国际肿瘤学杂志››2016,Vol. 43››Issue (8): 631-633.doi:10.3760/cma.j.issn.1673422X.2016.08.018
王豪,张庆玲
出版日期:
2016-08-08发布日期:
2016-07-05通讯作者:
张庆玲,Email: zqllc8@126.com E-mail:zqllc8@126.com基金资助:
国家自然科学基金(81272760; 81472712)
Wang Hao, Zhang Qingling
Online:
2016-08-08Published:
2016-07-05Contact:
Zhang Qingling, Email: zqllc8@126.com E-mail:zqllc8@126.comSupported by:
National Natural Science Foundation of China(81272760; 81472712)
摘要:结直肠癌(CRC)的早期症状隐匿,多数患者在诊断时已经发生转移。化疗与靶向药物的联合治疗是目前治疗转移性CRC的主要策略,在CRC中高频出现异常激活的磷脂酰肌醇-3-激酶(PI3K)信号通路与CRC的发生发展有着十分密切的关系,对CRC的诊断与治疗具有重要的价值。
王豪,张庆玲. PI3K信号通路在结直肠癌中的作用[J]. 国际肿瘤学杂志, 2016, 43(8): 631-633.
Wang Hao, Zhang Qingling. PI3K signaling pathway in colorectal cancer[J]. Journal of International Oncology, 2016, 43(8): 631-633.
[1] Torre LA, Bray F, Siegel RL, et al. Global cancer statistics, 2012[J]. CA Cancer J Clin, 2015, 65(2): 87-108. DOI: 10.3322/caac.21262. [2] Thorpe LM, Yuzugullu H, Zhao JJ. PI3K in cancer: divergent roles of isoforms, modes of activation and therapeutic targeting[J]. Nat Rev Cancer, 2015, 15(1): 7-24. DOI: 10.1038/nrc3860. [3] Kato S, Iida S, Higuchi T, et al. PIK3CA mutation is predictive of poor survival in patients with colorectal cancer[J]. Int J Cancer, 2007, 121(8): 1771-1778. DOI: 10.1002/ijc.22890. [4] Ogino S, Liao X, Imamura Y, et al. Predictive and prognostic analysis of PIK3CA mutation in stage Ⅲ colon cancer intergroup trial[J]. J Natl Cancer Inst, 2013, 105(23): 1789-1798. DOI: 10.1093/jnci/djt298. [5] Kaur J, Sanyal SN. PI3kinase/Wnt association mediates COX-2/PGE(2) pathway to inhibit apoptosis in early stages of colon carcinogenesis: chemoprevention by diclofenac[J]. Tumour Biol, 2010, 31(6): 623-631. DOI: 10.1007/s13277-010-0078-9. [6] Liao X, Lochhead P, Nishihara R, et al. Aspirin use, tumor PIK3CA mutation, and colorectalcancer survival[J]. N Engl J Med, 2012, 367(17): 1596-1606. DOI: 10.1056/NEJMoa1207756. [7] Domingo E, Church DN, Sieber O, et al. Evaluation of PIK3CA mutation as a predictor of benefit from nonsteroidal antiinflammatory drug therapy in colorectal cancer[J]. J Clin Oncol, 2013, 31(34): 4297-4305. DOI: 10.1200/JCO.2013.50.0322. [8] Van Cutsem E, Khne CH, Láng I, et al. Cetuximab plus irinotecan, fluorouracil, and leucovorin as firstline treatment for metastatic colo-rectal cancer: updated analysis of overall survival according to tumor K-RAS and BRAF mutation status[J]. J Clin Oncol, 2011, 29(15): 2011-2019. DOI: 10.1200/JCO.2010.33.5091. [9] SartoreBianchi A, Martini M, Molinari F, et al. PIK3CA mutations in colorectal cancer are associated with clinical resistance to EGFRtargeted monoclonal antibodies[J]. Cancer Res, 2009, 69(5): 1851-1857. DOI: 10.1158/0008-5472.CAN-08-2466. [10] Mao M, Tian F, Mariadason JM, et al. Resistance to BRAF inhibition in BRAF-mutant colon cancer can be overcome with PI3K inhibition or demethylating agents[J]. Clin Cancer Res, 2013, 19(3): 657-667. DOI: 10.1158/1078-0432.CCR-11-1446. [11] Zhu YF, Yu BH, Li DL, et al. PI3K expression and PIK3CA mutations are related to colorectal cancer metastases[J]. World J Gastroenterol, 2012, 18(28): 3745-3751. DOI: 10.3748/wjg.v18.i28.3745. [12] Wang G, Wang F, Ding W, et