关于肝癌治疗的策略

汤钊猷

关于肝癌治疗的策略

汤钊猷

复旦大学附属中山医院肝癌研究所

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中图分类号: R735.7
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出版历程
- 出版日期: 2011-04-20

Treatment strategies for liver cancer

Tang ZhaoYou

摘要

摘要: 近年肝癌各种疗法的5年生存率已接近高限,瓶颈主要是转移复发。20世纪肝癌治疗均以消灭肿瘤为目标,近年已转变为消灭和改造并举。在消灭肿瘤的基础上,出现了多种调变残癌和调变机体的办法,如合并应用细胞因子、抗炎剂、分子靶向治疗剂、全身性干预以及中医中药等。还出现了一些潜在的治疗途径,如小RNA等,一些"无关药物"（如治疗结核病的利福平）也可望用于肝癌治疗。实验研究表明,常规疗法常通过上皮-间质转化而促进转移,研究其干预是提高现有疗法疗效的一条捷径,但同时需要提防"过度治疗"。总之,消灭肿瘤仍然是基本的,而调变肿瘤和机体则是重要的补充。
- 肝肿瘤
Abstract: In the recent years, the 5-year survival rate of various treatment modalities for liver cancer have reached their upper limits.Cancer metastasis remains the key obstacle.The goal of liver cancer treatment in the 20th century was mainly cancer eradication, and is changing to the combination of eradication and modulation recently.Besides the cancer eradication modalities, many novel approaches emerged, such as the combination of cytokines, anti-inflammatory agents, molecular targeted agents, systemic interventions, and herbal compounds.Potential treatment strategies have also attracted attentions, such as microRNA, as well as "unrelated drugs" (such as rifampicin for tuberculosis) for treatment of liver cancer.Experimental studies revealed that metastatic potential was enhanced by conventional therapies, in which, epithelial-mesenchymal transition is the main mechanism.Studies on their intervention will further improve their response rate.Meanwhile, overtreatment should be avoided.Overall, cancer eradication remains the major approach, but modulation will be important supplements.
- liver neoplasms

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参考文献(15)

[1]Jemal A, Siegel R, Ward E, et al.Cancer statistics, 2009[J].CA Cancer J Clin, 2009, 59 (4) :225-249.

[2]Ye QH, Qin LX, Forgues M, et al.Predicting hepatitis Bvirus-positive metastatic hepatocellular carcinomas usinggene expression profiling and supervised machine learning[J].Nat Med, 2003, 9 (4) :416-423.

[3]Gatenby RA.A change of strategy in the war on cancer[J].Nature, 2009, 459 (7246) :508-509.

[4]Andre N, Pasquier E.For cancer, seek and destroy or liveand let live?[J].Nature, 2009, 460 (7253) :324.

[5]Mantovani A.Cancer:Inflaming metastasis[J].Nature, 2009, 457 (7225) :36-37.

[6]Dinarello CA.Anti-inflammatory agents:Present and future[J].Cell, 2010, 140 (6) :935-950.

[7]Hayden EC.Personalized cancer therapy gets closer[J].Nature, 2009, 458 (7235) :131-132.

[8] Ji J, Shi J, Budhu A, et al.MicroRNA expression, survival, and response to interferon in liver cancer[J].N Engl J Med, 2009, 361 (15) :1437-1447.

[9]Thaker PH, Han LY, Kamat AA, et al.Chronic stresspromotes tumor growth and angiogenesis in a mouse modelof ovarian carcinoma[J].Nat Med, 2006, 12 (8) :939-944.

[10]Xiong W, Ren ZG, Qiu SJ, et al.Residual hepatocellularcarcinoma after oxaliplatin treatment has increased metastaticpotential in a nude mouse model and is attenuated by SongyouYin[J].BMC Cancer, 2010, 10:219.

[11]Shichiri M, Fukai N, Kono Y, et al.Rifampicin as an oralangiogenesis inhibitor targeting hepatic cancers[J].CancerRes, 2009, 69 (11) :4760-4768.

[12]Liu L, Zhu XD, Wang WQ, et al.Activation of beta-cateninby hypoxia in hepatocellular carcinoma contributes toenhanced metastatic potential and poor prognosis[J].ClinCancer Res, 2010, 16 (10) :2740-2750.

[13]Yamauchi K, Yang M, Hayashi K, et al.Induction of cancermetastasis by cyclophosphamide pretreatment of host mice:an opposite effect of chemotherapy[J].Cancer Res, 2008, 68 (2) :516-520.

[14]Hayden EC.Cutting off cancer's supply lines[J].Nature, 2009, 458 (7239) :686-687.

[15]Loges S, Mazzone M, Hohensinner P, et al.Silencing orfueling metastasis with VEGF inhibitors:antiangiogenesisrevisited[J].Cancer Cell, 2009, 15 (3) :167-170.

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