恶性卵巢癌抗肿瘤间质治疗策略研究进展
The Progress of Antitumor Interstitial Treatment Strategy of Malignant Ovarian Cancer
DOI: 10.12677/ACROG.2013.14005, PDF, HTML, 下载: 3,055  浏览: 13,548  国家科技经费支持
作者: 郭振超, 张天柱, 顾 宁:东南大学生物科学与医学工程学院,江苏省生物材料与器件重点实验室,南京
关键词: 卵巢癌化疗耐药肿瘤间质生存率Ovarian Cancer; Chemotherapy Resistance; Tumor Interstitium; Survival Rate
摘要: 超过80%的卵巢癌患者对化疗药物出现耐药性而复发,使得卵巢癌死亡率居妇科恶性肿瘤之首。与肿瘤细胞分化高度异质性相比,肿瘤间质细胞遗传性稳定,不大可能产生获得性突变而导致抗药性。本文综述了卵巢癌针对肿瘤间质的治疗策略,为恶性妇科肿瘤治疗降低毒副作用、防止复发和转移,进一步提高生存率指明了方向。
Abstract: More than 80% of the patients with ovarian cancer chemotherapy relapse due to drug resistance, which makes the highest ovarian cancer mortality rates among the gynecologic malignancies. Compared with the highly heterogeneous tumor cell differentiation, tumor stroma cells have genetic stability, and it is unlikely to produce acquired mutations and lead to drug resistance. In view of the treatment strategies for tumor interstitium, ovarian cancer is reviewed in this paper. At the same time, we pointed out the direction for reducing toxicity, preventing the cancer recurrence and metastasis, improving the survival rate in the treatment of gynecologic malignancies.
文章引用:郭振超, 张天柱, 顾宁. 恶性卵巢癌抗肿瘤间质治疗策略研究进展[J]. 亚洲妇产科病例研究, 2013, 1(4): 19-23. http://dx.doi.org/10.12677/ACROG.2013.14005

参考文献

[1] 张桂荣, 翟云起, 杜少敏, 等 (2003) 卵巢上皮癌治疗及预后影响因素研究.肿瘤学杂志, 2, 68-70.
[2] Teng, P.-N., Wang, G., et al. (2014) Identification of candidate circulating cisplatin-resistant biomarkers from epithelial ovarian carcinoma cell secretomes. British Journal of Cancer, 110, 123132.
[3] 减荣余, 张志毅, 李子庭, 等 (200l) 晚期上皮性卵巢癌的预后影响因素. 复旦学报(医学科学版), 1, 46-47.
[4] Stalberg, K., Svensson, T., et al. (2012) Evaluation of prevalent and incident ovarian cancer co-morbidity. British Journal of Cancer, 106, 1860-1865.
[5] 何义富, 孙玉蓓, 陈健, 等 (2009) 腹腔内应用重组人血管内皮抑制素联合氟尿嘧啶治疗恶性腹水的初步探讨. 临床肿瘤学杂志, 3, 252.
[6] Marcucci, F., Bellone, M., et al. (2013) Pushing tumor cells towards a malignant phenotype: Stimuli from the microenvironment, intercellular communications and alterna-tive roads. International Journal of Cancer, 1, 1-12.
[7] Junttila, M.R., de Sauvage, F.J. (2013) Influence of tumour micro-environment heterogeneity on therapeutic response. Nature, 19, 346-354.
[8] Kim, S., Cho, H.B., et al. (2010) Autoantibodies against StressInduced Phosphoprotein-1 as a Novel Biomarker Candidate for Ovarian Cancer. Genes, Chromosomes & Cancer, 49, 585-595.
[9] Beyer, I., Li, Z., et al. (2011) Controlled Extracellular Matrix Degradation in Breast Cancer Tumors Improves Therapy by Trastuzumab. Molecular Therapy, 3, 479-489.
[10] Shashidharamurthy, R., Bozeman, E.N., et al. (2012) Immunotherapeutic Strategies for Cancer Treatment: A Novel ProteinTransfer Approach for Cancer Vaccine Development. Medicinal Research Reviews, 6, 1197-1219.
[11] Bukovsky, A. (2011) Immune Maintenance of Self in Morphostasis of Distinct Tissues, Tumour Growth and Regenerative Medicine. Scandinavian Journal of Immunology, 73, 159-189.
[12] Ning, N., Pan, Q., Zheng, F., et al. (2012) Cancer stemcell vaccination confers significant antitumor immunity. Cancer Research, 7, 18-53.
[13] Luo, L., Zeng, J., Liang, B., et al. (2011) Ovarian cancer cells with the CD117 phenotype are highly tumorigenic and are related to chemotherapy outcome. Experimental and Molecular Pathology, 2, 596-602.
[14] El-Kenawi, A.E. and El-Remessy, A.B. (2013) Angiogenesis inhibitors in cancer therapy: mechanistic perspective on classification and treatment rationales. British Journal of Pharmacology, 170, 712-729.
