Page 158 - 南京医科大学自然科学版第1期
P. 158
第41卷第1期
·152 · 南 京 医 科 大 学 学 报 2021年1月
dogenous RNA,ceRNA)机制促进肾细胞癌的增殖、 [7] RINI B I,POWLES T,ATKINS M B,et al. Atezolizumab
侵袭和转移。但是关于circRNA在肾细胞癌对舒尼 plus bevacizumab versus sunitinib in patients with previ⁃
替尼耐药机制中的作用目前几无文献报道。这也 ously untreated metastatic renal cell carcinoma(IMmo⁃
许是一个有价值的研究方向。 tion151):a multicentre,open⁃label,phase 3,randomised
controlled trial[J]. Lancet,2019,393(1189):2404-2415
4 总结与展望 [8] CHOUEIRI T K,HESSEL C,HALABI S,et al. Cabozan⁃
tinib versus sunitinib as initial therapy for metastatic re⁃
上述lncRNA及miRNA功能的研究显示,作为舒
nal cell carcinoma of intermediate or poor risk(Alliance
尼替尼作用主要靶点的VEGFR和PDGFR被抑制后, A031203 CABOSUN randomised trial):progression⁃free
其他促进肿瘤进展的通路和功能被激活,从而引发肿 survival by Independent review and overall survival up⁃
瘤耐药,这可以看作是舒尼替尼对肾细胞癌的一种选 date[J]. Eur J Cancer,2018,94:115-125
择作用。而在这一过程中,非编码RNA受到其他通 [9] MOTZER R J,PENKOV K,HAANEN J,et al. Avelumab
路调节,lncRNA自身启动子序列甲基化也可以影响 plus axitinib versus sunitinib for advanced renal⁃cell car⁃
其表达。这似乎说明非编码RNA自身并不是整个耐 cinoma[J]. N Engl J Med,2019,380(12):1103-1115
[10] MOTZER R J,RINI B,MCDERMOTT D F,et al. Niv⁃
药过程的始动环节。circRNA在肾细胞癌对舒尼替
olumab plus ipilimumab versus sunitinib in first ⁃ line
尼耐药机制中的作用目前研究较少,值得挖掘。
treatment for advanced renal cell carcinoma:extended fol⁃
尽管非编码 RNA 的表达水平有望成为肾细胞 low⁃up of efficacy and safety results from a randomised,
癌对舒尼替尼敏感性的预测指标和耐药产生后的 controlled,phase 3 trial[J]. Lancet Oncol,2019,20(10):
新治疗靶点,我们仍然需要更多研究进一步发现非 1370-1385
编码 RNA 在肾细胞癌对舒尼替尼反应性中发挥的 [11] RINI B,PLIMACK E R,STUS V,et al. Pembrolizumab
作用,以及在这些非编码RNA上游是否存在更初始 plus axitinib versus sunitinib for advanced renal⁃cell car⁃
的调控机制;并且确定切实可行的利用非编码RNA cinoma[J]. N Engl J Med,2019,380(12):1116-1127
对患者预后进行预测和对耐药患者进行治疗的方法。 [12] 刘 平,杨韬樾,常 磊,等. 酪氨酸激酶抑制剂联合局
部病灶处理治疗转移性肾癌[J]. 南京医科大学学报
[参考文献]
(自然科学版),2018,38(3):363-366
[1] SIEGEL R L,MILLER K D,JEMAL A. Cancer statistics, [13] LOO V,SALGIA M,BERGEROT P,et al. First⁃line sys⁃
2016[J]. CA Cancer J Clin,2016,66(1):7-30 temic therapy for metastatic clear⁃cell renal cell carcino⁃
[2] LALANI A A,MCGREGOR B,ALBIGES L,et al. Syste⁃ ma:critical appraisal of emerging options[J]. Target On⁃
mic treatment of metastatic clear cell renal cell carcinoma col,2019,14(6):639-645
in 2018:current paradigms,use of immunotherapy,and [14] FOGLI S,PORTA C,DEL RE M,et al. Optimizing treat⁃
future directions[J]. Eur Urol,2019,75(1):100-110 ment of renal cell carcinoma with VEGFR⁃TKIs:a com⁃
[3] DABESTANI S,THORSTENSON A,LINDBLAD P,et al. parison of clinical pharmacology and drug⁃drug interac⁃
Renal cell carcinoma recurrences and metastases in pri⁃ tions of anti ⁃ angiogenic drugs[J]. Cancer Treat Rev,
mary non ⁃ metastatic patients:a population ⁃ based study 2020,84:101966
[J]. World J Urol,2016,34(8):1081-1086 [15] ELGENDY M,FUSCO J P,SEGURA V,et al. Identifica⁃
[4] ESCUDIER B,PORTA C,SCHMIDINGER M,et al. Re⁃ tion of mutations associated with acquired resistance to
nal cell carcinoma:ESMO clinical practice guidelines for sunitinib in renal cell cancer[J]. Int J Cancer,2019,145
diagnosis,treatment and follow⁃up[J]. Ann Oncol,2019, (7):1991-2001
30(5):706-720 [16] BERTONE P,STOLC V,ROYCE T E,et al. Global identi⁃
[5] LJUNGBERG B,ALBIGES L,ABU⁃GHANEM Y A,et al. fication of human transcribed sequences with genome til⁃
European association of urology guidelines on renal cell ing arrays[J]. Science,2004,306(575):2242-2246
carcinoma:the 2019 update[J]. Eur Urol,2019,75(5): [17] CHENG J,KAPRANOV P,DRENKOW J,et al. Transcrip⁃
799-810 tional maps of 10 human chromosomes at 5 ⁃ nucleotide
[6] MCDERMOTT D F,HUSENI M A,ATKINS M B,et al. resolution[J]. Science,2005,308(5725):1149-1154
Clinical activity and molecular correlates of response to [18] KAPRANOV P,CHENG J,DIKE S,et al. RNA maps re⁃
atezolizumab alone or in combination with bevacizumab veal new RNA classes and a possible function for perva⁃
versus sunitinib in renal cell carcinoma[J]. Nat Med, sivetranscription[J]. Science,2007,316(5830):1484-1488
2018,24(6):749-757 [19] PENG W X,KOIRALA P,MO Y Y. LncRNA⁃mediated