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Biomedical subjects

Dan Xie

Publications and source records attributed to Dan Xie.

At least 37 records · Page 2Linked to original sources
PubMed2005

Tumor cyclooxygenase-2 levels correlate with tumor invasiveness in human hepatocellular carcinoma.

AIM: Recent studies suggested that cyclooxygenase-2 (COX-2) enhances tumor angiogenesis via upregulation of vascular endothelial growth factor (VEGF). Although COX-2 expression has been demonstrated in hepatocellular carcinoma (HCC), the significance of COX-2 in progression of HCC remains unclear. This study evaluated the clinico-pathological correlation of COX-2 level and its relationship with VEGF level in HCC. METHODS: Fresh tumor tissues were obtained from 100 patients who underwent resection of HCC. COX-2 protein expression was examined by immunohistochemistry, and quantitatively by an enzyme immunometric assay (EIA) of tumor cytosolic COX-2 levels. Tumor cytosolic VEGF levels were measured by an ELISA. RESULTS: Immunostaining showed expression of COX-2 in tumor cells. Tumor cytosolic COX-2 levels correlated with VEGF levels (r = 0.469, P<0.001). Correlation with clinicopathological features showed significantly higher tumor cytosolic COX-2 levels in the presence of multiple tumors (P = 0.027), venous invasion (P = 0.030), microsatellite lesions (P = 0.037) and advanced tumor stage (P = 0.008). Higher tumor cytosolic COX-2 levels were associated with worse patient survival. CONCLUSION: This study shows that elevated tumor COX-2 levels correlate with elevated VEGF levels and invasiveness in HCC, suggesting that COX-2 plays a significant role in the progression of HCC.

Adolescent↗
PubMed2005

Discovery and investigation of a novel class of thiophene-derived antagonists of the human glucagon receptor.

A novel class of antagonists of the human glucagon receptor (hGCGR) has been discovered. Systematic modification of the lead compound identified substituents that were essential for activity and those that were amenable to further optimization. This SAR exploration resulted in the synthesis of 13, which exhibited good potency as an hGCGR functional antagonist (IC50 = 34 nM) and moderate bioavailability (36% in mice).

Humans↗
PubMed2005

Up-regulated expression of cytoplasmic clusterin in human ovarian carcinoma.

BACKGROUND: Recently, tumorigenic roles of the clusterin gene in several human malignancies have been suggested, but its potential role in the development and progression of ovarian carcinoma is unclear. METHODS: In the current study, immunohistochemistry was used to examine the expression status of clusterin in 10 normal ovaries, 20 ovarian cystadenomas, 15 borderline ovarian tumors, and 240 ovarian carcinomas (nonmetastatic and metastatic) by tissue microarray. In addition, the apoptotic index of each tumor was assessed with a terminal deoxyuridine triphosphate nick-end labeling assay. RESULTS: Positive staining for clusterin in different ovarian tissues was observed primarily a cytoplasmic pattern. Cytoplasmic overexpression of clusterin was detected in none of the normal ovaries, in 17% of cystadenomas, in 38% of borderline tumors, and in 58% of invasive ovarian carcinomas. A significant association was observed (P < 0.001) between the overexpression of clusterin and late clinical stage according to the International Federation of Gynecology and Obstetrics staging system. In addition, the overexpression of clusterin was detected more frequently in metastatic lesions than that in their matched primary tumors. The current results also provided evidence that the overexpression of cytoplasmic clusterin in carcinomas was correlated inversely with the tumors' apoptotic index, demonstrating an antiapoptotic function of cytoplasmic clusterin in ovarian carcinomas. CONCLUSIONS: The current results suggested that the overexpression of cytoplasmic clusterin may represent an acquired malignant phenotypic feature of ovarian carcinoma and may be one of the important factors in determining the aggressive nature of ovarian carcinoma.

Adult↗
PubMed2005

Correlation of AIB1 overexpression with advanced clinical stage of human colorectal carcinoma.

