GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Increased Cyclooxygenase‐2 Expression Associated with Inflammatory Cellular Infiltration in Elderly Patients with Vulvar Cancer
    Wiley ; 2007
    In:  Annals of the New York Academy of Sciences Vol. 1095, No. 1 ( 2007-01), p. 143-153
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1095, No. 1 ( 2007-01), p. 143-153
    Abstract: Abstract :  As the relationship between inflammation and carcinogenesis grows stronger, the role of cyclooxygenase‐2 (COX‐2) and epidermal growth factor (EGFR) has been highlighted in the pathogenesis and progression of human cancer. In view of the fact that vulvar cancer is characterized by precancerous inflammatory changes in elderly patients, the expressions of COX‐2 and EGFR are expected to show different patterns of distribution according to age and other prognostic factors. To verify whether there was a relationship between their expression and clinicopathologic parameters in vulvar cancer, we investigated the inflammatory cellular infiltration and the expression of COX‐2 and EGFR by immunohistochemical analysis. Eleven of 19 samples (57.8%) were stained positive for COX‐2, and 17 (89.4%) for EGFR. The portion of inflammatory cellular infiltration in adjacent normal tissue was also higher in the older age group, and showed a strong correlation with COX‐2 positivity ( P = 0.002). Furthermore, COX‐2 expression was significantly more frequent in patients over 60 years of age compared to those under 50 years ( P = 0.009). COX‐2 expression was noted to be high in moderate and well‐differentiated cases, whereas, poorly differentiated carcinoma was negative for COX‐2 expression ( P = 0.023). However, EGFR expression was not differently distributed on the basis of stage, age, tumor grading, or presence of lymph node metastasis. Our article suggests that vulvar cancer in elderly patients may be associated with inflammation, and thus with increased COX‐2 expression. In light of these findings, a clinical trial designed to assess the addition of COX‐2 targeted therapy to conventional treatment in vulvar cancer would be helpful for consideration of additional treatment options and possibly avoiding the serious surgical morbidity in elderly patients.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1397.018
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Genistein Inhibits Cell Growth by Modulating Various Mitogen‐Activated Protein Kinases and AKT in Cervical Cancer Cells
    Wiley ; 2009
    In:  Annals of the New York Academy of Sciences Vol. 1171, No. 1 ( 2009-08), p. 495-500
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1171, No. 1 ( 2009-08), p. 495-500
    Abstract: Genistein, a soy‐derived isoflavone, inhibits growth of tumor cells from various malignancies. Here we investigated the effect of genistein on the growth of cervical cancer cells (HeLa and CaSki) and its possible mechanism. Genistein significantly suppressed cell growth of HeLa and CaSki cells at concentrations of 20 and 60 μmol/L, respectively, for 24 h. Western blotting analysis showed that genistein reduced phosphorylation of AKT and extracellular signal–regulated kinase (ERK)‐1/2 and induced phosphorylation of p38 mitogen‐activated protein kinase (MAPK) and c‐Jun N‐terminal kinase (JNK). Moreover, inhibition of ERK1/2 activity enhanced cell growth inhibition by genistein, whereas inhibition of p38 MAPK activity rescued from genistein‐mediated growth inhibition. Interestingly, inhibition of AKT activity recovered genistein‐induced growth inhibition in CaSki cells but did not in HeLa cells. However, inhibition of JNK activity seemed to have little effect on cell growth inhibition by genistein. Taken together, these results suggest that genistein could inhibit cell growth by inhibiting ERK1/2 activity and activating p38 MAPK.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.2009.1171.issue-1
    DOI: 10.1111/j.1749-6632.2009.04899.x
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Lack of Association of the Cyclooxygenase‐2 and Inducible Nitric Oxide Synthase Gene Polymorphism with Risk of Cervical Cancer in Korean Population
    Wiley ; 2007
    In:  Annals of the New York Academy of Sciences Vol. 1095, No. 1 ( 2007-01), p. 134-142
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1095, No. 1 ( 2007-01), p. 134-142
