Biomedical subjects

Yan Xin

Publications and source records attributed to Yan Xin.

26 records · Page 2Linked to original sources

PubMed2003

Role of PTEN and MMP-7 expression in growth, invasion, metastasis and angiogenesis of gastric carcinoma.

To investigate the role of PTEN and matrix metalloproteinase-7 (MMP-7) expression in tumorigenesis and progression of gastric carcinoma, their expression in 113 gastric carcinomas was studied by immunohistochemistry. Microvessel density (MVD) was counted using the anti-CD34 antibody. The expressions of PTEN and MMP-7, and MVD were compared with the clinicopathological parameters of tumors, and the relationship between PTEN and MMP-7 expression and MVD was analyzed. It was found that PTEN was expressed less frequently in primary gastric carcinoma cells than in adjacent epithelial cells (P < 0.05), whereas this was reversed for MMP-7 (P < 0.05). PTEN expression was negatively correlated with invasion, metastasis, growth pattern, Lauren's classification and histological classification (P < 0.05). Matrix metalloproteinase-7 expression was positively associated with tumor size, Borrmann's classification, invasive depth, metastasis and TNM staging (P < 0.05), but negative with PTEN expression (P < 0.05). A positive correlation of MVD with tumor size, invasive depth, metastasis and TNM staging was found (P < 0.05). Microvessel density depended on decreased PTEN expression and increased MMP-7 expression (P < 0.05). The results of the present study suggested that down-regulated PTEN expression and up-regulated MMP-7 expression were greatly implicated in tumorigenesis and progression of gastric carcinoma. Close correlation between PTEN on MMP-7 expression provided a novel insight into the regulatory effects of PTEN on MMP-7 expression in gastric carcinoma.

Adenocarcinoma↗

PubMed2003

PTEN encoding product: a marker for tumorigenesis and progression of gastric carcinoma.

AIM: To detect the expression of PTEN encoding product in normal mucosa, intestinal metaplasia (IM), dysplasia and carcinoma of the stomach, and to investigate its clinical implication in tumorigenesis and progression of gastric carcinoma. METHODS: Formalin-fixed paraffin embedded specimens from 184 cases of gastric carcinoma, their adjacent normal mucosa, IM and dysplasia were evaluated for PTEN protein expression by SABC immunohistochemistry. PTEN expression was compared with tumor stage, lymph node metastasis, Lauren's and WHO's histological classification of gastric carcinoma. Expression of VEGF was also detected in 60 cases of gastric carcinoma and its correlation with PTEN was concerned. RESULTS: The positive rates of PTEN protein were 100 %(102/102), 98.5 %(65/66), 66.7 % (4/6) and 47.8 %(88/184) in normal mucosa, IM, dysplasia and carcinoma of the stomach, respectively. The positive rates in dysplasia and carcinoma were lower than in normal mucosa and IM (P<0.01). Advanced gastric cancers expressed less frequent PTEN than early gastric cancer (42.9 % vs 67.6 %, P<0.01). The positive rate of PTEN protein was lower in gastric cancer with than without lymph node metastasis (40.3 % vs 63.3 %, P<0.01). PTEN was less expressed in diffuse-type than in intestinal-type gastric cancer (41.5 % vs 57.8 %, P<0.05). Signet ring cell carcinoma showed the expression of PTEN at the lowest level (25.0 %, 7/28); less than well and moderately differentiated ones (P<0.01). Expression of PTEN was not correlated with expression of VEGF (P>0.05). CONCLUSION: Loss or reduced expression of PTEN protein occures commonly in tumorigenesis and progression of gastric carcinoma. It is suggested that PTEN can be an objective marker for pathologically biological behaviors of gastric carcinoma.

Biomarkers, Tumor↗

PubMed2003

Expression of Fas ligand and caspase-3 contributes to formation of immune escape in gastric cancer.