AIB1, a member of the steroid receptor coactivator 1 family, has been cloned on 20q12 and is a candidate oncogene in human breast cancer. It is commonly amplified and overexpressed in several types of human cancers. In this study, we examined the expression of AIB1, as related to clinicopathologic features, in 85 human colorectal cancers (CRCs). The status of the number of AIB1 copies, p53 expression, and DNA ploidy was also analyzed. The overexpression of AIB1 was detected in 35% of CRCs. Amplification of AIB1 was observed in 10% of CRCs. In addition, the overexpression of AIB1 was observed more frequently in CRCs in later clinical stages (T3 N1 M0/T3 N0 2M1), compared with that in T3 N0 M0 stage (P < .05). These results suggest that overexpression of AIB1 might provide a selective advantage for the developmental growth and/or progression of subsets of CRCs. In addition, a significant correlation (P < .05) of overexpression of AIB1 with p53 overexpression as well as with aneuploid DNA content was observed in these CRCs. The overexpression of p53 was also correlated significantly with CRC DNA ploidy (P < .05). Furthermore, there was a substantial population of CRCs showing overexpression of both AIB1 and p53 protein and all had aneuploid DNA content; most of these were in the later clinical stage. These findings suggest a possible convergence of AIB1 with a pathway involving p53, which might induce chromosomal instability and affect the clinical phenotype of a subset of CRCs.

Acetyltransferases↗
PubMed2005

Enzymatic hydrolysis of steam-exploded and ethanol organosolv-pretreated Douglas-Firby novel and commercial fungal cellulases.

Softwood residues are the most abundant feedstock available for bioconversion in many northern countries. However, the high costs for delignification and enzymatic hydrolysis currently deter commercialization of softwood bioconversion processes. This study evaluates the abilities of two novel fungal preparations (MSUBC1 and MSUBC2) and two commercial cellulase preparations (TR1 and TR2) to hydrolyze cellulose in Douglas-firpretreated by steam explosion or ethanol organosolv process. MSUBC1 showed significantly better performance than the other preparations on both lignocellulosic substrates. In particular, MSUBC1 achieved >76% cellulose conversion for hydrolysis of steam-exploded Douglas-fir (approximately 44% lignin) after 72 h at low enzyme loading (10 filter paper units/g of cellulose) and without beta-glucosidase supplementation.

Biodegradation, Environmental↗
PubMed2005

Strategies to enhance the enzymatic hydrolysis of pretreated softwood with high residual lignin content.

Pretreatment of Douglas-fir by steam explosion produces a substrate containing approx 43% lignin. Two strategies were investigated for reducing the effect of this residual lignin on enzymatic hydrolysis of cellulose: mild alkali extraction and protein addition. Extraction with cold 1% NaOH reduced the lignin content by only approx 7%, but cellulose to glucose conversion was enhanced by about 30%. Before alkali extraction, addition of exogenous protein resulted in a significant improvement in cellulose hydrolysis, but this protein effect was substantially diminished after alkali treatment. Lignin appears to reduce cellulose hydrolysis by two distinct mechanisms: by forming a physical barrier that prevents enzyme access and by non-productively binding cellulolytic enzymes. Cold alkali appears to selectively remove a fraction of lignin from steam-exploded Douglas-fir with high affinity for protein. Corresponding data for mixed softwood pretreated by organosolv extraction indicates that the relative importance of the two mechanisms by which residual lignin affects hydrolysis is different according to the pre- and post-treatment method used.

Cell Culture Techniques↗
PubMed2005

[Expressions of inducible nitric oxide synthase and vascular endothelial growth factor and their relationship with microvessel density in hepatocellular carcinoma].

BACKGROUND & OBJECTIVE: Inducible nitric oxide synthase (iNOS), and vascular endothelial growth factor (VEGF) are recognized as key factors required for angiogenesis of tumors. They can influence pathologic development and prognosis of tumors. This study was to investigate the correlation of expressions of iNOS and VEGF to angiogenesis of hepatocellular carcinoma (HCC). METHODS: Tissue microarray of 147 specimens of HCC was prepared, VEGF and microvessel density (MVD) were detected using immunohistochemistry, iNOS mRNA was detected by in situ hybridization. RESULTS: Positive rates of iNOS, and VEGF in HCC tissues were higher than those in adjacent noncancerous tissues (86.39% vs. 33.33%, 78.91% vs. 40.82%). Expression levels of iNOS, and VEGF in HCC tissues were significantly higher than those in adjacent noncancerous tissues (P<0.01). MVD in HCC tissues was significantly higher than that in adjacent noncancerous tissues (56.5+/-12.8 vs. 8.4+/-3.6, P<0.01). Expression of iNOS was related with tumor size, and surface antigen of hepatitis B (HBsAg) (P<0.05), but didn't relate with metastasis, and differentiation of the cancer (P>0.05). Expression of VEGF, and MVD were correlated to tumor size, and metastasis (P<0.05), not to HbsAg, and tumor differentiation (P>0.05). In cancer tissues, MVD was positively correlated with expressions of VEGF and iNOS (P<0.01), expression of VEGF was positively correlated with that of iNOS (P<0.01). CONCLUSION: iNOS and VEGF may play important roles in angiogenesis of HCC. Expression levels of iNOS and VEGF, and MVD in HCC tissues were higher than those in adjacent noncancerous tissues.