    Abstract: Abstract :  Currently, many studies have shown that nitric oxide (NO) and prostaglandin (PG) are main inflammatory mediators involved in a variety of pathophysiological processes including inflammation and carcinogenesis. In this article, we explored the possible association of polymorphisms, of two representative inflammatory mediators, with the risk for cervical cancer. This study included 176 cases of histologically confirmed invasive cervical cancer, and 172 healthy controls. Allele frequency of 12 single‐nucleotide polymorphisms (SNPs) of cyclooxygenase‐2 (COX‐2) and COX5 of the inducible nitric oxide synthase (iNOS) genes in 43 different normal populations were analyzed. We found that 14 of 17 showed a monomorphic or minimal minor allele frequency; therefore, we did not continue with additional analysis. Three SNPs (2 for COX‐2, 1 for iNOS) were chosen for the study. Genotyping of three SNPs (SNP‐rs5275 in the untranslated region of exon 10 and rs5277 in the coding region of exon 3 of COX‐2, and iNOS Ser 608 Leu allele C/T polymorphism within exon 16 of the iNOS reductase domain) was performed. No significant increase was found in any of the genotypes of the COX‐2 or iNOS in the cancer group. We investigated the possible correlation between the genotypes and the clinicopathologic parameters of cervical cancer. No significant association of the genotypes studied was found with respect to clinical stage, lymph node (LN) status, histologic type, or parametrial invasion. Our data did not reveal an association between COX‐2 and iNOS polymorphisms with cervical cancer in Korean women.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1397.017
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Apoptotic Effect of Celecoxib Dependent Upon p53 Status in Human Ovarian Cancer Cells
    Wiley ; 2007
    In:  Annals of the New York Academy of Sciences Vol. 1095, No. 1 ( 2007-01), p. 26-34
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1095, No. 1 ( 2007-01), p. 26-34
    Abstract: Abstract :  Celecoxib, a selective cyclooxygenase‐2 (COX‐2) inhibitor, induces the apoptosis in various cancers in COX‐2 dependent and/or independent manners. The p53 protein is mutated in 50% of all human tumors and plays a key role in apoptosis, cell cycle, and the expression of several proteins. In ovarian cancer, the rate of p53 mutation has been shown to be very high and associated with poor prognosis. To explore the importance of functional status of p53 in apoptosis by celecoxib in ovarian cancer cells, the cellular response to celecoxib was determined in SK‐OV3 ovarian cancer cells with null type p53 and PA‐1 with wild‐type p53. Our results showed that celecoxib inhibited cell growth more in PA‐1 than in SK‐OV3. The underlying antiproliferative mechanism may differ between these two cell types dependent upon the functional status of p53, which plays integral roles in regulating cell cycle and survival. Higher sub‐G1 was shown in PA‐1 than in SK‐OV3 in response to celecoxib (PA‐1 versus SK‐OV3; 60.28% versus 6.69%). Caspase ‐8, ‐9, and ‐3 were activated in PA‐1 cells, but not in SK‐OV3 cells. These results suggest that death receptor and mitochondria‐mediated apoptotic pathways may be involved in celecoxib‐induced apoptosis dependent upon the functional status of p53. Our article demonstrated that the celecoxib effectively inhibited cell growth and induced apoptosis in human ovarian cancer cells with wild‐type p53. Thus, apoptotic effect by celecoxib seemed to be different dependent upon the functional status of p53.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1397.004
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Aromatase Expression Was Not Detected by Immunohistochemistry in Endometrial Cancer
    Wiley ; 2007
    In:  Annals of the New York Academy of Sciences Vol. 1095, No. 1 ( 2007-01), p. 70-75
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1095, No. 1 ( 2007-01), p. 70-75
    Abstract: Abstract :  Several studies suggested that aromatase could play an important role in tumor progression and prognosis in endometrial cancer because androstenedione is converted to estrogen by the enzyme. For better understanding of the aromatase expression in endometrial cancer and its relation to diverse clinicopathological parameters, we conducted this study. This study was carried out with 141 endometrial cancer patients, all of whom had undergone operations in our institution from 1993 to 2002. Paraffin‐embedded tissue blocks were sectioned and immunostained with monoclonal antiaromatase antibody using human placental tissue as positive control. Clinicopathological variables of all patients were also reviewed. Despite quite a high aromatase expression in positive control, there was no endometrial cancer specimen showing the enzyme expression. Our result, although needs further investigation on the cause of the difference from other studies, suggested that aromatase might not have an important role in endometrial cancer.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1397.010
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    DNA Hypomethylation of CAGE Promotors in Squamous Cell Carcinoma of Uterine Cervix
    Wiley ; 2006
    In:  Annals of the New York Academy of Sciences Vol. 1091, No. 1 ( 2006-12), p. 218-224
