Biomedical subjects

C W Chi

Publications and source records attributed to C W Chi.

155 records · Page 9Linked to original sources

PubMedDate not supplied

Serum matrix metalloproteinase-9 level associated with stromal reaction in patients with gastric cancer.

BACKGROUND: Matrix metalloproteinase 9 (MMP-9) plays an important role in cancer invasion and metastasis. The relationship between serum MMP-9 levels and clinicopathological factors in gastric cancer patients is not clear. MATERIALS AND METHODS: Preoperative serum was obtained from 170 patients who had undergone gastrectomy for gastric cancer at the Veterans General Hospital-Taipei. The serum MMP-9 level was measured using a sandwich enzyme-linked immunoassay by monoclonal antibodies. RESULTS: The median serum MMP-9 level was 368.6 ng/mL (range: 43.9-1871.3 ng/mL). Univariate analysis showed that stromal reaction and Lauren's histological classification were two factors related to serum MMP-9 levels (p = 0.014 and p = 0.030 respectively). Multivariate analysis revealed that stromal reaction was the only factor independently (odds ratio: 1.695) associated with MMP-9 levels. Patients with a serum MMP-9 level < 368.5 ng/mL had a tendency towards better survival rate (5-year survival rate: 64.4%) than those with > 368.5 ng/mL (58.5%), but this tendency did not reach statistical significance (p = 0.512). CONCLUSION: These data suggests that serum MMP-9 levels are associated with stromal reaction in gastric cancer.

Aged↗

PubMedDate not supplied

Adamantyl maleimide induced changes in adhesion molecules and ROS are involved in apoptosis of human gastric cancer cells.

BACKGROUND: We have previously found that N-1-adamantyl maleimide (AMI) inhibited the growth of SC-M1 tumors in vitro and in vivo. The cytotoxicity of AMI on SC-M1 was accompanied by a decrease of adherent cells and the suppressive effect was associated with conformational changes in cell membrane protein. In order to determine the cellular targets of AMI in human gastric cancer SC-M1 cells, we examined AMI-induced changes in the levels of adhesion molecules CD29 (beta 1 integrin) and CD54 (ICAM-1) and GSH. In addition, we also analyzed changes of apoptosis markers such as annexin V binding to membrane and caspase 3 activity in SC-M1 cells after treatment with AMI. MATERIALS AND METHODS: Changes in CD29, CD54, annexin V binding and GSH levels were examined using FITC-conjugated antibodies or fluorescence probes and flowcytometry. Caspase 3 activity was assayed with spectrofluorometry. RESULTS: We found that the expression of CD29 and CD54 on SC-M1 was decreased and the caspase 3 activity was increased during the early apoptosis induced by AMI. Moreover, it was found that the GSH content of the cell was depleted within 30 minutes and then recovered. CONCLUSION: These results suggest that the cell membrane proteins, such as adhesion molecules (CD29, CD54) and intracellular GSH, were the targets of AMI on SC-M1 cells. Since these membrane alterations were prior to apoptosis they may have transduced a death signal to SC-M1 cells.

Adamantane↗

PubMedDate not supplied

Expression of cyclooxygenase-2 in prostate adenocarcinoma and benign prostatic hyperplasia.

Elevated expression of cyclo-oxygenase (COX)-2 has been found in several human cancers, including prostate adenocarcinoma. To evaluate the potential prognostic role of COX-2 in prostate cancer, we assessed the expression of COX-2 in benign prostatic hyperplasia (BPH) and prostate cancer samples employing immunohistochemistry. COX-2 was over-expressed in 15 out of 18 (83%) prostate cancer samples whereas it was detected in only 22% (4 of 18) paired benign tissues. The intensity of immunostaining correlated with the tumor grading. In addition, COX-2 was expressed in 7 of the 22 (32%) BPH samples examined. The significance a COX-2 expression in the BPH samples is not known at present. This data suggest that COX-2 is over-expressed in prostate cancer and COX-2 inhibitors may be useful in combination chemotherapy or chemoprevention for prostate cancer.

Adenocarcinoma↗

PubMedDate not supplied

Tie-1 tyrosine kinase is an independent prognostic indicator for invasive breast cancer.