Adolescent↗
PubMed2005

[Characteristics of neoplasm occurrence of renal allograft recipients and their prognosis].

BACKGROUND & OBJECTIVE: Renal allograft recipients are more likely to develop neoplasm than general population because of long-term immunosuppressive treatment and concurrent infections. This study was designed to analyze the clinical features of neoplasm occurrence of renal allograft recipients, and the effect of radical surgery (RS) on their prognosis. METHODS: Records of 2 160 renal allograft recipients treated in our center from Oct. 1987 to Apr. 2003 were retrospectively studied. The time to neoplasm development, pathologic type of tumor, patients' survival time were analyzed to explore the clinical features of neoplasm developing after kidney transplantation. Recipients developed neoplasms were divided into RS group and non-RS group according to their treatment pattern. The effect of RS on patients' survival was estimated. RESULTS: A total of 33 patients developed neoplasms after transplantation. Among them,11(33.3%) developed neoplasms in digestive system. The median survival time of RS group (10 patients) was 41.5 months, that of non-RS group (23 patients) was 6.0 months. The 20-month survival rate of RS group was 70.0%, while that of non-RS group was 13.0%. CONCLUSIONS: Renal allograft recipients are more likely to develop neoplasm than general population. Moreover, their main malignancies are liver cancer, skin cancer, lymphoma and thyroid carcinoma, which differ from those observed in general population. Early diagnosis and treatment, especially feasible RS, will improve short-term outcome, while long-term therapeutic effect needs to be further observed.

Adult↗
PubMed2005

Establishment and characterization of a human non-small cell lung cancer cell line.

Lung cancer is one of the most common causes of cancer death worldwide. Although many efforts have been made to explore the mechanisms involved in the development of lung cancer, the genetic events involved in the pathogenesis of lung cancer are still unclear. For a better mechanistic scope of study, a well-established cellular model is essential. We report the establishment of a squamous cell carcinoma (SCC) cell line of human lung, SCC-37. Chromosomal abnormalities and global genomic alterations of SCC-37 were studied by spectral karyotyping (SKY) and comparative genomic hybridization (CGH), respectively. Results showed that SCC-37 was a hypodiploid with complex chromosomal rearrangements. Some of the alterations, such as the gain of 1q25-qter in SCC-37, have been correlated to the tumor recurrence of non-small cell lung cancer (NSCLC). Other interesting findings include the amplification of 3q25-qter and 12q13, suggesting the existence of important oncogenes in the amplicons. This cell line may thus provide a useful cellular resource for studying the pathogenesis of SCC of the lung in the future.

Aged↗
PubMed2005

[Correlation of NY-ESO-1 gene and protein expression to metastasis and clinicopathologic features of hepatocellular carcinoma].

BACKGROUND & OBJECTIVE: NY-ESO-1 belongs to cancer-testis antigen family. It can inspire both cellular and humoral immune responses in tumor patients, and is regarded as the strongest tumor antigen. This study was to investigate the expression of NY-ESO-1 gene and its correlation with clinicopathologic features of hepatocellular carcinoma (HCC). METHODS: NY-ESO-1 mRNA expression was detected by reverse transcription-polymerase chain reaction (RT-PCR) in 62 specimens of HCC and adjacent liver tissue. NY-ESO-1 protein expression and its distribution were detected by immunohistochemistry (IHC) in a tissue microarray contained 132 eligible cases of HCC. RESULTS: Positive rate of NY-ESO-1 mRNA was 27.4% in HCC; it was higher in HCC with tumor embolus of portal vein than in HCC without tumor embolism (40.0% vs. 18.9%). Positive rate of NY-ESO-1 protein was 18.9% in HCC tissue microarray; it was significantly higher in HCC with metastasis than in HCC without metastasis (29.6% vs. 11.5%, P < 0.05). NY-ESO-1 protein mainly located in cytoplasm of HCC cells. Positive rates of NY-ESO-1 mRNA and protein were 28.3% and 19.1% respectively in HBsAg positive HCC, and were 29.5% and 20.7% respectively in HCC with alpha fetoprotein (AFP) of > 20 ng/ml. Both NY-ESO-1 mRNA and protein were not detected in adjacent normal liver tissue. CONCLUSIONS: NY-ESO-1 gene specifically expresses in HCC, and may correlates with progress and metastasis of HCC. It may be a candidate target for antigen-specific immunotherapy for HCC with metastatic lesion. NY-ESO-1 expression has no correlation with HBsAg/AFP status of HCC.

