冷冻消融对前列腺癌血管生成影响研究及相关数学模型计划系统初步构建
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摘要
背景：冷冻消融逐渐成为治疗局限性前列腺癌的一线治疗手段,对于残存肿瘤血管生成活性的研究可以解释临床常见的实际问题。目的：复制激素难治性前列腺癌肺转移模型,评价冷冻消融治疗前列腺癌移植瘤后残存前列腺癌组织的血管生成活性,探讨联合治疗的可行性与必要性。并建立数学模型计划系统,服务于临床实际。材料与方法：通过表达谱基因芯片研究及荧光定量PCR研究,获得冷冻消融后残存瘤体m-RNA表达的差异。并使用双向电泳蛋白质谱分析手段验证蛋白表达的变化。在此基础之上利用免疫组化方法动态检测冷冻治疗术后相关蛋白空间与时间的变化特点。设立新的实验分组,研究氩氦冷冻消融联合抗血管内皮药物YH-16的联合治疗策略所产生的影响,以所得结果构建数学模型及靶向计划程序,获得完整的治疗计划及预后评测系统,直接辅助临床工作。结果：1)基因表达谱芯片筛选结果提示肿瘤细胞凋亡、血管生成及肿瘤细胞侵袭增殖能力变化等过程具有显著性差异。2)荧光定量PCR证实筛选出的HIF-1α, VEGFA, MMP2, Caspase3及Caspase6均出现了显著性变化。3)二维双向电泳技术蛋白质谱分析进一步验证了基因表达谱芯片及荧光定量PCR的研究结果。4)对于VEGF、MMP2及MVD时间分布的研究结果证实了冷冻消融后,随着时间推移,与血管生成活性相关的蛋白指标呈现显著增长,其可以为YH-16联合治疗策略所有效阻断,提示在冷冻消融治疗的基础上,联合抗血管生成靶向药物治疗,可能获得较好的治疗收益。对于VEGF、MMP2、MVD及Caspase3空间分布的研究结果说明了,血管生成增强剂凋亡增加在冷冻消融治疗后的残存前列腺癌组织中同时存在,但空间分布呈现互补态势。5)本研究在合理假设的前提基础上,成功地建立了数学模型靶向计划实验系统,以此系统为蓝本的初步临床实验,在相关性回归分析的方法中,确立了重要的模型参数,其使得数学模型靶向计划实验系统与临床表现具有较高的一致性。结论：冷冻消融治疗后,残存前列腺癌组织以血管生成活性为代表的生物学行为特征发生了复杂的改变,血管生成活性分布具有空间特征,联合抗血管生成治疗可能成为可选择的治疗策略。建立的数学模型靶向计划实验系统,可以为临床工作提供辅助性技术理论平台。
Background:Cryoablation has become primary treatment of localized prostate cancer treatment, the residual activity of tumor angiogenesis may explain common clinical practice problems. Objective:To copy the hormone refractory prostate cancer lung metastasis model to evaluate cryoablation of surviving prostate cancer tumor angiogenesis in prostate cancer activity, explore the feasibility and necessity of combination therapy. Planning system and the establishment of mathematical models, services in clinical practice. Materials and Methods:The expression profiles by cDNA microarray and quantitative PCR studies, access to residual tumor after cryoablation m-RNA expression differences. And use the means of two-dimensional electrophoresis proteomic analysis of protein expression changes verified. On this basis, the dynamic use of immunohistochemical detection of proteins after cryoablation, the changes of space and time. Establishment of a new group to study the argon-helium cryoablation combined vascular endothelial drugs YH-16combined impact of treatment strategies to build mathematical models and the results of targeted planning process, a complete treatment plan and prognosis evaluation system, direct support of clinical work. Results:1) gene chip screening results suggest that tumor cell apoptosis, angiogenesis and proliferation of tumor cell invasion process of change, significant differences.2) The fluorescence quantitative PCR screening confirmed the HIF-1α, VEGFA, MMP2, Caspase3and Caspase6there were significant changes.3) two-dimensional spectral analysis of two-dimensional electrophoresis technology to further validate the protein microarray and quantitative PCR results.4) For VEGF, MMP2and temporal distribution of MVD confirmed the findings after cryoablation, as time goes on, and angiogenesis activity of protein targets associated with significant growth, which can be as YH-16combined treatment strategies are effective in blocking, Tip cryoablation, based on the joint anti-angiogenic targeted drug therapy may be a better therapeutic gains. For VEGF, MMP2, MVD, and the spatial distribution of Caspase3results suggest that angiogenesis enhancer increased apoptosis after the frozen remnant ablation therapy in prostate cancer exist, but a complementary distribution trend.5) In this study, based on the premise of reasonable assumptions, the mathematical model successfully established experimental system targeted programs, this system is modeled on the initial clinical trials, the relevance of the method of regression analysis to establish an important model parameters The mathematical model makes the targeted programs and clinical manifestations of experimental system has a higher consistency. Conclusion:Cryoablation treatment, residual prostate cancer to angiogenic activity represented characteristics of the biological behavior of complex changes have taken place, angiogenesis activity of distribution of spatial characteristics, combined anti-angiogenesis therapy might be alternative treatment strategies. Targeted programs established mathematical model experimental system for providing assistive technology clinical theory of platform.
