effector mechanisms, we investigated the role of apoptosis in ADCC mediated by LAK cells and Ch FU-MK-1 against MKN-74 cells. The implication of the apoptosis during ADCC was demonstrated by means of both a terminal-deoxynucleotidyltransferase-mediated dUTP-biotin nick-end-labeling assay and a propidium iodide staining method. In vivo antitumor activity of combination treatment with LAK cells and Ch FU-MK-1 was estimated using SCID mice inoculated s.c. with MKN-74 cells. The i.v. administration of LAK cells and i.p. administration of Ch FU-MK-1 and interleukin-2 (IL-2) produced a marked growth inhibition of MKN-74 tumors in SCID mice. When the actual tumor weights were measured 16 days after initiation of treatment, more than 70% reduction was observed in the group receiving LAK cells plus Ch FU-MK-1 plus IL-2 as compared to the control untreated group. Together these results suggest that Ch FU-MK-1 may serve as a potentially useful immunotherapeutic reagent for human MK-1-expressing tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002620050561
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  • 4
    Electronic Resource
    Electronic Resource
    A Possible Role of Multidrug Resistance-Associated Protein (MRP) in Basic Fibroblast Growth Factor Secretion by AIDS-Associated Kaposi's Sarcoma Cells: A Survival Molecule? (1998)
    Springer
    Journal of clinical immunology 18 (1998), S. 256-263 
    Details
    ISSN: 1573-2592
    Keywords: Apoptosis ; multidrug resistance-associated protein ; Kaposi's sarcoma ; basic fibroblast growth factor ; P-glycoprotein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Kaposi's sarcoma (KS) is considered a disorder of cytokines. Basic fibroblast growth factor (bFGF) is produced by AIDS-associated KS (AIDS-KS) cells and supports their growth in an autocrine and paracrine manner. bFGF lacks a signal sequence; therefore, its mechanism of secretion is unclear. In this study, we investigate the role of two important members of ATP-binding cassette transport proteins, the P-glycoprotein (P-gp) and multidrug resistance-associated protein (MRP), in the secretion of bFGF from AIDS-KS cells. Expression of P-gp and MRP was examined at both the protein and the mRNA levels by flow cytometry and RT-PCR respectively. Intracellular and secreted bFGF was measured by ELISA. AIDS-KS cells expressed MRP at both the mRNA and the protein levels; however, no P-gp expression was detected at either the mRNA or the protein level, Probenecid, a putative inhibitor of MRP efflux function, in a concentration-dependent manner, inhibited bFGF secretion, with a concomitant increase in intracellular bFGF, demonstrating that probenecid blocks bFGF secretion without inhibiting its synthesis. In addition, probenecid induced apoptosis in AIDS-KS cells. AIDS-KS cells expressed fas, bcl-2, and bcl-xL genes but lacked fasL and bax gene expression. These data suggest that bFGF is secreted from AIDS-KS cells via a probenecid-sensitive transporter, most likely by MRP. Furthermore, probenecid appears to induce apoptosis in AIDS-KS cells by depriving them of the growth promoting activity of bFGF. These data suggest that MRP may play a role as a survival molecule in AIDS-KS cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1027381705962
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  • 5
    Electronic Resource
    Electronic Resource
    Programmed cell death in the interdigital tissue of the fetal mouse limb is apoptosis with DNA fragmentation (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 242 (1995), S. 103-110 
    Details
    ISSN: 0003-276X
    Keywords: Apoptosis ; Programmed cell death ; DNA fragmentation ; Fetal limb ; Mouse ; Interdigital tissue ; Joint ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Background: Programmed cell death is an essential event during mammalian morphogenesis which eliminates unnecessary cells to accomplish histogenesis and organogenesis. Cell death in interdigital spaces of the developing limb is a classical example of morphogenetic cell death. We investigated whether classical programmed cell death in the interdigital tissue of the developing limb in mice is apoptosis with fragmentation of nuclear DNA and also examined sequentially the occurrence of programmed cell death and cell proliferation in the developing limb of mouse fetuses to analyze their interrelation.Methods: We examined the occurrence of apoptotic cell death in the developing limbs of mouse fetuses by using Nile blue sulphate staining, agarose gel electrophoresis for detecting DNA laddering, and a cytochemical labeling of DNA fragmentation. We also labeled proliferating cells using BrdU/anti-BrdU immunohistochemistry and examined the interrelation between apoptotic programmed cell death and cell proliferation.Results: DNA ladders, a biochemical evidence of apoptosis, were detected in DNA extracts from the interdigital tissue of day 13 mouse fetuses by agarose gel electrophoresis. Programmed cell death and DNA fragmentation were detected by Nile blue staining and cytochemical labeling of DNA fragmentation, respectively, in the interdigital mesoderm and in the regions of presumptive joints of the digit. BrdU/anti-BrdU immunohistochemistry for identifying proliferating S-phase cells revealed that interdigital mesenchymal cells cease DNA synthesis before programmed cell death and DNA fragmentation begin.Conclusions: We confirmed that both cytological apoptotic alterations and fragmentation of nuclear DNA occur in the interdigital tissue and presumptive joint areas of fetal mouse limbs, and they appear to play a significant role in the separation of digits as well as the formation of joint cavities. © 1995 Wiley-Liss, Inc.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092420114
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