Adult↗
PubMed2005

[Correlation of clusterin expression to prognosis of bladder carcinoma].

BACKGROUND & OBJECTIVE: Clinically, molecular prognostic markers for bladder carcinoma are still rare. Recently, up-regulation of clusterin protein has been suggested to relate with development and prognosis of several human cancers, but its relation with bladder cancer is unclear. This study was to analyze correlation of expression of clusterin protein to clinicopathologic parameters and prognosis of bladder cancer with tissue chip. METHODS: A tissue microarray containing 81 cases of bladder carcinoma was constructed. The expression of clusterin was detected by immunohistochemistry; its correlation with clinicophathologic parameters was analyzed. RESULTS: Of the 81 cases of bladder cancer, 69 were detectable by immunohistochemistry, 32 (46.4%) of which showed overexpression of clusterin protein. Overexpression rate of clusterin was significantly higher in poorly differentiated (G3 grade) tumors than in well differentiated (G1-G2 grades) tumors (75.0% vs. 34.7%, P=0.002), and was significantly higher in invasive (T2-T4 stages) tumors than in superficial (Ta-T1 stages) tumors (65.4% vs. 34.9%, P=0.014). Expression of clusterin was negatively correlated with prognosis of bladder cancer patients (log-rank=5.88, P=0.015); the recurrence-free survival time of patients with overexpression of clusterin was shorter than that of patients with normal expression of clusterin (37.3 months vs. 48.8 months). CONCLUSION: The overexpression of clusterin might be a molecular prognostic marker of bladder cancer.

Adenocarcinoma↗
PubMed2005

[Expression and amplification of steroid receptor coactivator-3 gene in colorectal carcinoma and its clinicopathological significance].

OBJECTIVE: To investigate the expression and amplification of steroid receptor coactivator- 3(SRC- 3) gene in colorectal carcinoma (CRC) and its clinicopathological significance. METHODS: Immunohistochemistry and fluorescence in situ hybridization (FISH) were used to detect the expression and amplification of SRC- 3 gene in CRC, and its association with patient's clinical pathological features was analyzed. RESULTS: A total of 60 patients with CRC were studied. SAR- 3 proteins were overexpressed in 23 cases (38% ). There was a significant association between SAR- 3 overexpression and neoplasm staging (P< 0.01). SRC- 3 protein was overexpressed in 62% of patients with Dukes C or D stage, whereas SRC- 3 protein was normally expressed in 74% of patients with Dukes A or B stage. As for FISH study, 47 cases were informative. High- level amplification of SRC- 3 gene was detected in 6 cases(13% ) and all showed overexpression of SRC- 3 protein. Low- level amplification of SRC- 3 was observed in 9 cases (19% ). Overexpression of SRC- 3 was detected in 6 cases. The remaining 9 of 32 patients(28% ) without amplification of SRC- 3 gene were observed with overexpression of SRC- 3 protein. In addition, 91% patients with CRC were found overexpression of SRC- 3 as well as overexpression of P53. CONCLUSION: The abnormal expression of SRC- 3 gene might impact on the function of P53 and development of CRC. There might exist some unknown mechanisms other than gene amplification of SRC- 3 to regulate its encoded protein expression in CRC.

Biomarkers, Tumor↗
PubMed2004

Oncogenic role of eIF-5A2 in the development of ovarian cancer.

