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Xin Ma,
Hongzhao Li,
Xu Zhang, Qingbo Huang,
Baojun Wang,
Taoping Shi,
Dongliang Hu,
Qing Ai,
Shangwen Liu,
Jiangping Gao,
Yong Yang,
Jun Dong,
Tao Zheng
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ABSTRACT: BACKGROUND: In a previous experience, anatomical retroperitoneoscopic adrenalectomy (ARA) was proven safe, effective, and technically efficient for surgical adrenal diseases. However, laparoscopic adrenalectomy for adrenal metastasis is controversial. We evaluated the safety, effectiveness, and efficiency of modified ARA technique for adrenal metastasis and predicted survival factors. METHODS: From 2000 to 2010, a consecutive series of 75 patients with adrenal metastases underwent 78 ARAs (three bilateral ARAs). Three modifications and one key procedure were specified in this study. Medical records and follow-up data were retrospectively studied. Then, the surgery data of ARA were compared with those of other approaches to evaluate its safety, effectiveness, and efficiency. Additionally, univariate and multivariate analyses were used to predict the risk factors for survival. RESULTS: The most common primary tumor was renal cell carcinoma (RCC, n = 26), followed by non-small-cell lung carcinoma (NSCLC, n = 23), and hepatocellular carcinoma (HCC, n = 12). A total of 76 successful ARAs and two conversions to open surgery were performed, with a median operation time of 53 (range, 40-250) min and median estimated blood loss of 25 (range, 10-700) mL. The local recurrence rate was 5.3 %, and the median survival was 24 months. These data were comparable with or even better than other approaches in previous studies. The independent prognostic factors of survival were body mass index (BMI, p < 0.001), tumor type (p < 0.001), tumor size (≥4 cm vs. <4 cm, p = 0.017), and margin status (negative vs. positive, p = 0.011). CONCLUSIONS: ARA is a safe and effective approach for the management of adrenal metastasis in selected patients. BMI, tumor type, tumor size, and margin status may independently predict survival.
Surgical Endoscopy 12/2012; · 4.01 Impact Factor
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Qing Ai,
Xin Ma, Qingbo Huang,
Shangwen Liu,
Taoping Shi,
Chao Zhang,
Mingyang Zhu,
Yu Zhang,
Baojun Wang,
Dong Ni,
Hongzhao Li,
Tao Zheng,
Xu Zhang
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ABSTRACT: Although metastasis of clear cell renal cell carcinoma (ccRCC) is basically observed in late stage tumors, T1 stage metastasis of ccRCC can also be found with no definite molecular cause resulting inappropriate selection of surgery method and poor prognosis. Notch signaling is a conserved, widely expressed signal pathway that mediates various cellular processes in normal development and tumorigenesis. This study aims to explore the potential role and mechanism of Notch signaling in the metastasis of T1 stage ccRCC.
The expression of Notch1 and Jagged1 were analyzed in tumor tissues and matched normal adjacent tissues obtained from 51 ccRCC patients. Compared to non-tumor tissues, Notch1 and Jagged1 expression was significantly elevated both in mRNA and protein levels in tumors. Tissue samples of localized and metastatic tumors were divided into three groups based on their tumor stages and the relative mRNA expression of Notch1 and Jagged1 were analyzed. Compared to localized tumors, Notch1 expression was significantly elevated in metastatic tumors in T1 stage while Jagged1 expression was not statistically different between localized and metastatic tumors of all stages. The average size of metastatic tumors was significantly larger than localized tumors in T1 stage ccRCC and the elevated expression of Notch1 was significantly positive correlated with the tumor diameter. The functional significance of Notch signaling was studied by transfection of 786-O, Caki-1 and HKC cell lines with full-length expression plasmids of Notch1 and Jagged1. Compared to the corresponding controls, all cell lines demonstrated significant promotion in cell proliferation and migration while cell cycle remained unaffected.
High-level expression of Notch signaling increased the risk of metastasis in T1 stage ccRCC by stimulating the proliferation and migration of tumor cells, which may be helpful for the selection of suitable operation method and prognosis of ccRCC.
PLoS ONE 01/2012; 7(4):e35022. · 4.09 Impact Factor
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ABSTRACT: OBJECTIVES: Although NOTCH1 plays a wide-ranging role in controlling cell fate, differentiation, and development, its pathologic roles in clear cell renal cell carcinoma (CCRCC) are still unclear. In the present study, the expression pattern of NOTCH1 was examined in CCRCC tissues, and the interaction of NOTCH1 with the phosphatase and tensin homologue deleted on chromosome 10 (PTEN)/phosphatidylinositol 3-kinase (PI3K)/AKT pathway was investigated in vitro. MATERIALS AND METHODS: Thirty-six paired CCRCC and adjacent non-neoplastic renal samples were analyzed by Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR). The alteration of NOTCH1, hairy and enhancer of split 1 (HES1), PTEN, AKT (phosphorylated at Ser473) in CCRCC cell line (786-O), and the human normal kidney tubule epithelial cell line (HKC) were analyzed by Western blotting and qRT-PCR, before and after transfection with siRNA against NOTCH1 or the plasmid containing the ORF clone of NOTCH1. The effects of NOTCH1 signaling pathway on cells proliferation, apoptosis, invasion, and migration were detected by MTS assay, flow cytometry analyses, and transwell chamber assay, respectively. RESULTS: The NOTCH1 expression levels were significantly increased in CCRCC tissues compared with the adjacent non-neoplastic renal samples, while it had no significant association with the pathologic parameters. NOTCH1 signaling cascade was constitutively active in human CCRCC cell lines. Blocking NOTCH1 signaling resulted in the attenuation of proliferation, invasion, and migration, as well as PTEN up-regulation with decreased AKT phosphorylation. NOTCH1 overexpression had an opposite effect to NOTCH1 knockdown. CONCLUSIONS: Our findings indicated that NOTCH1 receptor expression was up-regulated in CCRCC, and that NOTCH1 could regulate PTEN expression and the activity of the PI3K/AKT pathway via HES1 in 786-O and HKC cell lines. These might provide a basis for the designing new therapeutic strategies for CCRCC.
Urologic Oncology 10/2011; · 3.22 Impact Factor