Background:Cryoablation has become primary treatment of localized prostate cancer treatment, the residual activity of tumor angiogenesis may explain common clinical practice problems. Objective:To copy the hormone refractory prostate cancer lung metastasis model to evaluate cryoablation of surviving prostate cancer tumor angiogenesis in prostate cancer activity, explore the feasibility and necessity of combination therapy. Planning system and the establishment of mathematical models, services in clinical practice. Materials and Methods:The expression profiles by cDNA microarray and quantitative PCR studies, access to residual tumor after cryoablation m-RNA expression differences. And use the means of two-dimensional electrophoresis proteomic analysis of protein expression changes verified. On this basis, the dynamic use of immunohistochemical detection of proteins after cryoablation, the changes of space and time. Establishment of a new group to study the argon-helium cryoablation combined vascular endothelial drugs YH-16combined impact of treatment strategies to build mathematical models and the results of targeted planning process, a complete treatment plan and prognosis evaluation system, direct support of clinical work. Results:1) gene chip screening results suggest that tumor cell apoptosis, angiogenesis and proliferation of tumor cell invasion process of change, significant differences.2) The fluorescence quantitative PCR screening confirmed the HIF-1α, VEGFA, MMP2, Caspase3and Caspase6there were significant changes.3) two-dimensional spectral analysis of two-dimensional electrophoresis technology to further validate the protein microarray and quantitative PCR results.4) For VEGF, MMP2and temporal distribution of MVD confirmed the findings after cryoablation, as time goes on, and angiogenesis activity of protein targets associated with significant growth, which can be as YH-16combined treatment strategies are effective in blocking, Tip cryoablation, based on the joint anti-angiogenic targeted drug therapy may be a better therapeutic gains. For VEGF, MMP2, MVD, and the spatial distribution of Caspase3results suggest that angiogenesis enhancer increased apoptosis after the frozen remnant ablation therapy in prostate cancer exist, but a complementary distribution trend.5) In this study, based on the premise of reasonable assumptions, the mathematical model successfully established experimental system targeted programs, this system is modeled on the initial clinical trials, the relevance of the method of regression analysis to establish an important model parameters The mathematical model makes the targeted programs and clinical manifestations of experimental system has a higher consistency. Conclusion:Cryoablation treatment, residual prostate cancer to angiogenic activity represented characteristics of the biological behavior of complex changes have taken place, angiogenesis activity of distribution of spatial characteristics, combined anti-angiogenesis therapy might be alternative treatment strategies. Targeted programs established mathematical model experimental system for providing assistive technology clinical theory of platform.
引文
[1]Jeffrey KC, Miller RJ, Ahmed S, et al. Ten-Year Biochemical Disease Control for Patients with Prostate Cancer Treated with Cryosurgery as Primary Therapy[J]. Urology.2008;71:515-518.
[2]Gary O, David V, Richard L, et al. "Male Lumpectomy":Focal Therapy for Prostate Cancer Using Cryoablation[J]. Urology.2007;70:16-21.
[3]Bharat G, Damien G. Cryotherapy for the prostate:an in vitro and clinical study of two new developments; advanced cryoneedles and a temperature monitoring system[J]. BJU International 2007; 100:295-302.
[4]Gary Onik. Rationale for a "Male Lumpectomy," a Prostate Cancer targeted approach using cryoablation:results in 21 patients with at Least 2 years of follow-up[J]. Cardiovasc Intervent Radiol 2008;31:98-106
[5]Yang L,W ang JW,Cui CX,et al.Rh-endostatin(YH-16)in combination w ith vinorelbine and cisp latin for advanced non-small cell lung cancer:a multicenter phase 11 trial[J].Chin J New D rugs,2005,14(2):2041.
[6]Polascik TJ, Nosnik I, Mayes JM, et al. Short-Term Cancer Control After Primary Cryosurgical Ablation for Clinically Localized Prostate Cancer Using Third-Generation Cryotechnology[J]. Urology 2007;70:117-121.
[7]Siddiqui SA, Mynderse LA, Zincke H,et al. Treatment of Prostate Cancer Local Recurrence After Radical Retropubic Prostatectomy with 17-Gauge Interstitial Transperineal Cryoablation:Initial Experience[J]. Urology 2007;70:80-85.
[8]Hayek ORE, Alfer Jr. W, Reggio E, et al. Percutaneous prostate cryoablation as treatment for high-risk prostate cancer[J]. Clinics.2007;62(2):109-12.
[9]Scott GH, Michael DF, Paul FS, et al. Single center experience with third-generation cryosurgery for management of organ-confine prostate cancer: critical evaluation of short-term outcome,complications, and patient quality of life[J]. Journal of endourology 2007; 21(12):1521-1531.
[10]Forest V, Peoc'h M, Campos L et al. Benefit of a combined treatment of cryotherapy and chemotherapy on tumour growth and late cryo-induced angiogenesis in a non-small-cell lung cancer model[J]. Lung Cancer.2006 Oct;54(1):79-86.
[11]Yang L,W ang JW,Cui CX,et al.Rh-endostatin(YH-16)in combination w ith vinorelbine and cisp latin for advanced non-small cell lung cancer:a multicenter phase Ⅱ trial[J].Chin J New D rugs,2005,14(2):2041.
[12]Herbst RS,Johnson DH,Mininberg E,et al.Phase Ⅰ/Ⅱ trial evaluating the anti-vascular endothelial growth factor monoclonal antibody bevacizumab in combination with the HER-1/epidermal growth factor receptor tyrosine kinase inhibitor erlotinib for patients with recurrent non-small-cell lung cancer[J].J Clin Oncol,2005,23(11):2544-2555.
[13]Pao W,Miller VA.Epidermal growth factor receptor muta-tions,small-molecule kinase inhibitors,and non-small-cell lung cancer:current knowledge and future directions[J].J Clin Oncol,2005,23(11):2556-2568.
[14]Dong QQHuang JS.Epidermal growth factor receptor mutations in Chinese patients with adenocarcinoma of the lung[J]. ancer,006, (26) 271-275.
[15]Laack E, SchefflerA, Burkholder I, et al. Pretreatment vascular endothelial growth fact or (VEGF) and matrix metalloproteinase-9 (MMP29) serum levels in patients with metastatic non-small cell lung cancer (NSCLC)[J]. Lung Cancer,2005,50(1):51-58.
[16]Sapra P, Kraft P, Pastorino F, Potent and sustained inhibition of HIF-1α and downstream genes by a polyethyleneglycol-SN38 conjugate, EZN-2208, results in anti-angiogenic effects[J]. Angiogenesis.2011 Mar 31
[17]Chang CC, Lin MT, Lin BR, et al. Effect of connective tissue growth factor on hypoxia-inducible factor lalpha degradation and tumor angiogenesis[J]. J Natl Cancer Inst.2006 Jul 19;98(14):984-95.
[18]Choi KS, Bae MK, Jeong JW, et al. Hypoxia-induced angiogenesis during carcinogenesis[J]. J Biochem Mol Biol.2003 Jan 31;36(1):120-7.
[19]Yamakawa M, Liu LX, Date T, et al. Hypoxia-inducible factor-1 mediates activation of cultured vascular endothelial cells by inducing multiple angiogenic factors[J]. Circ Res.2003 Oct 3;93(7):664-73.
[20]Choi KS, Bae MK, Jeong JW, et al. Hypoxia-induced angiogenesis during carcinogenesis[J]. J Biochem Mol Biol.2003 Jan 31;36(1):120-7.
[21]Mazure NM, Brahimi-Horn MC, Pouyssegur J. Protein kinases and the hypoxia-inducible factor-1, two switches in angiogenesis[J]. Curr Pharm Des. 2003;9(7):531-41.