AIM: To study the role of Fas ligand (FasL) and Caspase-3 expression in carcinogenesis and progression of gastric cancer and molecular mechanisms of relevant immune escape. METHODS: FasL and Caspase-3 expression was studied in adjacent epithelial cells, cancer cells and lymphocytes of primary foci, and cancer cells of metastatic foci from 113 cases of gastric cancer by streptavidin-biotin-peroxidase (S-P) immunohistochemistry. Expression of both proteins in cancer cells of primary foci was compared with clinicopathological features of gastric cancer. The relationship between FasL expression in cancer cells and Caspase-3 expression in cancer cells or infiltrating lymphocytes of primary foci was investigated. RESULTS: Cancer cells of primary foci expressed FasL in 53.98 % (61/113) of gastric cancers, more than their adjacent epithelial cells (34.51 %, 39/113) (P=0.003, chi(2)=8.681), while the expression of Caspase-3 in cancer cells of primary foci was detected in 32.74 % (37/113) of gastric cancers, less than in the adjacent epithelial cells (50.44 %, 57/113) (P=0.007, chi(2)=7.286). Infiltrating lymphocytes of the primary foci showed positive immunoreactivity to Caspase-3 in 70.80 % (80/113) of gastric cancers, more than their corresponding adjacent epithelial cells (P=0.001, chi(2)=10.635) or cancer cells of primary foci (P=0.000, chi(2)=32.767). FasL was less expressed in cancer cells of metastases (51.16 %, 22/43) than in those of the corresponding primary foci (81.58 %, 31/38) (P=0.003, chi(2)=9.907). Conversely, Caspase-3 was more expressed in cancer cells of metastases (58.14 %, 25/43) than in those of the corresponding primary foci (34.21 %, 13/38) (P=0.031, chi(2)=4.638). FasL expression was significantly correlated with tumor size (P=0.035,rs=0.276), invasive depth (P=0.039, rs=0.195), metastasis (P=0.039, rs=0.195), differentiation (P=0.015, rs=0.228) and Lauren's classification (P=0.038, rs=0.196), but not with age or gender of patients, growth pattern or TNM staging of gastric cancer (P>0.05). In contrast, Caspase-3 expression showed no correlation with any clinicopathological parameters described above in cancer cells of the primary foci (P>0.05). Interestingly, FasL expression in primary gastric cancer cells paralleled to Caspase-3 expression in infiltrating lymphocytes of the primary foci (P=0.016, chi(2)=5.825). CONCLUSION: Up-regulated expression of FasL and down-regulated expression of Caspase-3 in cancer cells of primary foci play an important role in gastric carcinogenesis. As an effective marker to reveal the biological behaviors, FasL is implicated in differentiation, growth, invasion and metastasis of gastric cancer by inducing apoptosis of infiltrating lymphocytes. Chemical substances derived from the primary foci and metastatic microenvironment can inhibit the growth of metastatic cells by enhancing Caspase-3 expression and diminishing FasL expression.

Adenocarcinoma↗

PubMed2003

Growth, invasion, metastasis, differentiation, angiogenesis and apoptosis of gastric cancer regulated by expression of PTEN encoding products.