Amplification of 3q26 is one of the most frequent chromosomal alterations in many solid tumors, including ovarian, lung, esophageal, prostate, breast, and nasopharyngeal cancers. A candidate oncogene to eukaryotic initiation factor 5A2 (eIF-5A2), a member of eukaryotic initiation factor 5A subfamily, has been isolated from a frequently amplified region at 3q26.2. In this work, the tumorigenic ability of eIF-5A2 was demonstrated by anchorage-independent growth in soft agar and tumor formation in nude mice. Furthermore, antisense DNA against eIF-5A2 could inhibit cell growth in ovarian cancer cell line UACC-1598 with amplification of eIF-5A2 in form of double minutes. Cell growth rate in UACC-1598 was also inhibited when the expression level of EIF-5A2 was decreased by the reduction of the copy number of double minutes. The correlation of EIF-5A2 overexpression and clinical features of ovarian cancer was investigated using tissue microarray, and the result showed that eIF-5A2 overexpression was significantly associated with the advanced stage of ovarian cancer. These findings suggest that eIF-5A2 plays important roles in ovarian pathogenesis.

Animals↗
PubMed2004

Recurrent chromosomal imbalances in nonsmall cell lung carcinoma: the association between 1q amplification and tumor recurrence.

BACKGROUND: Lung carcinoma is a leading cause of cancer deaths worldwide. To better understand this disease, the authors studied genetic alterations in nonsmall cell lung carcinoma (NSCLC) and the association between genetic changes and clinical features. METHODS: Genetic alterations in 30 patients with adenocarcinoma (AC) and 39 patients with squamous cell carcinoma (SCC) were analyzed by comparative genomic hybridization. The genetic changes in patients with AC and SCC were compared and the associations of these changes with clinical features were studied. RESULTS: A gain of 3q with a minimal amplified region at 3q25.3-qter was significantly higher in patients with SCC compared with patients with AC (72% vs. 27%; P < 0.001). A gain of 20q and loss of chromosome 9 were detected more frequently in patients with AC compared with patients with SCC (P < 0.05). Gains of 5p and 20q and loss of 5q were significantly correlated with an advanced stage of NSCLC (P < 0.05). Amplification of 1q was significantly associated with NSCLC recurrence (P = 0.04). CONCLUSIONS: The results of the current study suggested that different chromosomal aberrations may contribute to the types and pathologic stages of NSCLC.

Adenocarcinoma↗
PubMed2004

Small molecule biaryl FSH receptor agonists. Part 1: Lead discovery via encoded combinatorial synthesis.

High-throughput screening of two million compounds in 37 distinct encoded combinatorial libraries using FSH receptor transfected cells provided small molecule agonists such as 1 (EC(50)=3 microM) and 2 (EC(50)=3.9 microM), based on which a focused combinatorial library with a total of 31372 compounds was designed, synthesized, and screened to reveal 72 novel biaryl FSH receptor agonists such as 8a-c as well as a unique combinatorial SAR.

Combinatorial Chemistry Techniques↗
PubMed2004

Association of Vimentin overexpression and hepatocellular carcinoma metastasis.

The poor prognosis of hepatocellular carcinoma (HCC) has been associated with recurrence and metastasis. Recently, we established a pair of HCC cell lines from a primary (H2-P) and its matched metastatic (H2-M) HCC tumors. A high density of cDNA microarray with 9184 human cDNA was used to identify the differentially expressed genes between H2-P and H2-M. Comparing with H2-P, eight upregulated and six downregulated genes were detected in H2-M. One interesting finding is the overexpression of Vimentin (VIM), a well-defined intermediate filament, which has been linked to a more aggressive status in various tumors. The correlation of overexpression of VIM and HCC metastasis was studied by immunohistochemistry using a tissue microarray with 200 primary HCCs and 60 pairs of primary and matched metastatic HCC samples. Tissue microarray demonstrated that the overexpression of VIM was significantly associated with HCC metastasis (P<0.01). This finding strongly suggests that the overexpression of VIM may play an important role in the metastasis of HCC.

Adult↗
PubMed2004

Establishment of cell lines from a primary hepatocellular carcinoma and its metastatis.

Hepatocellular carcinoma (HCC) is one of the most common malignancies in the world with a very poor prognosis that has been associated with tumor metastasis. The molecular mechanism of HCC metastasis is still unclear. In this study, we established cell lines from a primary tumor (H2-P) and its metastasis (H2-M). G-banding karyotyping, comparative genomic hybridization, and fluorescence in situ hybridization were applied to study these two cell lines and the results demonstrated that they are of the same origin. These cell lines provide a very useful tool to identify genetic alterations associated with HCC metastasis.

Adult↗