[22]Chang CC, Lin MT, Lin BR, et al. Effect of connective tissue growth factor on hypoxia-inducible factor lalpha degradation and tumor angiogenesis[J]. J Natl Cancer Inst.2006 Jul19;98(14):984-95.
[23]Berra E, Pages G, Pouyssegur J. et al. MAP kinases and hypoxia in the control of VEGF expression[J]. Cancer Metastasis Rev.2000; 19(1-2):139-45.
[24]Hashizurne H, Falcon BL, Kuroda T, et al. Complementary actions of inhibitors of angiopoietin-2 and VEGF on tumor angiogenesis and growth[J]. Cancer Res. 2010 Mar 15;70(6):2213-23.
[25]Diaz-Rubio E. Vascular endothelial growth factor inhibitors in colon cancer[J]. Adv Exp Med Biol.2006;587:251-75.
[26]Hicklin DJ, Ellis LM. Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis[J]. J Clin Oncol.2005 Feb 10;23(5):1011-27.
[27]Veeravagu A, Hsu AR, Cai W, et al. Vascular endothelial growth factor and vascular endothelial growth factor receptor inhibitors as anti-angiogenic agents in cancer therapy[J]. Recent Pat Anticancer Drug Discov.2007 Jan;2(1):59-71.
[28]Shinkaruk S, Bayle M, Lain G, et al. Vascular endothelial cell growth factor (VEGF), an emerging target for cancer chemotherapy[J]. Curr Med Chem Anticancer Agents.2003 Mar;3(2):95-117.
[29]Ferrara N. Role of vascular endothelial growth factor in physiologic and pathologic angiogenesis:therapeutic implications[J]. Semin Oncol.2002 Dec;29(6):10-4.
[30]Jain RK. Tumor angiogenesis and accessibility:role of vascular endothelial growth factor[J]. Semin Oncol.2002 Dec;29(6):3-9.
[31]Pradeep CR, Sunila ES, Kuttan G. Expression of vascular endothelial growth factor (VEGF) and VEGF receptors in tumor angiogenesis and malignancies[J]. Integr Cancer Ther.2005 Dec;4(4):315-21.
[32]Kerigh BF, Bahrami A, Shamsa A, et al. Assessment of angiogenic factor, vascular endothelial growth factor, serum and urine level changes in superficial bladder tumor immunotherapy by intravesical Bacillus Calmette-Guerin[J]. Urol Ann.2010 Sep;2(3):91-5.
[33]Kaur B, Khwaja FW, Severson EA, Hypoxia and the hypexia inducible factor pathway in glioma growth and angiogenesis[J]. Neuro Oncol.2005 Apr;7(2):134-53.
[34]Jensen RL, Ragei BT, Whang K, et al. Inhibition of hypoxia inducible factor-1 alpha (HIF-1 alpha) decreases vascular endothelial growth factor (VEGF) secretion and tumor growth in malignant gliomas[J]. J Neurooncol.2006 Jul;78(3):233-47.
[35]Zagzag D, Lukyanov Y, Lan L, et al.Hypoxia-inducible factor 1 and VEGF upregulate CXCR4 in glioblastoma:implications for angiogenesis and glioma cell invasion[J]. Lab Invest.2006 Dec;86(12):1221-32.
[36]Overall CM, Dean RA. Degradomics:systems biology of the protease web. Pleiotropic roles of MMPs in cancer[J]. Cancer Metastasis Rev.2006 Mar;25(1):69-75.
[37]Dean RA, Overall CM. Proteomics discovery of metalloproteinase substrates in the cellular context by iTRAQ labeling reveals a diverse MMP-2 substrate degradome[J]. Mol Cell Proteomics.2007 Apr;6(4):611-23.
[38]Prudova A, auf dem Keller U, Butler GS, et al. Multiplex N-terminome analysis of MMP-2 and MMP-9 substrate degradomes by iTRAQ-TAILS quantitative proteomics[J]. Mol Cell Proteomics.2010 May;9(5):894-911.
[39]Overall CM, Dean RA. Degradomics:systems biology of the protease web. Pleiotropic roles of MMPs in cancer[J]. Cancer Metastasis Rev.2006 Mar;25(1):69-75.
[40]Dean RA, Overall CM. Proteomics discovery of metalloproteinase substrates in the cellular context by iTRAQ labeling reveals a diverse MMP-2 substrate degradome[J]. Mol Cell Proteomics.2007 Apr;6(4):611-23.
[41]Butler GS, Dean RA, Tam EM, et al. Pharmacoproteomics of a metalloproteinase hydroxamate inhibitor in breast cancer cells:dynamics of membrane type 1 matrix metalloproteinase mediated membrane protein shedding[J]. Mol Cell Biol. 2008 Aug;28(15):4896-914.
[42]Butler GS, Overall CM. Proteomic validation of protease drug targets: pharmacoproteomics of matrix metalloproteinase inhibitor drugs using isotope-coded affinity tag labelling and tandem mass spectrometry[J]. Curr Pharm Des.2007;13(3):263-70.
[43]Morrison CJ, Butler GS, Rodriguez D, et al. Matrix metalloproteinase proteomics: substrates, targets, and therapy[J]. Curr Opin Cell Biol.2009 Oct;21(5):645-53.
[44]Butler GS, Overall CM. Updated biological roles for matrix metalloproteinases and new "intracellular" substrates revealed by degradomics[J]. Biochemistry. 2009 Nov 24;48(46):10830-45.
[45]Rodriguez D, Morrison CJ, Overall CM. Matrix metalloproteinases:what do they not do? New substrates and biological roles identified by murine models and proteomics[J]. Biochim Biophys Acta.2010 Jan;1803(1):39-54.
[46]Tam EM, Morrison CJ, Wu YI, et al. Membrane protease proteomics: Isotope-coded affinity tag MS identification of undescribed MT1-matrix metalloproteinase substrates[J]. Proc Natl Acad Sci U S A.2004 May 4;101(18):6917-22.
[47]Dean RA, Butler GS, Hamma-Kourbali Y, et al. Identification of candidate angiogenic inhibitors processed by matrix metalloproteinase 2 (MMP-2) in cell-based proteomic screens:disruption of vascular endothelial growth factor (VEGF)/heparin affin regulatory peptide (pleiotrophin) and VEGF/Connective tissue growth factor angiogenic inhibitory complexes by MMP-2 proteolysis[J]. Mol Cell Biol.2007 Dec;27(24):8454-65.