AIM: To investigate expression of PTEN in gastric cancer and to explore its roles in tumorigenesis and progression of gastric cancer. METHODS: Formalin-fixed and paraffin-embedded tissues of adjacent non-tumor mucosa and primary foci from 113 cases of gastric cancers were studied for the expression of PTEN and Caspase-3 and microvessel density (MVD) by streptavidin-peroxidase (S-P) immunohistochemistry with antibodies against PTEN, Caspase-3, and CD34. The relationship between PTEN and Caspase 3 expression and clinicopathological parameters of tumors was compared. RESULTS: Primary gastric cancer cells expressed PTEN less frequently than adjacent epithelial cells of primary foci (54.9 % vs 89.4 %; P=0.000, chi(2)=33.474). PTEN expression was significantly associated with invasive depth (P=0.003, rs=0.274), metastasis (P=0.036, rs=0.197), growth pattern (P=0.008, rs=0.282), Lauren's classification (P=0.000, rs=0.345), and histological classification (P=0.005, rs=0.262) of tumors, but not with tumor size (P=0.639, rs=0.045), Borrmann's classification (P=0.544, rs=0.070) or TNM staging (P=0.172, rs=0.129). PTEN expression was negatively correlated with MDV in primary gastric cancer (P=0.020, F=5.558). Primary gastric cancer cells showed less frequent immunoreactivity to Caspase-3 than adjacent epithelial cells of primary foci (32.7 % vs 50.4 %; P=0.007, chi(2)=7.286). Caspase-3 expression was dependent of PTEN expression in primary gastric cancer cells (P=0.000, chi(2)=15.266). CONCLUSION: Down-regulated expression of PTEN plays an important role in tumorigenesis, progression, growth, differentiation and angiogenesis of gastric cancer. Low expression of PTEN can decrease expression of Caspase-3 to disorder apoptosis of tumor cells, which might explain the molecular mechanisms of PTEN contributions to tumorigenesis and progression of gastric cancer.

Adult↗

PubMed2003

Variations of mitochondrial D-loop region plus downstream gene 1 2S rRNA-tRNA(phe) and gastric carcinomas.

AIM: To explore the instabilities, polymorphisms and other variations of mitochondrial D-loop region and downstream gene 12S rRNA-tRNA(phe) in gastric cancers, and to study their relationship with gastric cancer. METHODS: Three adjacent regions (D-loop, tRNA(phe) and 12S rRNA) were detected for instabilities, polymorphisms and other variations via PCR amplification followed by direct DNA sequencing in 22 matched gastric cancerous tissues and para-cancerous normal tissues. RESULTS: PolyC or (CA) (n) instabilities were detected in 13/22(59.1 %) gastric cancers and 9/22(40.9 %) in the control (P>0.05). There existed 2/12(16.7 %) and 6/10(60 %) alterations of 12S rRNA-tRNA(phe) in well differentiated gastric cancers and poorly differentiated ones, respectively (P<0.05). Some new variations were found, among which np 318 and np 321 C-T transitions in D-loop region were two of the five bases for H-strand replication primer. np 523 AC-deletion and np 527 C-T transition occurred at mtTF1 binding site (mtTFBS), which were associated with the transcription of downstream mitochondrial genome. Seven samples showed the np 16 182 polyC instabilities, five of which simultaneously showed np 16 189 T-C transitions. CONCLUSION: There is no statistic significance of instabilities and polymorphisms in mitochondrial D-loop region between gastric cancerous and para-cancerous normal tissues, which suggests that the instability might relate to heredity or be dependent on aging. There is a significant correlation between differentiation degree of gastric cancer and variant frequencies of 12S rRNA-tRNA(phe). The poorly differentiated gastric cancers are more prone to 12S rRNA-tRNA(phe) variations, or gastric cancers with 12S rRNA-tRNA(phe) variations are more likely to be poorly differentiated. np 16 189 T-C transition may be one of the important reasons for polyC instability in gastric cancer.

Base Sequence↗

PubMed2003

[Expression of PTEN-encoding product in different stages of carcinogenesis and progression of gastric carcinoma].