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1091, No. 1 ( 2006-12), p. 218-224
    Abstract: Abstract:  This study was performed to determine whether promotor hypomethylation of CAGE is involved in cervical carcinogenesis. The surgical specimens of 40 cervical squamous cell carcinoma patients treated at Seoul National University Hospital and those of 48 healthy controls were used, with informed consent. We investigated the promotor hypomethylation status of CAGE by methylation‐specific polymerase chain reaction (MSP) using primers specific for unmethylated sequences, and found hypomethylation of CAGE promotor at a frequency approaching 90% in cervical squamous cell carcinomas (35/40, 87.5%) , but at less than 4% in controls ( P 〈 0.001). This finding provides experimental evidence of the frequent hypomethylation of normally methylated CAGE promotor CpG islands in cervical cancer, and indicates that this hypomethylation is likely to be a valuable surrogate marker for the expression of CAGE . It also provides a clue concerning the molecular mechanisms of carcinogenesis in cervical squamous cell carcinoma.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1378.068
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Involvement of Both Extrinsic and Intrinsic Apoptotic Pathways in Apoptosis Induced by Genistein in Human Cervical Cancer Cells
    Wiley ; 2009
    In:  Annals of the New York Academy of Sciences Vol. 1171, No. 1 ( 2009-08), p. 196-201
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1171, No. 1 ( 2009-08), p. 196-201
    Abstract: Genistein, a naturally occurring isoflavonoid abundant in soy products, has anticancer activity in multiple tumor cells. In this study, we evaluated the apoptotic effect of genistein on cervical cancer cells and its mechanism of apoptosis. Genistein inhibited the proliferation of cervical cancer cells (HeLa, CaSki, and C33A). HeLa cells were the most sensitive to genistein, whereas CaSki and C33A cells were less sensitive. Sub‐G 1 analysis showed that genistein increased apoptotic cells up to 45% at a concentration of 60 μmol/L in HeLa cells, whereas it produced 21% and 17% apoptotic cells in CaSki and C33A cells, respectively, at the same concentration. To determine the apoptotic pathway induced by genistein in the cervical cancer cells, we assessed activation of caspase‐3, ‐8, and ‐9 by immunoblotting. Procaspase‐3, ‐8, and ‐9 were decreased and PARP cleavage increased in a time‐dependent manner after the treatment of genistein in HeLa cells. Also, inhibition of caspase‐3, ‐8, and ‐9 with pharmacological inhibitors reduced genistein‐mediated apoptosis. Interestingly, inhibition of caspase‐8 resulted in remarkable reduction of genistein‐induced apoptosis. Bax expression was increased and total bid decreased, whereas bcl‐2 level was not changed by genistein. Taken together, these results suggest that genistein could induce apoptosis through both extrinsic and intrinsic pathways in human cervical cancer cells.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.2009.1171.issue-1
    DOI: 10.1111/j.1749-6632.2009.04902.x
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Phase I/IIa Study of Combination Chemotherapy with CKD‐602 and Cisplatin in Patients with Recurrent Epithelial Ovarian Cancer
    Wiley ; 2009
    In:  Annals of the New York Academy of Sciences Vol. 1171, No. 1 ( 2009-08), p. 627-634
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1171, No. 1 ( 2009-08), p. 627-634
    Abstract: The aim of this study was to determine the maximum tolerated dose (MTD) and therapeutic efficacy of a newly developed CKD‐602 topoisomerase I inhibitor and cisplatin in patients with recurrent epithelial ovarian cancer. CKD‐602 (0.30 mg/m 2 daily for 5 days) and cisplatin (60 mg/m 2 on day 5) were administered to patients every 3 weeks with dose adjustment of CKD‐602 by 0.05 mg/m 2 daily until the MTD was reached. Dose‐limiting toxicity was defined as grade ≥ 3 neutropenia or thrombocytopenia for more than 4 days or accompanied by fever ≥ 38.5°C, infection, hemorrhage, or transfusion; grade ≥ 3 nonhematological toxicity except for alopecia, nausea, and vomiting. We enrolled 26 patients with recurrent epithelial ovarian cancer who had measurable disease (MD) estimated by computed tomography scan ( n = 12) and nonmeasurable disease (NMD) evaluated by serum CA‐125 levels ( n = 14). All patients received 188 cycles of CKD‐602 and cisplatin with a median number of six cycles per patient (range, 2 to 12). MTD of CKD‐602 was 0.30 mg/m 2 daily. The overall response rate was 69.2% (18/26) with 58.3% (7/12) and 78.6% (11/14) in MD and NMD, respectively. Among the responsive patients, 14 were platinum sensitive (14/18, 77.7%) and four were platinum resistant (4/8, 50.0%). The most common toxicity was grade ≥ 3 neutropenia developing in 17 patients (65.4%) and 72 cycles (38.3%). Grade 3 nausea and anorexia were the most common gastrointestinal toxicities, developing in 15 cycles (8.0%) of four patients (15.4%) and 10 cycles (5.3%) of five patients (19.3%), respectively. The median disease‐free interval was 6 months (range 0–26 months). CKD‐602 at a concentration of 0.3 mg/m 2 daily for 5 days and cisplatin at 60 mg/m 2 on day 5 every 3 weeks showed high efficacy, with acceptable toxicity, against platinum‐sensitive/resistant recurrent epithelial ovarian cancer.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.2009.1171.issue-1