Receptor tyrosine kinases are known to be involved in the growth, progression and metastasis of solid tumors. We investigated the relationship between tie-1 expression and progression of invasive ductal breast carcinoma with immunohistochemical analysis. Tie-1 protein was detected in the microvessel endothelial cells and cytoplasm of tumor cells. The tumor size and stage were significantly associated with the expression of tie-1, which portends a worse 5-year disease-free status (39.3% v 59.2%, p = 0.07) and overall survival rate (67.3% v 93%, p = 0.02) than those without tie-1 expression. Multivariate analysis demonstrated that larger tumor size, presence of lymph node metastasis and tie-1 expression were independent prognostic parameters, both in 5-year disease-free survival and overall survival. Patients with lymph node metastases and tie-1 expression had the worst 5-year disease-free survival (0%) and overall survival (42.4%) compared to those without tie-1 expression (50.2%, 85%). In lymph node negative patients, those without tie-1 expression had better 5-year disease-free survival and overall survival (72.9%, 100%) compared to those with tie-1 expression (65.5%, 87.7%). We conclude that tie-1 expression is an independent prognostic factor for invasive ductal breast carcinoma, adversely affecting survival of breast cancer patients with positive nodes to a significant extent.

Biomarkers, Tumor↗

PubMedDate not supplied

Conformational changes in gastric carcinoma cell membrane protein correlated to cell viability after treatment with adamantyl maleimide.

BACKGROUND: In order to investigate the mechanism of the effects of the anticancer drug adamantyl maleimide (AMI) on the in vitro growth of a human gastric carcinoma cell line (SC-M1), the membrane protein conformation on the cell surface after treatment with AMI was studied. MATERIALS AND METHODS: The interaction of AMI with SC-M1 cell line was studied by reflectance Fourier transform infrared (FT-IR) microspectroscopy. The cell viability was also determined by the trypan blue exclusion method. RESULTS: FT-IR microscopic study provided evidence that the conformational conversion of the membrane proteins of the SC-M1 cell line from alpha-helix to beta-sheet was found evident, but was dependent on the AMI concentrations used and the time of treatment. AMI not only interacted with the membrane protein on the cell surface, but also entered into cells to interact with the nucleic acids. CONCLUSIONS: The relationship between membrane protein conformational changes and the cell viability of SC-M1 cell line was evident. The AMI-induced apoptosis in SC-M1 cell line was also supposed.

Adamantane↗

PubMedDate not supplied

Effect of hepatocyte growth factor on cell cycle and c-met expression in human gastric cancer cells.

Hepatocyte growth factor (HGF) was found to stimulate the growth and progression of gastric cancer cells through hepatocyte growth factor receptor (HGFR). In the present study, the effects of HGF on the expression of HGFR in relation to cell cycle progression of human gastric cancer cells were investigated by two-parameter flow cytometric analysis. We found that the expression of HGFR in SC-M1 and KATO-III gastric cancer cells was cycle dependent, the level of HGFR increased from GO-G1 to S phase and the highest level of HGFR was found in G2-M phases. The level of HGFR was higher in KATO-III than SC-M1 cells. However, HGF treatment induced a dose-dependent stimulation of growth as well as down-regulation of HGFR in SC-M1 cells but not in KATO-III cells. These results suggest that functional HGFR rather than overexpressed HGFR may be more important for the growth of gastric cancer cells.

Adenocarcinoma↗

PubMedDate not supplied

Abnormal transcripts of FHIT gene in thyroid cancer.

Abnormalities of the FHIT gene were found in many carcinoma cell lines and human tumors as reported which suggest an etiological function in tumorigenesis. To investigate whether the FHIT gene is a target of thyroid tumor specific 3p alterations, we screened the FHIT gene for alteration in thyroid tumors and found that the tumors exhibited aberrant FHIT gene expression. The complete sequence of the FHIT gene in seven cases was determined and deletions between exon 2-9 in different regions were found. Goiter samples as control had normal FHIT transcripts while both normal and aberrant transcripts of FHIT were found not only in the tumor samples but also in the adjacent non-tumorous portion of the thyroid tumor. Our results support the hypothesis that FHIT gene alteration is involved in tumorigenetic development of human neoplasms in thyroid glands.