[48]Hashimoto G, Inoki I, Fujii Y, et al. Matrix metalloproteinases cleave connective tissue growth factor and reactivate angiogenic activity of vascular endothelial growth factor 165[J]. J Biol Chem.2002 Sep 27;277(39):36288-95.
[49]Inoki I, Shiomi T, Hashimoto G, et al. Connective tissue growth factor binds vascular endothelial growth factor (VEGF) and inhibits VEGF-induced angiogenesis[J]. FASEB J.2002 Feb; 16(2):219-21.
[50]Liu XD, Fan RF, Zhang Y, et al. Down-regulation of telomerase activity and activation of caspase-3 are responsible for tanshinone I-induced apoptosis in monocyte leukemia cells in vitro[J]. Int J Mol Sci.2010 May 26;11(6):2267-80.
[51]Xu Q, Li ZX, Peng HQ, et al. Artesunate inhibits growth and induces apoptosis in human osteosarcoma HOS cell line in vitro and in vivo[J]. J Zhejiang Univ Sci B.2011 Apr.;12(4):247-255.
[52]Ji BC, Hsu WH, Yang JS, et al. Gallic acid induces apoptosis via caspase-3 and mitochondrion-dependent pathways in vitro and suppresses lung xenograft tumor growth in vivo[J]. J Agric Food Chem.2009 Aug 26;57(16):7596-604.
[53]Lu HF, Chie YJ, Yang MS,et al. Apigenin induces caspase-dependent apoptosis in human lung cancer A549 cells through Bax-and Bcl-2-triggered mitochondrial pathway[J]. Int J Oncol.2010 Jun;36(6):1477-84.
[54]Chen QY, Lu GH, Wu YQ, et al. Curcumin induces mitochondria pathway mediated cell apoptosis in A549 lung adenocarcinoma cells[J]. Oncol Rep.2010 May;23(5):1285-92.
[55]Gyrd-Hansen M, Meier P. IAPs:from caspase inhibitors to modulators of NF-kappaB, inflammation and cancer[J]. Nat Rev Cancer.2010 Aug;10(8):561-74.
[56]LaCasse EC, Baird S, Korneluk RG, et al. The inhibitors of apoptosis (IAPs) and their emerging role in cancer[J]. Oncogene.1998 Dec 24; 17(25):3247-59.
[57]Hunter AM, LaCasse EC, Korneluk RG. The inhibitors of apoptosis (IAPs) as cancer targets[J]. Apoptosis.2007 Sep; 12(9):1543-68.
[58]Fulda S, Gorman AM, Hori O, et al. Cellular stress responses:cell survival and cell death[J]. Int J Cell Biol.2010;2010:214074.
[59]Katacka S, Tsuruo T. Physician Education:Apoptosis[J]. Oncologist. 1996;1(6):399-401.
[60]Park HJ, Kim MJ, Ha E, et al. Apoptotic effect of hesperidin through caspase3 activation in human colon cancer cells, SNU-C4[j]. Phytomedicine.2008 Jan; 15(1-2):147-51.
[61]Larsen BD, Rampalli S, Burns LE, et al. Caspase 3/caspase-activated DNase promote cell differentiation by inducing DNA strand breaks[J]. Proc Natl Acad Sci USA.2010 Mar 2;107(9):4230-5.
[62]Hu D, Liu S, Shi L, et al. Cleavage of survivin by Granzyme M triggers degradation of the survivin-X-linked inhibitor of apoptosis protein (XIAP) complex to free caspase activity leading to cytolysis of target tumor cells[J]. J Biol Chem.2010 Jun 11;285(24):18326-35.
[63]Yin S, Sethi S, Reddy KB. Protein kinase C8 and caspase-3 modulate TRAIL-induced apoptosis in breast tumor cells[J]. J Cell Biochem.2010 Nov 1;111(4):979-87.
[64]Yang X, Wang D, Zhong Z, et al. The Comparison of Clinical Effect of Rh-endostar on Retreated Non-Small Cell Lung Cancer and Colorectal Cancer[J]. Zhongguo Fei Ai ZaZhi.2009 Nov 20; 12(11):1184-7.
[65]Zhang DW, Li HL, Yao Q, et al. The synergistic effect of recombinant human endostatin (YH-16) combined with oxaliplatin on human colorectal carcinoma[J]. J Int Med Res.2010 Jan-Feb;38(1):111-26.
[66]Wu H, Deng J, Yu S, et al. The inhibitory effects of rh-endostatin (YH-16) in combination with radiotherapy on lung adenocarcinoma A549 in mice and the underlying mechanisms[J].J Huazhong Univ Sci Technolog Med Sci.2010 Feb;30(1):108-12.
[67]Wu G, Zhang R, Ren J, et al. Autophagic cell death of human hepatoma cells induced by endostar, a recombinant human endostatin[J]. Cancer Biother Radiopharm.2008 Dec;23(6):735-40.
[68]Jiang HQ, Li YL, Zou J.Effect of recombinant human endostatin on endometriosis in mice.Chin Med J (Engl)[J].2007 Jul 20; 120(14):1241-6
[69]Wang J, Sun Y, Liu Y, et al. Results of randomized, multicenter, double-blind phase III trial of rh-endostatin (YH-16) in treatment of advanced non-small cell lung cancer patients[J]. Zhongguo Fei Ai Za Zhi.2005 Aug 20;8(4):283-290.
[70]El Zouhairi M, Charabaty A, Pishvaian MJ. Molecularly targeted therapy for metastatic colon cancer:proven treatments and promising new agents[J]. Gastrointest Cancer Res.2011 Jan;4(1):15-21.
[1]Jeffrey K.C, Miller RJ, Ahmed S, et al. Ten-Year Biochemical Disease Control for Patients with Prostate Cancer Treated with Cryosurgery as Primary Therapy. Urology.2008;71:515-518.
[2]Gary O, David V, Richard L, et al. "Male Lumpectomy":Focal Therapy for Prostate Cancer Using Cryoablation. Urology.2007;70:16-21.
[3]Bharat G, Damien G. Cryotherapy for the prostate:an in vitro and clinical study of two new developments; advanced cryoneedles and a temperature monitoring system. BJU International 2007; 100:295-302.
[4]Gary Onik. Rationale for a "Male Lumpectomy," a Prostate Cancer targeted approach using cryoablation:results in 21 patients with at Least 2 years of follow-up. Cardiovasc Intervent Radiol 2008;31:98-106
[5]Bahn DK, Lee F, Badalament R, et al. Targeted cryoablation of the prostate: 7-year outcomes in the primary treatment of prostate cancer. Urology.2002; 60(suppl2A):3-11.
