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Träfflista för sökning "WFRF:(Zhang Zhi Yong) srt2:(2006-2009)"

Sökning: WFRF:(Zhang Zhi Yong) > (2006-2009)

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1.
  • Zhao, Zeng-Ren, et al. (författare)
  • Overexpression of Id-1 protein is a marker in colorectal cancer progression
  • 2008
  • Ingår i: Oncology Reports. - 1021-335X. ; 19:2, s. 419-424
  • Tidskriftsartikel (refereegranskat)abstract
    • The inhibitor of differentiation/DNA binding 1 (Id-1), a negative regulator of basic helix-loop-helix transcription factors, plays an important role in the regulation of cell proliferation and differentiation. We examined the Id-1 expression by immunohistochemistry in 9 adenomas, 79 primary colorectal adenocarcinomas matched with 40 adjacent normal mucosa specimens and its relationship with clinicopathological factors. The Id-1 expression was increased in the carcinoma compared to the adjacent normal mucosa either in the unmatched and matched samples or to the adenoma. There was no significant difference in the Id-1 expression between normal mucosa and adenoma. The Id-1 expression of carcinoma was increased from Dukes' stages A to B, to C and to D. The cases with lymph node metastasis had a higher rate of a stronger Id-1 expression than those without lymph node metastasis. In conclusion, Id-1 overexpression plays an important role in colorectal cancer progression.
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2.
  • Zhao, Zeng-Ren, et al. (författare)
  • Particularly interesting new cysteine-histidine rich protein expression in colorectal adenocarcinomas
  • 2006
  • Ingår i: World Journal of Gastroenterology. - 1007-9327. ; 12:2, s. 298-301
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: To study the relationship between particularly interesting new cysteine-histidine rich protein (PINCH) expression and clinicopathological factors in Chinese colorectal cancer patients. Methods: The expression of PINCH was examined by immumohistochemistry in 141 samples of primary colorectal adenocarcinoma and 92 normal samples of colorectal mucosa. Eighty of the cases had both primary tumour and normal mucosa from the same patients. Results: PINCH was expressed in the stroma of normal mucosa and tumours. PINCH expression in tumourassociated stroma was increased compared to normal mucosa in both unmatched cases (n = 141, X2 = 85.79, df = 3, P<0.0001) and matched cases (n = 80, X2 = 45.86, df = 3, P<0.0001). Among 135 tumours with visible invasive margin, 86 (64%) showed stronger PINCH expression at the invasive margin than in the intratumoural stroma. The frequency of PINCH strong expression in mucinous and signet-ring cell carcinomas was higher (52%) compared to non-mucinous carcinomas (29%, X2= 5.13, P= 0.02). We did not find that PINCH expression was related to patient's gender, age, tumour location, tumour size, gross status, histological type, differentiation, invasion depth, lymph node status and Dukes' stage (P>0.05). Conclusion: The expression of PINCH was upregulated in colorectal cancers, and especially at the margin of tumours, and further was related to mucinous and signet-ring cell carcinomas. The results suggest that expression of PINCH may be involved in the tumourigenesis and aggressiveness of colorectal cancers. © 2006 The WJG Press. All rights reserved.
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3.
  • Hua, Dong, et al. (författare)
  • Small interfering RNA-directed targeting of toll-like receptor 4 inhibits human prostate cancer cell invasion, survival, and tumorigenicity
  • 2009
  • Ingår i: Molecular Immunology. - 0161-5890. ; 46:15, s. 2876-2884
  • Tidskriftsartikel (refereegranskat)abstract
    • A major cause of tumor treatment failure is cancer cell metastasis. Toll-like receptor 4 (TLR4)-mediated signaling has been implicated in tumor cell invasion, survival, and metastasis in a variety of cancers. In this study, we investigated the biological roles of TLR4 in prostate metastatic cell invasion and survival, and the potential of gene silencing of TLR4 using small interfering RNA (siRNA) for treatment of cancer. In cultured human prostate cancer cell lines, TLR4 were higher PC3 and DU145 as compared with the poorly metastatic LNCaP indicating that up-regulation of TLR4 was positively correlated with metastasis of tumor cell. In the highly metastatic cancer cell PC3, gene silencing of TLR4 using siRNA significantly inhibited TLR4 mRNA expression and protein level. Knockdown of TLR4 in PC3 cells resulted in a dramatic reduction of tumor cell migration and invasion as indicated by a Matrigel invasion assay. Furthermore, TLR4 siRNA suppressed cell viability and ultimately caused the induction of apoptotic cell death. The effects were associated with abrogating TLR4-mediated signaling to downstream target molecules such as myeloid differentiation factor 88 (MyD88), adaptor-inducing IFN-beta (TRIF), and interferon regulatory factor-1 (IRF-1). In a mouse prostate cancer model, administration with the plasmid construct expressing siRNA for TLR4 obviously inhibited established tumor growth and survival. These studies revealed evidence of a multifaceted signaling network operating downstream of TLR4-mediated tumor cell invasion, proliferation, and survival. Thus, RNA interference-directed targeting of TLR4 may raise the potential of its application for cancer therapy.
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4.