    DOI: 10.1111/j.1749-6632.2009.04885.x
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Celecoxib Potentiates the Anticancer Effect of Cisplatin on Vulvar Cancer Cells Independently of Cyclooxygenase
    Wiley ; 2009
    In:  Annals of the New York Academy of Sciences Vol. 1171, No. 1 ( 2009-08), p. 635-641
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1171, No. 1 ( 2009-08), p. 635-641
    Abstract: Cyclooxygenase‐2 (COX‐2) has been found to be associated with the development and progression of various cancers. Our previous study showed a high expression rate of COX‐2 in paraffin‐embedded tissue specimens from patients with vulvar cancer. In this study, we evaluated the efficacy of celecoxib, a selective COX‐2 inhibitor, as a chemosensitizing agent with cisplatin in vulvar cancer cells A431 and SW962. COX‐2 was expressed in both A431 and SW962 vulvar cancer cell lines. COX‐1 was expressed in A431 but not in SW962. MTT [3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazoliumbromide] assay showed that treatment with 30 μmol/L celecoxib had no effect on cell growth in A431 cells for 72 h. However, combined treatment with celecoxib and cisplatin induced a significant reduction in cell growth compared to single treatment with cisplatin. Interestingly, single treatment with celecoxib or cisplatin and combined treatment of 10 μmol/L celecoxib with 10 μmol/L cisplatin increased COX‐2 expression. However, the combination of 30 μmol/L celecoxib and 30 μmol/L cisplatin reduced COX‐2 expression to the control state. Inhibition of cell growth by celecoxib alone and in combination with cisplatin was independent of the expression level of COX‐2 induced by these a gents. While treatment with 10 μmol/L celecoxib or 10 μmol/L piroxicam significantly suppressed the activity of COX enzymes, neither agent affected the growth of A431 and SW962 cells at this concentration. Taken together, celecoxib could be used as a chemosensitizing agent in vulva cancer cells; the anticancer activity of celecoxib seemed to be independent of COX.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.2009.1171.issue-1
    DOI: 10.1111/j.1749-6632.2009.04888.x
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    Akt Involvement in Paclitaxel Chemoresistance of Human Ovarian Cancer Cells
    Wiley ; 2007
    In:  Annals of the New York Academy of Sciences Vol. 1095, No. 1 ( 2007-01), p. 82-89
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1095, No. 1 ( 2007-01), p. 82-89
    Abstract: Abstract :  Paclitaxel (taxol) is extensively used for chemotherapy of various cancers including ovarian cancer. Although paclitaxel induces apoptosis in cancer cells, its exact mechanism of action still remains to be determined. Akt mediates survival signals which preserve various cancer cells from apoptosis pathway. Thus, Akt is considered an exciting target for therapeutics. Here, we demonstrated that inhibition of Akt increases the efficacy of the paclitaxel‐induced apoptosis in SKOV3 and PA‐1 human ovarian cancer cells. The sensitivity to paclitaxel of SKOV3 and PA‐1 cells was examined using the MTT assay. At a concentration of 30 nM, PA‐1 cells were more sensitive to paclitaxel than SKOV3 cells. Apoptosis was accompanied by the release of cytochrome c into the cytoplasm and cleavage of poly (ADP‐ribose) polymerase (PARP). To further elucidate the mechanism of apoptosis by paclitaxel, we compared the levels of phosphorylation of Akt between paclitaxel‐resistant SKOV3 cells and paclitaxel‐sensitive PA‐1 cells. The higher level of phosphorylated Akt was shown in SKOV3 cells than in PA‐1 cells. Interestingly, the treatment of paclitaxel decreased the amount of phosphorylated Akt in a time‐dependent manner in both cell lines. Furthermore, inhibition of Akt by specific phosphatidyinositol‐3‐kinase (PI3K)‐Akt inhibitors (Wortmannin, and LY294002) synergistically increased the efficacy of the paclitaxel‐induced apoptosis in both cell lines. These results suggest that the addition of the Akt inhibitor may increase the therapeutic efficacy of paclitaxel for patients with ovarian cancer.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1397.012
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...