[6]Polascik TJ, Nosnik I, Mayes JM, et al. Short-Term Cancer Control After Primary Cryosurgical Ablation for Clinically Localized Prostate Cancer Using Third-Generation Cryotechnology. Urology 2007;70:117-121.
[7]Siddiqui SA, Mynderse LA, Zincke H,et al. Treatment of Prostate Cancer Local Recurrence After Radical Retropubic Prostatectomy with 17-Gauge Interstitial Transperineal Cryoablation:Initial Experience. Urology 2007;70:80-85.
[8]Hayek ORE, Alfer Jr. W, Reggio E, et al. Percutaneous prostate cryoablation as treatment for high-risk prostate cancer. Clinics.2007;62(2):109-12.
[9]Scott GH, Michael DF, Paul FS, et al. Single center experience with third-generation cryosurgery for management of organ-confine prostate cancer: critical evaluation of short-term outcome,complications, and patient quality of life. Journal of endourology 2007; 21(12):1521-1531.
[10]Chin JL, C-K Ng, NJ Touma, et al. Randomized trial comparing cryoablation and external beam radiotherapy for T2C-T3B prostate cancer. Prostate Cancer and Prostatic Diseases 2007:1-6.
[11]Mohamed I, Shwan A, Christof K, et al. Salvage cryotherapy for recurrent prostate cancer after radiation failure:a prospective case series of the first 100 patients. BJU International 2007; 100:760-764
[12]Chee KN, Madeleine M, Donal BD,et al. Salvage Cryoablation of the Prostate: Followup and Analysis of Predictive Factors for Outcome. The journal of urologe 2007; 178:1253-1257,
[13]A1 B. Barqawi, E. David Crawford, The Current Use and Future Trends of Focal Surgical Therapy in. the Management of Localized Prostate Cancer. Cancer J 2007;13:313-317.
[14]Eggener SE, Scardino PT, Focal PR, et al. Therapy for Localized Prostate Cancer: A Critical Appraisal of Rationale and Modalities. The journal of urology 2007; 178:2260-2267,
[15]Vladimir M., Janice MM, John FM, et al. Analysis of Laterality and Percentage of Tumor Involvement in 1386 Prostatectomized Specimens for Selection of Unilateral Focal Cryotherapy. Technology in Cancer Research and Treatment 2007, Technology in Cancer Research and Treatment 2007; (2):91-95
[16]Ellis DS, Theodore BMJ, Rewcastle JC. Focal Cryosurgery Followed by Penile Rehabilitation as Primary Treatment for Localized Prostate Cancer:Initial Results. Urology 2007;70:9-15.
[17]den Brok MH, Sutmuller RP, Nierkens S, et al. Efficient loading of dendritic cells following cryo and radiofrequency ablation in combination with immune modulation induces anti-tumour immunity. Br J Cancer 2006,95(7):896-905.
[18]Osada S, Imai H, Tomita Ⅱ, et al. Serum Cytokine Levels in Response to Hepatic Cryoablation. J Surg Oncol 2007;95(6):491-498.
[19]Si TG, Guo Z, Hao XS, et al. Cryoablation for prostate cancer induce specific immune response. Cryobiology 2008;
[20]Clarke DM, Robilotto AT, VanBuskirk RG, et al. Targeted induction of apoptosis via TRAIL and cryoablation:a novel strategy for the treatment of prostate cancer. Prostate Cancer and Prostatic Diseases 2007; 10:175-184.
[21]Kang SH, Kim JW, Bae JH, et al. Targeted-cryosurgical ablation of the prostate with androgen deprivation therapy:quality of life in high-risk prostate cancer patients, Asian J Androl 2006; 8 (5):629-636.
[22]Clarke DM, Baust JM, VanBuskirk RG, et al. Addition of anticancer agents enhances freezing-induced prostate cancer cell death:implications of mitochondrial involvement. Cryobiology 2004;49:45-61.
[2]Gary O, David V, Richard L, et al. "Male Lumpectomy":Focal Therapy for Prostate Cancer Using Cryoablation[J]. Urology.2007;70:16-21.
[3]Bharat G, Damien G. Cryotherapy for the prostate:an in vitro and clinical study of two new developments; advanced cryoneedles and a temperature monitoring system[J]. BJU International 2007; 100:295-302.
[4]Gary Onik. Rationale for a "Male Lumpectomy," a Prostate Cancer targeted approach using cryoablation:results in 21 patients with at Least 2 years of follow-up[J]. Cardiovasc Intervent Radiol 2008;31:98-106
[5]Yang L,W ang JW,Cui CX,et al.Rh-endostatin(YH-16)in combination w ith vinorelbine and cisp latin for advanced non-small cell lung cancer:a multicenter phase 11 trial[J].Chin J New D rugs,2005,14(2):2041.
[6]Polascik TJ, Nosnik I, Mayes JM, et al. Short-Term Cancer Control After Primary Cryosurgical Ablation for Clinically Localized Prostate Cancer Using Third-Generation Cryotechnology[J]. Urology 2007;70:117-121.
[7]Siddiqui SA, Mynderse LA, Zincke H,et al. Treatment of Prostate Cancer Local Recurrence After Radical Retropubic Prostatectomy with 17-Gauge Interstitial Transperineal Cryoablation:Initial Experience[J]. Urology 2007;70:80-85.
[8]Hayek ORE, Alfer Jr. W, Reggio E, et al. Percutaneous prostate cryoablation as treatment for high-risk prostate cancer[J]. Clinics.2007;62(2):109-12.
[9]Scott GH, Michael DF, Paul FS, et al. Single center experience with third-generation cryosurgery for management of organ-confine prostate cancer: critical evaluation of short-term outcome,complications, and patient quality of life[J]. Journal of endourology 2007; 21(12):1521-1531.
[10]Forest V, Peoc'h M, Campos L et al. Benefit of a combined treatment of cryotherapy and chemotherapy on tumour growth and late cryo-induced angiogenesis in a non-small-cell lung cancer model[J]. Lung Cancer.2006 Oct;54(1):79-86.
[11]Yang L,W ang JW,Cui CX,et al.Rh-endostatin(YH-16)in combination w ith vinorelbine and cisp latin for advanced non-small cell lung cancer:a multicenter phase Ⅱ trial[J].Chin J New D rugs,2005,14(2):2041.