Acid Anhydride Hydrolases↗

PubMedDate not supplied

Serum tumor necrosis factor in patients with gastric cancer.

We have measured serum TNF-alpha levels in 220 gastric cancer patients, 9 patients with gastric polyps or ulcers, 9 hepatitis B carriers and 85 normal controls. The results showed that no positive TNF-alpha value (> 10 pg/ml) was detected in Hepatitis B carriers and benign gastric lesions' patients and normal controls. In the cancer group, 17 out of 220 patients (7.7%) had positive-TNF-alpha values. The proportion of TNF-alpha positive was 6.8% in stage I disease, 6.5% in stage II disease, 3.7% stage III, and 12.9% stage IV. No clinicopathologic factors were related to positive TNF-alpha value. TNF-alpha value was not an independent prognostic indicator The role of TNF-alpha in gastric cancer remains obscures.

Age Factors↗

PubMedDate not supplied

Serum hepatocyte growth factor level associate with gastric cancer progression.

We have measured serum HGF levels from 80 gastric cancer patients and 51 normal subjects by enzyme-linked immunosorbent assay. The results showed that the mean value of serum HGF level in gastric cancer patients was significantly higher than in normal subjects (0.30 +/- 0.02 vs 0.22 +/- 0.05 ng/ml; p = 0.005). The increase was stage related. Patients with serum HGF < or = 0.30 ng/ml survived longer than those with serum HGF > 0.30 ng/ml (p = 0.02). These data suggest that HGF involve in progression of gastric cancer.

Adenocarcinoma↗

PubMedDate not supplied

Differential paclitaxel-induced cytotoxicity in rodent and human hepatoma cell lines.

Hepatoma is the leading cause of death in male cancer patients in Taiwan. In this study, we examined the effect of Paclitaxel on the in vitro growth of 2 rodent and 4 human hepatoma cell lines. Differential Paclitaxel-induced cytotoxicity was observed among hepatoma cell lines. In Paclitaxel-sensitive Hep3B and N1S1 cells, Paclitaxel-induced cytotoxicity was dose- and time-dependent. The effective doses of Paclitaxel were in the range 0.1-1.0 microM. Flow cytometric analysis showed that Paclitaxel-treated hepatoma cells were arrested in G2-M phases prior to apoptosis. In addition, growth inhibition by Paclitaxel was accompanied by an increase in the expression of proliferating cell nuclear antigen (PCNA) in hepatoma cells. For Paclitaxel-resistant hepatoma cells, cytostatic response and/or polyploidization was observed. Our results indicated that two thirds of the hepatoma cell lines examined showed some degree of resistance to Paclitaxel treatment in vitro. The expression of p53 gene had no direct effect on Paclitaxel-induced cytotoxicity. The expression of PCNA and the development of polyploidization appear to be good markers for measuring Paclitaxel response. These findings suggest that Paclitaxel alone appears to by cytostatic to hepatoma cells, combination of Paclitaxel with other chemotherapeutic agents may show better cytotoxic effects.

Animals↗

PubMedDate not supplied

Submicromolar paclitaxel induces apoptosis in human gastric cancer cells at early G1 phase.

Paclitaxel induced apoptosis has been reported in many cancer cell lines, but the relationship between G2/M phase arrest and apoptosis is not clear. We have reported that low dose (10 nM) paclitaxel induced apoptosis in gastric cancer cells without G2/M phase arrest. In this study, SC-M1 gastric cancer cells were synchronized at early G1, late G1, S and G2/M phases by staurosporine, mimosine, hydroxyurea and berberine, respectively. We have found that paclitaxel could not induce apoptosis of gastric cancer cells in late G1, S and G2/M phases; however, paclitaxel induced apoptosis in the early G1 phase. Our results suggest that cells arrested at G2/M phase by paclitaxel eventually entered the early G1 phase then proceeded to apoptosis.

Antineoplastic Agents, Phytogenic↗