OBJECTIVE: To illustrate the significance of expression of phosphatase and tensin homologue derived from chromosome ten (PTEN) encoding product in normal mucosa, intestinal metaplasia (IM), dysplasia and carcinoma of the stomach, and to evaluate its clinical implication in tumorigenesis and progression of gastric carcinoma. METHODS: Formalin-fixed and paraffin-embedded tissues from 184 cases of gastric carcinoma, its adjacent normal mucosa, IM and dysplasia were evaluated for the expression of PTEN by SABC immunohistochemistry. PTEN expression was assessed as to tumor stage, lymph node metastasis, Lauren's classification and WHO histological classification of gastric carcinoma. Expression of VEGF protein was also studied in 60 cases of gastric carcinoma, with its correlation with PTEN concerned. RESULTS: The positive rates of PTEN protein were 100% (102/102), 98.5% (65/66), 66.7% (4/6) and 47.8% (88/184) in normal mucosa, IM, dysplasia and carcinoma of stomach, respectively. The positive rates in the last two groups were lower than the first two (P < 0.01). PTEN was less expressed in advanced gastric carcinoma than in early ones (42.9% vs 67.6%, P < 0.01). The positive rate of PTEN protein was lower in gastric carcinoma with lymph node metastasis than without (40.3% vs 63.3%, P < 0.01). PTEN was less expressed in diffuse-type gastric carcinoma than in intestinal-type (41.5% vs 57.8%, P < 0.05). Signet ring cell carcinoma expressed PTEN stood the lowest (25.0%, 7/28), which was less than well and moderately differentiated ones (61.8%, 21/34) (P < 0.01). Expression of PTEN was inversely correlated with expression of VEGF though without any significance (P > 0.05). CONCLUSION: Loss or reduced expression of PTEN protein is common in carcinogenesis and progression of gastric cancer. Altered expression of PTEN may contribute to carcinogenesis and progression of gastric cancer by increasing angiogenesis, cellular adhesion and mobility and so on. PTEN may be an objective marker for pathologically biological behavior of gastric carcinoma.

Adult↗

PubMed2002

[Advances in research for relationship between mitochondrial DNA and solid tumor].

Mitochondrial DNA (mtDNA) encodes the polypeptides required for oxidative phosphorylation and genesis of ATP. It has been though to be involved in carcinogenesis because of its high mutation rate and lacking effective repair mechanism in contrast to nuclear DNA. Since mtDNA lacks introns, it has been suggested that most mutations will occur in this coding sequence and subsequent accumulation of mutation may lead to tumor formation. Alteration in expression of mitochondrial DNA may be a general characteristic of cancer cells. The research on mtDNA such as the mitochondrial genome instability (mtGI) and the integration between the mtDNA and nuclear genome have, mainly in solid tumor, been reported recently, meanwhile it will be a critical topic in solid tumors. In this paper, we reviewed the advances in research for relationship among mitochondrial DNA mutation, abnormal expression, integration, and mtGI in solid tumors lately.

Adenosine Triphosphate↗

PubMed2002

Expression of midkine in benign, premalignant and malignant vulvar tumors.

OBJECTIVE: To clarify the role of midkine (MK) in vulvar carcinogenesis though examination of its expression in vulvar lesions including vulvar condyloma acuminata (VCA), vulvar intraepithelial neoplasia (VIN) and vulvar squamous cell carcinomas (VSCC), and to analyze the relationship between MK expression and human papilloma virus (HPV) infection. METHODS: Thirty VSCC, 15 VIN and 10 VCA patients were studied by streptavidin-biotin-immunoperoxidase method. MK expression was compared with clinicopathologic features of vulvar tumors. RESULTS: MK was expressed in 26 of 30 VSCC (87%), 3 of 5 VIN III and all VCA samples, whereas no MK expression was detected in the VIN I-II samples or in normal epithelium. The difference of MK expression between VIN III and VSCC was statistically significant (P < 0.05). MK was more intensely expressed in differentiated-type (well differentiated and moderately differentiated) VSCC than in undifferentiated-type (poorly differentiated) VSCC. There was no statistically significant correlation between MK expression and clinical stage, lymph node metastasis and HPV infection in VSCC. MK expression were observed in all HPV-positive specimens including 2 VSCC, 1 VIN III and all VCA. CONCLUSIONS: MK gene expression may be a late event in vulvar squamous cell malignant transformation, and may be associated with vulvar tumor cell differentiation. HPV-positive vulvar tumors expressed MK protein.

Carcinoma, Squamous Cell↗