[12]Herbst RS,Johnson DH,Mininberg E,et al.Phase Ⅰ/Ⅱ trial evaluating the anti-vascular endothelial growth factor monoclonal antibody bevacizumab in combination with the HER-1/epidermal growth factor receptor tyrosine kinase inhibitor erlotinib for patients with recurrent non-small-cell lung cancer[J].J Clin Oncol,2005,23(11):2544-2555.
[13]Pao W,Miller VA.Epidermal growth factor receptor muta-tions,small-molecule kinase inhibitors,and non-small-cell lung cancer:current knowledge and future directions[J].J Clin Oncol,2005,23(11):2556-2568.
[14]Dong QQHuang JS.Epidermal growth factor receptor mutations in Chinese patients with adenocarcinoma of the lung[J]. ancer,006, (26) 271-275.
[15]Laack E, SchefflerA, Burkholder I, et al. Pretreatment vascular endothelial growth fact or (VEGF) and matrix metalloproteinase-9 (MMP29) serum levels in patients with metastatic non-small cell lung cancer (NSCLC)[J]. Lung Cancer,2005,50(1):51-58.
[16]Sapra P, Kraft P, Pastorino F, Potent and sustained inhibition of HIF-1α and downstream genes by a polyethyleneglycol-SN38 conjugate, EZN-2208, results in anti-angiogenic effects[J]. Angiogenesis.2011 Mar 31
[17]Chang CC, Lin MT, Lin BR, et al. Effect of connective tissue growth factor on hypoxia-inducible factor lalpha degradation and tumor angiogenesis[J]. J Natl Cancer Inst.2006 Jul 19;98(14):984-95.
[18]Choi KS, Bae MK, Jeong JW, et al. Hypoxia-induced angiogenesis during carcinogenesis[J]. J Biochem Mol Biol.2003 Jan 31;36(1):120-7.
[19]Yamakawa M, Liu LX, Date T, et al. Hypoxia-inducible factor-1 mediates activation of cultured vascular endothelial cells by inducing multiple angiogenic factors[J]. Circ Res.2003 Oct 3;93(7):664-73.
[20]Choi KS, Bae MK, Jeong JW, et al. Hypoxia-induced angiogenesis during carcinogenesis[J]. J Biochem Mol Biol.2003 Jan 31;36(1):120-7.
[21]Mazure NM, Brahimi-Horn MC, Pouyssegur J. Protein kinases and the hypoxia-inducible factor-1, two switches in angiogenesis[J]. Curr Pharm Des. 2003;9(7):531-41.
[22]Chang CC, Lin MT, Lin BR, et al. Effect of connective tissue growth factor on hypoxia-inducible factor lalpha degradation and tumor angiogenesis[J]. J Natl Cancer Inst.2006 Jul19;98(14):984-95.
[23]Berra E, Pages G, Pouyssegur J. et al. MAP kinases and hypoxia in the control of VEGF expression[J]. Cancer Metastasis Rev.2000; 19(1-2):139-45.
[24]Hashizurne H, Falcon BL, Kuroda T, et al. Complementary actions of inhibitors of angiopoietin-2 and VEGF on tumor angiogenesis and growth[J]. Cancer Res. 2010 Mar 15;70(6):2213-23.
[25]Diaz-Rubio E. Vascular endothelial growth factor inhibitors in colon cancer[J]. Adv Exp Med Biol.2006;587:251-75.
[26]Hicklin DJ, Ellis LM. Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis[J]. J Clin Oncol.2005 Feb 10;23(5):1011-27.
[27]Veeravagu A, Hsu AR, Cai W, et al. Vascular endothelial growth factor and vascular endothelial growth factor receptor inhibitors as anti-angiogenic agents in cancer therapy[J]. Recent Pat Anticancer Drug Discov.2007 Jan;2(1):59-71.
[28]Shinkaruk S, Bayle M, Lain G, et al. Vascular endothelial cell growth factor (VEGF), an emerging target for cancer chemotherapy[J]. Curr Med Chem Anticancer Agents.2003 Mar;3(2):95-117.
[29]Ferrara N. Role of vascular endothelial growth factor in physiologic and pathologic angiogenesis:therapeutic implications[J]. Semin Oncol.2002 Dec;29(6):10-4.
[30]Jain RK. Tumor angiogenesis and accessibility:role of vascular endothelial growth factor[J]. Semin Oncol.2002 Dec;29(6):3-9.
[31]Pradeep CR, Sunila ES, Kuttan G. Expression of vascular endothelial growth factor (VEGF) and VEGF receptors in tumor angiogenesis and malignancies[J]. Integr Cancer Ther.2005 Dec;4(4):315-21.
[32]Kerigh BF, Bahrami A, Shamsa A, et al. Assessment of angiogenic factor, vascular endothelial growth factor, serum and urine level changes in superficial bladder tumor immunotherapy by intravesical Bacillus Calmette-Guerin[J]. Urol Ann.2010 Sep;2(3):91-5.
[33]Kaur B, Khwaja FW, Severson EA, Hypoxia and the hypexia inducible factor pathway in glioma growth and angiogenesis[J]. Neuro Oncol.2005 Apr;7(2):134-53.
[34]Jensen RL, Ragei BT, Whang K, et al. Inhibition of hypoxia inducible factor-1 alpha (HIF-1 alpha) decreases vascular endothelial growth factor (VEGF) secretion and tumor growth in malignant gliomas[J]. J Neurooncol.2006 Jul;78(3):233-47.
[35]Zagzag D, Lukyanov Y, Lan L, et al.Hypoxia-inducible factor 1 and VEGF upregulate CXCR4 in glioblastoma:implications for angiogenesis and glioma cell invasion[J]. Lab Invest.2006 Dec;86(12):1221-32.
[36]Overall CM, Dean RA. Degradomics:systems biology of the protease web. Pleiotropic roles of MMPs in cancer[J]. Cancer Metastasis Rev.2006 Mar;25(1):69-75.
[37]Dean RA, Overall CM. Proteomics discovery of metalloproteinase substrates in the cellular context by iTRAQ labeling reveals a diverse MMP-2 substrate degradome[J]. Mol Cell Proteomics.2007 Apr;6(4):611-23.
[38]Prudova A, auf dem Keller U, Butler GS, et al. Multiplex N-terminome analysis of MMP-2 and MMP-9 substrate degradomes by iTRAQ-TAILS quantitative proteomics[J]. Mol Cell Proteomics.2010 May;9(5):894-911.