[15] Buergy, D., Wenz, F., et al. (2012) Tumor-platelet interaction in solid tumors. In-ternational Journal of Cancer, 130, 2747-2760.
[16] Koyanagi, T. and Suzuki, Y. (2013) In Vivo delivery of siRNA targeting vasohibin-2 decreases tumor angiogenesis and suppresses tumor growth in ovarian cancer. Cancer Science, 12, 1705-1710.
[17] Wu, F.T.H., Stefanini, M.O., et al. (2010) A systems biology perspective on sVEGFR1: its biological function, pathogenic role and therapeutic use. Journal of Cellular and Molecular Medicine, 3, 528-552.
[18] McKeage, M.J. and Baguley, B.C. (2010) Disrupting Established Tumor Blood Vessels. Cancer, 15, 1859-1866.
[19] Khalid, B., et al. (1998) Absence of Host Plasminogen Activator Inhibitor 1 Prevents Cancer Invasion and Vas-cularization. Nature Medicine, 8, 923-928.
[20] Hanna, E., Quick, J. and Libutti, S.K. (2009) The tuour microenviroment: A novel target for cancer therapy. Oral Diseases, 1, 8-17.
[21] Wong, G.S. and Rustgi, A.K. (2013) Matricellular proteins: priming the tumour microenviron-ment for cancer development and metastasis. British Journal of Cancer, 108, 755-761.
[22] Akerman, S., Fisher, M., et al. (2013) Influence of soluble or matrix-bound isoforms of vascular endothelial growth factor-A on tumor response to vascular-targeted strategies. International Journal of Cancer, 133, 2563-2576.
[23] Provenzano, P.P. and Hingorani, S.R. (2013) Hyaluronan, fluid pressure, and stromal resistance in pancreas cancer. British Journal of Cancer, 108, 1-8.
[24] Mueller, M.M. and Fuening, N.E. (2004) Friend or foes-bipolar effect of the tumor stroma in cancer. Nature Reviews Cancer, 11, 839-849.
[25] Anton, K. and Glod, J. (2009) Targeting the tumor stroma in cancer therapy. Current Pharmaceutical Biotechnology, 2, 185191.
[26] Mani, T., Wang, F., et al. (2013) Small-molecule inhibition of the uPAR, uPA interaction: Synthesis, biochemical, cellular, in vivo pharmacokinetics and efficacy studies in breast cancer metastasis. Bioorganic & Medicinal Chemistry, Bioorganic & Medicinal Chemistry, 21, 2145-2155.
[27] Nordengren, J., Pilka, R., Noskova, V., et al. (2004) Differential localization and expression of urokinase plasminogen activator (uPA), its receptor (uPAR), and its inhibitor (PAI-1) mRNA and protein in endometrial tissue during the menstrual cycle. Molecular Human Reproduction, 9, 655-663.
[28] Hofmeister, V., Schrama, D. and Becker, J.C. (2008)Anti-cancer therapy targeting the tumor stroma. Cancer Immu-nology, Immunotherapy, 1, 1-17.
[29] Blansfield, J.A., Caragaciam, D., Alexander, H.R., et al. (2008) Combining agents that target the tumor microenvironment improves the efficacy of anticancer therapy. Clini-cal Cancer Research, 1, 270-280.
[30] Liu, M., Xu, J., et al. (2011) Tangled Fibroblasts in TumorStroma interactions. International Jour-nal of Cancer, 129, 17951805.
[31] Mitra, S., Stemke-Hale, K., et al. (2012) Interactions between tumor cells and microenvironment in breast cancer: A new opportunity for targeted therapy. Cancer Science, 3, 400-407.
[32] Kosaka, N., Ogawa, M., et al. (2010) Semiquantita-tive assessment of the microdistribution of fluorescence-labeled mo-noclonal antibody in small peritoneal disseminations of ovarian cancer. Cancer Science, 3, 820-825.
[33] Kenny, H.A., Krausz, T., Yamada, S.D. and Lengyel, E. (2007) Use of a novel 3D culture model to eluci-date the role of mesothelial cells, fibroblasts and extra-cellular matrices on adhesion and invasion of ovarian cancer cells to the omentum. International Journal of Cancer, 121, 1463-1472 .
[34] Katoh, M. and Nakagama, H. (2014) FGF Receptors: Cancer Biology and Therapeutics. Medicinal Research Reviews, 2, 280300.
[35] 王纯燕, 李联昆, 祁秀峪, 等 (2000) 卵巢正常大小的原发性卵巢上皮性癌综合征的临床特点与预后影响因素.中华妇产科杂志, 2, 420.
[36] 张蓉, 吴令英, 章文华, 等 (2003) 年轻妇女卵巢上皮细胞癌预后因素分析.中华肿瘤杂志, 25, 264-266.
[37] 李孟达, 李玉沽 (2004) 影响上皮性卵巢癌远期疗效的因素分析. 癌症, 11, 1306-1311.
[38] Zhang, Y., Xu, B., et al. (2012) The ovarian cancer-derived secretory/releasing proteome: A repertoire of tumor markers. Proteomics, 12, 1883-1891.