• 1.湖南吉首大學醫(yī)學院（吉首 416000）;;
  • 2.中南大學湘雅二醫(yī)院肝膽研究室（長沙 410011）;

目的研究芳香化酶（aromatase, Arom）和存活素（survivin, Surv）在原發(fā)性肝癌（primary hepatocarcinoma, PHC）中的表達情況，探討它們間的相互關系以及與PHC臨床病理特征之間的關系。
方法應用ABC免疫組化染色法對47例PHC手術切除標本切片分別檢測Arom和Surv的表達，并于高倍鏡下評分。
結果47例PHC癌組織中Arom和Surv的表達陽性率和表達評分均顯著高于癌旁組織： Arom, 40.43% vs 21.38%（P＜0.05）, 1.53±1.69 vs 0.79±1.41 （P＜0.05）; Surv, 63.83% vs 31.91%（ P＜0.01）, 2.40±1.96 vs 1.45±1.80 （P＜0.05）。除Surv在腫塊最大徑＜5 cm的癌組織中的表達評分（4.00±2.10）顯著高于腫塊最大徑≥5 cm者（2.17±1.86）外（P＜0.05），Arom和Surv在PHC中的表達情況與PHC其他主要臨床病理特征之間均無明顯關系； 癌組織中Arom與Surv的表達評分呈正相關（r=0.316，P＜0.05）。結論Arom和Surv的表達在PHC發(fā)生、發(fā)展中可能有著密切的關系。

引用本文： 向志鋼,楊竹林,鄧星輝. 原發(fā)性肝癌組織中芳香化酶和存活素的表達及其臨床病理意義. 中國普外基礎與臨床雜志, 2006, 13(3): 321-324. doi: 復制

1. Harada N, Ota H, Yoshimura N, et al. Localized aberrant expression of cytochrome P450 aromatase in primary and metastatic malignant tumors of human liver [Ｊ]. J Clin Endocrinol Metab, 1998; 83(2)∶ 697.
2. Kappler M, Kotzsch M, Bartel F, et al. Elevated expression level of survivin protein in softtissue sarcomas is a strong independent predictor of survival [Ｊ]. Clin Cancer Res, 2003; 9(3)∶1098.
3. 胡淳玲， 喻倫銀， 陳德基， 等. 大鼠試驗性肺鱗癌癌變各階段間質(zhì)微血管密度及VEGF、FLK1表達的動態(tài)變化 [Ｊ]. 癌癥， 2001; 20(10)∶713.
4. Meinhardt U, Mullis PE. The aromatase cytochrome P450 and its clinical impact [Ｊ]. Horm Res, 2002; 57(5-6)∶145.
5. Castagnetta LA, Agostara B, Montalto G, et al. Local estrogen formation by nontumoral, cirrhotic, and malignant human liver tissues and cells[Ｊ]. Cancer Res, 2003; 63(16)∶5041.
6. Shin S, Sung BJ, Cho YS, et al. An antiapoptotic protein human survivin is a direct inhibitor of caspase3 and 7[Ｊ]. Biochemistry, 2001; 40(4)∶1117.
7. 林木生， 伊新， 繆輝來， 等. 生存素和天冬氨酸特異性半胱氨酸蛋白酶3在肝癌中的表達及其關系[Ｊ]. 中華實驗外科雜志, 2004; 21(3)∶210.
8. Shekhar MP, Werdell J, Tait L. Interaction with endothelial cells is a prerequisite for branching ductalalveolar morphogenesis and hyperplasia of preneoplastic human breast epithelial cells: regulation by estrogen[Ｊ]. Cancer Res, 2000;60(2)∶439.
9. Kirma N, Gill K, Mandava U, et al. Overexpression of aromatase leads to hyperplasia and changes in the expression of genes involved in apoptosis, cell cycle, growth, and tumor suppressor functions in the mammary glands of transgenic mice [Ｊ]. Cancer Res, 2001; 61(5)∶1910.
10. Thiantanawat A, Long BJ, Brodie AM. Signaling pathways of apoptosis activated by aromatase inhibitors and antiestrogens[Ｊ]. Cancer Res, 2003; 63(22)∶8037.
  1. 1. Harada N, Ota H, Yoshimura N, et al. Localized aberrant expression of cytochrome P450 aromatase in primary and metastatic malignant tumors of human liver [Ｊ]. J Clin Endocrinol Metab, 1998; 83(2)∶ 697.
  2. 2. Kappler M, Kotzsch M, Bartel F, et al. Elevated expression level of survivin protein in softtissue sarcomas is a strong independent predictor of survival [Ｊ]. Clin Cancer Res, 2003; 9(3)∶1098.
  3. 3. 胡淳玲， 喻倫銀， 陳德基， 等. 大鼠試驗性肺鱗癌癌變各階段間質(zhì)微血管密度及VEGF、FLK1表達的動態(tài)變化 [Ｊ]. 癌癥， 2001; 20(10)∶713.
  4. 4. Meinhardt U, Mullis PE. The aromatase cytochrome P450 and its clinical impact [Ｊ]. Horm Res, 2002; 57(5-6)∶145.
  5. 5. Castagnetta LA, Agostara B, Montalto G, et al. Local estrogen formation by nontumoral, cirrhotic, and malignant human liver tissues and cells[Ｊ]. Cancer Res, 2003; 63(16)∶5041.
  6. 6. Shin S, Sung BJ, Cho YS, et al. An antiapoptotic protein human survivin is a direct inhibitor of caspase3 and 7[Ｊ]. Biochemistry, 2001; 40(4)∶1117.
  7. 7. 林木生， 伊新， 繆輝來， 等. 生存素和天冬氨酸特異性半胱氨酸蛋白酶3在肝癌中的表達及其關系[Ｊ]. 中華實驗外科雜志, 2004; 21(3)∶210.
  8. 8. Shekhar MP, Werdell J, Tait L. Interaction with endothelial cells is a prerequisite for branching ductalalveolar morphogenesis and hyperplasia of preneoplastic human breast epithelial cells: regulation by estrogen[Ｊ]. Cancer Res, 2000;60(2)∶439.
  9. 9. Kirma N, Gill K, Mandava U, et al. Overexpression of aromatase leads to hyperplasia and changes in the expression of genes involved in apoptosis, cell cycle, growth, and tumor suppressor functions in the mammary glands of transgenic mice [Ｊ]. Cancer Res, 2001; 61(5)∶1910.
  10. 10. Thiantanawat A, Long BJ, Brodie AM. Signaling pathways of apoptosis activated by aromatase inhibitors and antiestrogens[Ｊ]. Cancer Res, 2003; 63(22)∶8037.