[39]Overall CM, Dean RA. Degradomics:systems biology of the protease web. Pleiotropic roles of MMPs in cancer[J]. Cancer Metastasis Rev.2006 Mar;25(1):69-75.
[40]Dean RA, Overall CM. Proteomics discovery of metalloproteinase substrates in the cellular context by iTRAQ labeling reveals a diverse MMP-2 substrate degradome[J]. Mol Cell Proteomics.2007 Apr;6(4):611-23.
[41]Butler GS, Dean RA, Tam EM, et al. Pharmacoproteomics of a metalloproteinase hydroxamate inhibitor in breast cancer cells:dynamics of membrane type 1 matrix metalloproteinase mediated membrane protein shedding[J]. Mol Cell Biol. 2008 Aug;28(15):4896-914.
[42]Butler GS, Overall CM. Proteomic validation of protease drug targets: pharmacoproteomics of matrix metalloproteinase inhibitor drugs using isotope-coded affinity tag labelling and tandem mass spectrometry[J]. Curr Pharm Des.2007;13(3):263-70.
[43]Morrison CJ, Butler GS, Rodriguez D, et al. Matrix metalloproteinase proteomics: substrates, targets, and therapy[J]. Curr Opin Cell Biol.2009 Oct;21(5):645-53.
[44]Butler GS, Overall CM. Updated biological roles for matrix metalloproteinases and new "intracellular" substrates revealed by degradomics[J]. Biochemistry. 2009 Nov 24;48(46):10830-45.
[45]Rodriguez D, Morrison CJ, Overall CM. Matrix metalloproteinases:what do they not do? New substrates and biological roles identified by murine models and proteomics[J]. Biochim Biophys Acta.2010 Jan;1803(1):39-54.
[46]Tam EM, Morrison CJ, Wu YI, et al. Membrane protease proteomics: Isotope-coded affinity tag MS identification of undescribed MT1-matrix metalloproteinase substrates[J]. Proc Natl Acad Sci U S A.2004 May 4;101(18):6917-22.
[47]Dean RA, Butler GS, Hamma-Kourbali Y, et al. Identification of candidate angiogenic inhibitors processed by matrix metalloproteinase 2 (MMP-2) in cell-based proteomic screens:disruption of vascular endothelial growth factor (VEGF)/heparin affin regulatory peptide (pleiotrophin) and VEGF/Connective tissue growth factor angiogenic inhibitory complexes by MMP-2 proteolysis[J]. Mol Cell Biol.2007 Dec;27(24):8454-65.
[48]Hashimoto G, Inoki I, Fujii Y, et al. Matrix metalloproteinases cleave connective tissue growth factor and reactivate angiogenic activity of vascular endothelial growth factor 165[J]. J Biol Chem.2002 Sep 27;277(39):36288-95.
[49]Inoki I, Shiomi T, Hashimoto G, et al. Connective tissue growth factor binds vascular endothelial growth factor (VEGF) and inhibits VEGF-induced angiogenesis[J]. FASEB J.2002 Feb; 16(2):219-21.
[50]Liu XD, Fan RF, Zhang Y, et al. Down-regulation of telomerase activity and activation of caspase-3 are responsible for tanshinone I-induced apoptosis in monocyte leukemia cells in vitro[J]. Int J Mol Sci.2010 May 26;11(6):2267-80.
[51]Xu Q, Li ZX, Peng HQ, et al. Artesunate inhibits growth and induces apoptosis in human osteosarcoma HOS cell line in vitro and in vivo[J]. J Zhejiang Univ Sci B.2011 Apr.;12(4):247-255.
[52]Ji BC, Hsu WH, Yang JS, et al. Gallic acid induces apoptosis via caspase-3 and mitochondrion-dependent pathways in vitro and suppresses lung xenograft tumor growth in vivo[J]. J Agric Food Chem.2009 Aug 26;57(16):7596-604.
[53]Lu HF, Chie YJ, Yang MS,et al. Apigenin induces caspase-dependent apoptosis in human lung cancer A549 cells through Bax-and Bcl-2-triggered mitochondrial pathway[J]. Int J Oncol.2010 Jun;36(6):1477-84.
[54]Chen QY, Lu GH, Wu YQ, et al. Curcumin induces mitochondria pathway mediated cell apoptosis in A549 lung adenocarcinoma cells[J]. Oncol Rep.2010 May;23(5):1285-92.
[55]Gyrd-Hansen M, Meier P. IAPs:from caspase inhibitors to modulators of NF-kappaB, inflammation and cancer[J]. Nat Rev Cancer.2010 Aug;10(8):561-74.
[56]LaCasse EC, Baird S, Korneluk RG, et al. The inhibitors of apoptosis (IAPs) and their emerging role in cancer[J]. Oncogene.1998 Dec 24; 17(25):3247-59.
[57]Hunter AM, LaCasse EC, Korneluk RG. The inhibitors of apoptosis (IAPs) as cancer targets[J]. Apoptosis.2007 Sep; 12(9):1543-68.
[58]Fulda S, Gorman AM, Hori O, et al. Cellular stress responses:cell survival and cell death[J]. Int J Cell Biol.2010;2010:214074.
[59]Katacka S, Tsuruo T. Physician Education:Apoptosis[J]. Oncologist. 1996;1(6):399-401.
[60]Park HJ, Kim MJ, Ha E, et al. Apoptotic effect of hesperidin through caspase3 activation in human colon cancer cells, SNU-C4[j]. Phytomedicine.2008 Jan; 15(1-2):147-51.
[61]Larsen BD, Rampalli S, Burns LE, et al. Caspase 3/caspase-activated DNase promote cell differentiation by inducing DNA strand breaks[J]. Proc Natl Acad Sci USA.2010 Mar 2;107(9):4230-5.
[62]Hu D, Liu S, Shi L, et al. Cleavage of survivin by Granzyme M triggers degradation of the survivin-X-linked inhibitor of apoptosis protein (XIAP) complex to free caspase activity leading to cytolysis of target tumor cells[J]. J Biol Chem.2010 Jun 11;285(24):18326-35.
[63]Yin S, Sethi S, Reddy KB. Protein kinase C8 and caspase-3 modulate TRAIL-induced apoptosis in breast tumor cells[J]. J Cell Biochem.2010 Nov 1;111(4):979-87.
[64]Yang X, Wang D, Zhong Z, et al. The Comparison of Clinical Effect of Rh-endostar on Retreated Non-Small Cell Lung Cancer and Colorectal Cancer[J]. Zhongguo Fei Ai ZaZhi.2009 Nov 20; 12(11):1184-7.