  • Lewander, Andreas, 1973-, et al. (författare)
  • Polymorphism in the promoter region of the NFKB1 gene increases the risk of sporadic colorectal cancer in Swedish but not in Chinese populations
  • 2007
  • Ingår i: Scandinavian Journal of Gastroenterology. - 0036-5521. ; 42:11, s. 1332-1338
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective. An insertion/deletion polymorphism (-94ins/delATTG) in the promoter region of the NFKB1 gene correlates to an increased risk of ulcerative colitis, a known risk factor for colorectal cancer, but this polymorphism has not been studied in colorectal cancer patients. The purpose of this study was to investigate whether this polymorphism is related to colorectal cancer risk and clinicopathological variables. Material and methods. Case samples were taken from four groups of Swedish patients: 193 unselected patients, 90 patients with ≥3 affected 1st-degree relatives, 85 patients with 2 affected 1st-degree relatives, and 109 sporadic cancer patients, and one group of 193 unselected Chinese patients. Controls included 439 Swedish and 458 Chinese healthy individuals. Genotypes were determined by polymerase chain reaction (PCR)-restriction fragment length polymorphism. Results. The deletion increased the risk of colorectal cancer among Swedish unselected patients (OR=3.81, 95% CI: 2.17-6.69, p<0.0001 for heterozygote deletion, and OR=4.65, 95% CI: 2.43-8.89, p<0.0001 for homozygote deletion) and sporadic cancer patients (OR=7.73, 95% CI: 3.06-19.57, p<0.0001 for heterozygote deletion, and OR=6.58, 95% CI: 2.35-18.43, p<0.0001 for homozygote deletion) compared to homozygote insertion (wild-type), but not among the other Swedish or Chinese patients (p>0.05). Similar evidence was seen in age-adjusted analyses (p<0.0001). The polymorphism did not correlate to clinicopathological variables (p>0.05). Conclusions. Deletion of the polymorphism was associated with increased susceptibility to sporadic colorectal cancers in the Swedish population, but not in the Swedish patients with a family history of colorectal cancer or in Chinese patients. © 2007 Taylor & Francis.
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5.
  • Wang, Ming-Wei, et al. (författare)
  • Expression of PINCH protein in gliomas and its clinicopathological significance
  • 2007
  • Ingår i: Oncology. - 0890-9091. ; 72:5-6, s. 343-346
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: Particularly interesting new cysteine-histidine-rich protein (PINCH), as a LIM domain adapter protein, functions in the integrin and growth factor signal transduction pathway, and is upregulated in tumor-associated stroma in several types of cancers. However, no study of PINCH has been carried out in gliomas, therefore we examined PINCH expression in gliomas and its clinicopathological significance. Methods: PINCH expression was immunohistochemically examined in 82 gliomas, along with 26 matched adjacent normal brain samples and 10 recurred gliomas. Results: PINCH was strongly expressed in the primary (35%, p = 0.0001) or recurred tumors (40%, p = 0.004) and weak in normal brain tissue. PINCH expression was significantly increased in high-grade gliomas (55 vs. 24%, high- vs. low-grade gliomas, p = 0.004). There was no association of PINCH expression with gender, age, tumor number, size, histological type and tumor location (p > 0.05). Conclusions: PINCH expression may be involved in glioma development and differentiation. Copyright © 2008 S. Karger AG.
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6.
  • Wang, Ming-Wei, et al. (författare)
  • FXYD3 Expression in Gliomas and its Clinicopathological Significance
  • 2009
  • Ingår i: Oncology Research. - 0965-0407. ; 18:4, s. 133-139
  • Tidskriftsartikel (refereegranskat)abstract
    • FXYD3, interacting with Na+/K+-ATPase, is considered a cell surface regulator modulating the function of ion pumps and ion channels. The FXYD3 gene was originally cloned from murine mammary tumors and then from human breast tumors. However, no study of FXYD3 has been carried out in gliomas; therefore, we examined FXYD3 expression in gliomas and its clinicopathological significance. FXYD3 expression was immunohistochemically examined in 71 primary gliomas, along with 37 matched adjacent normal brain samples and 8 recurred gliomas. The frequency of strong FXYD3 expression was higher in the primary tumors in either unmatched (p = 0.046) or matched cases (p = 0.02), compared to normal brain tissue. FXYD3 expression was significantly more increased in females than males (p = 0.01), and in multiple site gliomas than single sites (p = 0.02). There was no difference of FXYD3 expression regarding age, tumor location, size, histological type, and tumor grade (p greater than 0.05). The results suggest that FXYD3 expression may be involved in glioma development, especially in multiple gliomas and female patients.
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7.
  • Zhang, Zhi-Yong, et al. (författare)
  • Nup88 expression in normal mucosa, adenoma, primary adenocarcinoma and lymph node metastasis in the colorectum
  • 2007
  • Ingår i: Tumor Biology. - 1010-4283. ; 28:2, s. 93-99
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: It was the aim of this study to investigate Nup88 expression in normal colorectal mucosa, adenoma, adenocarcinoma and lymph node metastasis, as well as the relationship between Nup88 expression and clinicopathological features. Methods: Nup88 expression was examined by immunohistochemistry in 84 normal mucosa samples, 32 adenomas, 181 primary adenocarcinomas, and 18 lymph node metastases from colorectal tumour patients. Results: Nup88 expression was observed in normal epithelial and tumour cells. The frequency of strong Nup88 expression was increased from normal mucosa or adenoma to primary tumour and lymph node metastasis (p < 0.0001). There was no significant difference in the expression between normal mucosa and adenoma (p = 0.41). The frequency of strong Nup88 expression was higher in ulcerated tumours (40%) than in polypoid/large fungating tumours (23%, p = 0.048). The frequency of strong Nup88 expression was significantly different among tumours with good (21%), moderate (42%) and poor differentiation (48%, p = 0.01). Nup88 expression was not related to the patients' gender, age, tumour location, size, histological type, invasive depth, lymph node status and Dukes stage (p > 0.05). Conclusion: Our results suggest that Nup88 may play a role during the development, aggressiveness and differentiation of colorectal tumours. Copyright © 2007 S. Karger AG.
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