自引率: 12%
被引量: 20778
通过率: 暂无数据
审稿周期: 1.07
版面费用: 暂无数据
国人发稿量: 71
投稿须知/期刊简介:
Anticancer Research (AR) publishes high quality works and reviews on all aspects of experimental and clinical cancer research. AR preferentially publishes papers advancing the understanding of cancer causation, and papers applying the results of basic research to cancer diagnosis, prognosis and therapy.
期刊描述简介:
Anticancer Research (AR) publishes high quality works and reviews on all aspects of experimental and clinical cancer research. AR preferentially publishes papers advancing the understanding of cancer causation, and papers applying the results of basic research to cancer diagnosis, prognosis and therapy.
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Hypoxia inducible factor-alpha expression correlates with vascular endothelial growth factor-C expression and lymphangiogenesis/angiogenesis in oral squamous cell carcinoma.
The number of blood vessels correlates with metastasis in solid tumors, including oral squamous cell carcinoma (OSCC). Hypoxia inducible factor-1alpha (HIF-1alpha) could play a role in tumor lymphangiogenesis by regulating the lymphatic expression of vascular endothelial growth factor-C (VEGF-C). HIF-1alpha protein expression, VEGF-C protein expression, lymphatic vessel density (LVD) and blood vessel density (BVD) in OSCC were investigated. HIF-1alpha and VEGF-C protein expression were investigated by means of immunohistochemistry in samples from 65 cases of OSCC. The density of the lymphatic microvessels and blood microvessels immunohistochemically stained by LYVE-1 and CD34 antibody, respectively, was calculated. The association between the HIF-1alpha expression and the clinicopathological parameters was evaluated. HIF-1alpha overexpression occurred in 43 out of the 65 tumor samples (66.2%), while VEGF-C overexpression was observed in 34 out of the 65 tumor samples (52.3%). Higher LVD was found in both high HIF-1alpha and high VEGF-C expression cases. HIF-1alpha overexpression was significantly correlated with VEGF-C overexpression (p = .018, Chi-square test), higher LVD (p < 0.001, Mann-Whitney U-test), and regional lymph nodal involvement (p = 0.004, Chi-square test) as well as UICC TMN classification (p = 0.043, Chi-square test), respectively. In addition, higher BVD existed in the high HIF-1alpha and VEGF-C expression groups (p < 0.001, Mann-Whitney U-test). HIF-1alpha might play a crucial role in regional lymph node metastasis as a regulator of lymphangiogenesis and angiogenesis in OSCC with a possible novel pathway involving VEGF-C. Therefore, HIF-1alpha might be a particularly promising target for controlling regional lymph node metastases by a combination of antiangiogenic and anti-lymphangiogenic effects in OSCC.
被引量：52 发表：2008
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Expression of hypoxia-inducible factor (HIF-1alpha), VEGF-C and VEGF-D in non-invasive and invasive breast ductal carcinomas.
Hypoxia-inducible factor 1 alpha (HIF-1alpha) is a transcription factor that may play an important role in tumour growth and metastasis by its regulation of angiogenesis and lymphangiogenesis to survive cellular hypoxia. Lymphangiogenesis is promoted by vascular endothelial growth factors (VEGF)-C and VEGF-D, but the correlation between the expression of HIF-1alpha and VEGF-C or VEGF-D in human breast carcinoma is not well elucidated. This study examined the pathobiological role of these molecules in human breast ductal carcinoma. The expressions of HIF-1alpha, VEGF-C and VEGF-D were analyzed in 10 normal mammary epithelia, 12 fibroadenomas, 20 ductal carcinomas in situ (DCISs and 36 invasive ductal carcinomas (IDCs) by immunohistochemistry, comparing clinicopathological parameters. HIF-1alpha expression in nuclei was found in DCIS and IDC, but not in normal or fibroadenoma cells. The HIF-1alpha labelling index was significantly correlated with the degree of VEGF-C expression in IDC (p < 0.001), but not in DCIS. HIF-1alpha expression was significantly correlated with tumour necrosis and with the Van Nuys prognostic index (VNPI) (p < 0.05, p < 0.05, respectively) in the 20 DCISs. On the other hand, VEGF-D levels, but not those of HIF-1alpha and VEGF-C, were significantly higher in cases with lymph node metastasis and estrogen receptor expression in carcinoma cells (p < 0.01, p < 0.05, respectively) in the 36 IDCs. These findings suggest that HIF-1alpha is expressed in the early stage of mammary carcinogenesis, in which the expression correlates with necrosis in the DCISs and with VEGF-C expression in the IDCs, the latter resulting in a higher frequency of metastasis to regional lymph nodes.
被引量：21 发表：2005
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Hypoxia-induced changes in the expression of VEGF, HIF-1 alpha and cell cycle-related molecules in ovarian cancer cells.
Hypoxia is important in cancer progression, and at the stage of detachment of the cancer cells from the primary lesion. This study was undertaken to analyze the effect of hypoxia on angiogenesis and cell proliferation in ovarian cancer. We first used immunohistochemistry to examine the expression of VEGF in 42 cases of ovarian carcinoma, with relevance to the p53 expression. Then, the expression of VEGF, HIF-1 alpha, cell cycle-related molecules and cell numbers were examined in 4 ovarian cancer cell lines with various p53 gene status. Immunohistochemistry showed that there was no significant correlation between VEGF and p53 expression. Moreover, hypoxia increased the expression of VEGF via up-regulation of HIF-1 alpha irrespective of p53 gene status. However hypoxia did not change the cell numbers, but influenced the expression of cell cycle-related molecules (increased p27 and decreased cyclin D1 and Rb). Hypoxia increased VEGF expression in ovarian cancer cells irrespective of p53 gene status.
被引量：19 发表：2002
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Caspase-activation and induction of inducible nitric oxide-synthase during TNF alpha-triggered apoptosis.
Activation of the intracellular "death domain" (DD) of the 55kD-TNF alpha-receptor by TNF alpha initiates signal and effector cascades with pro- and anti-apoptotic function. Co-activation of the adjacent "NO-domain" is followed by induction of inducible nitric oxide-synthase (iNOS) and generation of nitric oxide radicals (NO.). Recently, we have shown NO.-generation to be essential for TNF alpha-induced apoptosis of various tumor cell lines. However, the impact of iNOS activation in relation to other promoters of apoptosis, such as the caspases, is still unclear. Caspase activation, iNOS induction and death rate were therefore investigated in TNF alpha-treated MCF-7 cells. Incubation with TNF alpha (+/- cycloheximide) led to activation of the caspase cascade and was followed by apoptosis. Simultaneously, TNF alpha stimulated induction of iNOS and generation of NO.. Caspase inhibitors DEVD-CHO, YVAD-cmk and YVAD-CHO effectively inhibited caspase activation and prevented apoptosis. Apoptotic cell death was decreased to a similar degree following inhibition of iNOS by L-nitro-arginine-methyl-ester (L-NAME). Cell death suppression by caspase inhibition did not result in reduced iNOS activity, as well as L-NAME-dependent prevention of apoptosis was not associated with caspase inactivation. Taken together, TNF alpha induces apoptosis in MCF-7 cells by initiating a two-sided effector pathway including iNOS-induction and activation of caspase 1- and 3-like proteases. Both mechanisms seem to be equally essential for the execution of the death program. The exact nature of their cooperation needs further clarification.
被引量：8 发表：1999