[65]Zhang DW, Li HL, Yao Q, et al. The synergistic effect of recombinant human endostatin (YH-16) combined with oxaliplatin on human colorectal carcinoma[J]. J Int Med Res.2010 Jan-Feb;38(1):111-26.
[66]Wu H, Deng J, Yu S, et al. The inhibitory effects of rh-endostatin (YH-16) in combination with radiotherapy on lung adenocarcinoma A549 in mice and the underlying mechanisms[J].J Huazhong Univ Sci Technolog Med Sci.2010 Feb;30(1):108-12.
[67]Wu G, Zhang R, Ren J, et al. Autophagic cell death of human hepatoma cells induced by endostar, a recombinant human endostatin[J]. Cancer Biother Radiopharm.2008 Dec;23(6):735-40.
[68]Jiang HQ, Li YL, Zou J.Effect of recombinant human endostatin on endometriosis in mice.Chin Med J (Engl)[J].2007 Jul 20; 120(14):1241-6
[69]Wang J, Sun Y, Liu Y, et al. Results of randomized, multicenter, double-blind phase III trial of rh-endostatin (YH-16) in treatment of advanced non-small cell lung cancer patients[J]. Zhongguo Fei Ai Za Zhi.2005 Aug 20;8(4):283-290.
[70]El Zouhairi M, Charabaty A, Pishvaian MJ. Molecularly targeted therapy for metastatic colon cancer:proven treatments and promising new agents[J]. Gastrointest Cancer Res.2011 Jan;4(1):15-21.
[1]Jeffrey K.C, Miller RJ, Ahmed S, et al. Ten-Year Biochemical Disease Control for Patients with Prostate Cancer Treated with Cryosurgery as Primary Therapy. Urology.2008;71:515-518.
[2]Gary O, David V, Richard L, et al. "Male Lumpectomy":Focal Therapy for Prostate Cancer Using Cryoablation. Urology.2007;70:16-21.
[3]Bharat G, Damien G. Cryotherapy for the prostate:an in vitro and clinical study of two new developments; advanced cryoneedles and a temperature monitoring system. BJU International 2007; 100:295-302.
[4]Gary Onik. Rationale for a "Male Lumpectomy," a Prostate Cancer targeted approach using cryoablation:results in 21 patients with at Least 2 years of follow-up. Cardiovasc Intervent Radiol 2008;31:98-106
[5]Bahn DK, Lee F, Badalament R, et al. Targeted cryoablation of the prostate: 7-year outcomes in the primary treatment of prostate cancer. Urology.2002; 60(suppl2A):3-11.
[6]Polascik TJ, Nosnik I, Mayes JM, et al. Short-Term Cancer Control After Primary Cryosurgical Ablation for Clinically Localized Prostate Cancer Using Third-Generation Cryotechnology. Urology 2007;70:117-121.
[7]Siddiqui SA, Mynderse LA, Zincke H,et al. Treatment of Prostate Cancer Local Recurrence After Radical Retropubic Prostatectomy with 17-Gauge Interstitial Transperineal Cryoablation:Initial Experience. Urology 2007;70:80-85.
[8]Hayek ORE, Alfer Jr. W, Reggio E, et al. Percutaneous prostate cryoablation as treatment for high-risk prostate cancer. Clinics.2007;62(2):109-12.
[9]Scott GH, Michael DF, Paul FS, et al. Single center experience with third-generation cryosurgery for management of organ-confine prostate cancer: critical evaluation of short-term outcome,complications, and patient quality of life. Journal of endourology 2007; 21(12):1521-1531.
[10]Chin JL, C-K Ng, NJ Touma, et al. Randomized trial comparing cryoablation and external beam radiotherapy for T2C-T3B prostate cancer. Prostate Cancer and Prostatic Diseases 2007:1-6.
[11]Mohamed I, Shwan A, Christof K, et al. Salvage cryotherapy for recurrent prostate cancer after radiation failure:a prospective case series of the first 100 patients. BJU International 2007; 100:760-764
[12]Chee KN, Madeleine M, Donal BD,et al. Salvage Cryoablation of the Prostate: Followup and Analysis of Predictive Factors for Outcome. The journal of urologe 2007; 178:1253-1257,
[13]A1 B. Barqawi, E. David Crawford, The Current Use and Future Trends of Focal Surgical Therapy in. the Management of Localized Prostate Cancer. Cancer J 2007;13:313-317.
[14]Eggener SE, Scardino PT, Focal PR, et al. Therapy for Localized Prostate Cancer: A Critical Appraisal of Rationale and Modalities. The journal of urology 2007; 178:2260-2267,
[15]Vladimir M., Janice MM, John FM, et al. Analysis of Laterality and Percentage of Tumor Involvement in 1386 Prostatectomized Specimens for Selection of Unilateral Focal Cryotherapy. Technology in Cancer Research and Treatment 2007, Technology in Cancer Research and Treatment 2007; (2):91-95
[16]Ellis DS, Theodore BMJ, Rewcastle JC. Focal Cryosurgery Followed by Penile Rehabilitation as Primary Treatment for Localized Prostate Cancer:Initial Results. Urology 2007;70:9-15.
[17]den Brok MH, Sutmuller RP, Nierkens S, et al. Efficient loading of dendritic cells following cryo and radiofrequency ablation in combination with immune modulation induces anti-tumour immunity. Br J Cancer 2006,95(7):896-905.
[18]Osada S, Imai H, Tomita Ⅱ, et al. Serum Cytokine Levels in Response to Hepatic Cryoablation. J Surg Oncol 2007;95(6):491-498.
[19]Si TG, Guo Z, Hao XS, et al. Cryoablation for prostate cancer induce specific immune response. Cryobiology 2008;
[20]Clarke DM, Robilotto AT, VanBuskirk RG, et al. Targeted induction of apoptosis via TRAIL and cryoablation:a novel strategy for the treatment of prostate cancer. Prostate Cancer and Prostatic Diseases 2007; 10:175-184.
[21]Kang SH, Kim JW, Bae JH, et al. Targeted-cryosurgical ablation of the prostate with androgen deprivation therapy:quality of life in high-risk prostate cancer patients, Asian J Androl 2006; 8 (5):629-636.
[22]Clarke DM, Baust JM, VanBuskirk RG, et al. Addition of anticancer agents enhances freezing-induced prostate cancer cell death:implications of mitochondrial involvement. Cryobiology 2004;49:45-61.