al. April induces tumorigenesis and metastasis of colorectal cancer cells via activation of the PI3K/Akt pathway[J]. PLoS One, 2013, 8(1): e55298. DOI: 10.1371/journal.pone.0055298. [13] Lan YT, Jen-Kou L, Lin CH, et al. Mutations in the RAS and PI3K pathways are associated with metastatic location in colorectal cancers[J]. J Surg Oncol, 2015, 111(7): 905-910. DOI: 10.1002/jso.23895. [14] Bendell JC, Rodon J, Burris HA, et al. Phase I, doseescalation study of BKM120, an oral pan-Class I PI3K inhibitor, in patients with advanced solid tumors[J]. J Clin Oncol, 2012, 30(3): 282-290. DOI: 10.1200/JCO.2011.36.1360. [15] Hong DS, Bowles DW, Falchook GS, et al. A multicenter phase I trial of PX-866, an oral irreversible phosphatidylinositol 3-kinase inhibitor, in patients with advanced solid tumors[J]. Clin Cancer Res, 2012, 18(15): 4173-4182. DOI: 10.1158/1078-0432.CCR-12-0714. [16] Sarker D, Ang JE, Baird R, et al. Firstinhuman phase I study of pictilisib (GDC0941), a potent panclass I phosphatidylinositol-3-kinase (PI3K) inhibitor, in patients with advanced solid tumors[J]. Clin Cancer Res, 2015, 21(1): 77-86. DOI: 10.1158/1078-0432.CCR-14-0947. [17] Roper J, Richardson MP, Wang WV, et al. The dual PI3K/mTOR inhibitor NVPBEZ235 induces tumor regression in a genetically engineered mouse model of PIK3CA wildtype colorectal cancer[J]. PLoS One, 2011, 6(9): e25132. DOI: 10.1371/journal.pone.0025132. [18] Migliardi G, Sassi F, Torti D, et al. Inhibition of MEK and PI3K/mTOR suppresses tumor growth but does not cause tumor regression in patientderived xenografts of RASmutant colorectal carcinomas[J]. Clin Cancer Res, 2012, 18(9): 2515-2525. [19] Courtney KD, Corcoran RB, Engelman JA. The PI3K pathway as drug target in human cancer[J]. J Clin Oncol, 2010, 28(6): 1075-1083. DOI: 10.1200/JCO.2009.25.3641. [20] Yap TA, Yan L, Patnaik A, et al. Firstinman clinical trial of the oral panAKT inhibitor MK2206 in patients with advanced solid tumors[J]. J Clin Oncol, 2011, 29(35): 4688-4695. DOI: 10.1200/JCO.2011.35.5263. [21] Guertin DA, Sabatini DM. The pharmacology of mTOR inhibition[J]. Sci Signal, 2009, 2(67): pe24. DOI: 10.1126/scisignal.267pe24. [22] Wolpin BM, Ng K, Zhu AX, et al. Multicenter phase Ⅱ study of tivozanib (AV951) and everolimus (RAD001) for patients with refractory, metastatic colorectal cancer[J]. Oncologist, 2013, 18(4): 377-378. DOI: 10.1634/theoncologist.2012-0378. [23] Spindler KL, Sorensen MM, Pallisgaard N, et al. Phase Ⅱ trial of temsirolimus alone and in combination with irinotecan for K-RAS mutant metastatic colorectal cancer: outcome and results of K-RAS mutational analysis in plasma[J]. Acta Oncol, 2013, 52(5): 963970. DOI: 10.3109/0284186X.2013.776175. [24] Altomare I, Hurwitz H. Everolimus in colorectal cancer[J]. Expert Opin Pharmacother, 2013, 14(4): 505-513. DOI: 10.1517/14656566.2013.770473. [25] Shimizu T, Tolcher AW, Papadopoulos KP, et al. The clinical effect of the dualtargeting strategy involving PI3K/AKT/mTOR and RAS/MEK/ERK pathways in patients with advanced cancer[J]. Clin Cancer Res, 2012, 18(8): 2316-2325. DOI: 10.1158/1078-0432.CCR-11-2381. |
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