[1] Malempati S, Hawkins DS. Rhabdomyosarcoma:review of the Children's Oncology Group(COG) soft-tissue sarcoma committee experience and rationale for current COG studies[J].Pediatr Blood Cancer, 2012, 59(1):5-10. [2] Breneman JC, Lyden E, Pappo AS, et al. Prognostic factors and clinical outcomes in children and adolescents withmetastatic rhabdomyosarcoma——a report from the Intergroup Rhabdomyosarcoma Study Ⅳ[J]. J Clin Oncol, 2003, 21(1):78-84. [3] Skapek SX, Anderson J, Barr FG, et al. PAX-FOXO1 fusion status drives unfavorable outcome for children with rhabdomyosarcoma:A children's oncology group report[J].Pediatr Blood Cancer, 2013, 60(9):1411-1417. [4] 李栋梁, 刘春霞, 邹泓,等. 横纹肌肉瘤分子生物学研究进展[J].临床与实验病理学杂志, 2011, 27(2):181-184. [5] Chen X, Stewart E, Shelat AA, et al. Targeting oxidative stress in embryonal rhabdomyosarcoma[J]. Cancer Cell, 2013, 24(6):710-724. [6] Mosquera JM, Sboner A, Zhang L, et al. Recurrent NCOA2 gene rearrangements in congenital/infantile spindle cell rhabdomyosarcoma[J]. Genes Chromosomes Cancer, 2013, 52(6):538-550. [7] Shern JF, Yohe ME, Khan J. Pediatric rhabdomyosarcoma[J].Crit Rev Oncog, 2015, 20(3/4):227-243. [8] Norman G, Fayter D, Lewis-Light K, et al. An emerging evidence base for PET-CT in the management of childhood rhabdomyosarcoma:systematic review[J]. BMJ Open, 2015, 5(1):e006030. [9] 刘丽丽, 陈云新, 叶新青, 等. 横纹肌肉瘤临床病理及分子遗传学特征研究[J]. 中国矫形外科杂志, 2014, 22(17):1542-1546. [10] Biederer CH, Ries SJ, Moser M, et al. The basic helix-loop-helix transcription factor smyogenin and Id2 mediate specific induction of caveolin-3 gene expression during embryonic development[J]. J Biol Chem, 2000, 275(34):26245-26251. [11] Fine SW, Lisanti MP, Argani P, et al. Caveolin-3 is a sensitive and specific marker for rhabdomyosarcoma[J]. Appl Immunohistochem Mol Morphol, 2005, 13(3):231-236. [12] 王正, 陈建华, 范钦和. 横纹肌肉瘤中小窝蛋白3的表达及鉴别诊断意义[J]. 临床与实验病理学杂志, 2008, 24(2):203-206. [13] 童刚领, 孙晓非, 甄子俊, 等. p-mTOR和p-4EBP1在横纹肌肉瘤组织中的表达及其临床意义[J]. 中国肿瘤临床, 2011, 38(8):447-451. [14] 管雯斌, 许恪淳, 许艳春, 等. 儿童横纹肌肉瘤的病理学研究[J]. 上海交通大学学报:医学版, 2014, 34(1):70-74. [15] Calhabeu F, Hayashi S, Morgan JE, et al. Alveolar rhabdomyosarcoma-associated proteins PAX3/FOXO1A and PAX7/FOXO1A suppress the transcriptional activity of MyoD-target genes in muscle stem cells[J]. Oncogene, 2013, 32(5):651-662. [16] Gordon AT, Brinkschmidt C, Anderson J, et al. A novel and consistent amplicon at 13q31 associated with alveolar rhabdomyosarcoma[J]. Genes Chromosomes Cancer, 2000, 28(2):220-226. [17] Mehra S, de la Roza G, Tull J, et al. Detection of FOXO1(FKHR) gene break-apart by fluorescence in situ hybridization in formalin-fixed, paraffin-embedded alveolar rhabdomyosarcomas and its clinicopathologic correlation[J]. Diagn Mol Pathol, 2008, 17(1):14-20. [18] Kolb EA, Gorlick R, Lock R. Initial testing (stage 1) ofthe IGF-1 receptor inhibitor BMS-754807 by the pediatricpreclinical testing program[J]. Pediatr Blood Cancer, 2011, 56(4):595-603. [19] van Gaal JC, Flucke UE, Roeffen MH, et al. Anaplastic lymphoma kinase aberrations in rhabdomyosarcoma:clinical and prognostic implications[J]. J Clin Oncol, 2012, 30(3):308-315. [20] Bai RY, Ouyang T, Miething C, et al. Nucleophosmin-anaplastic lymphoma kinase associated with anaplastic large-cell lymphoma activates the phosphatidylinositol 3-kinase/Akt antiapoptotic signaling pathway[J]. Blood, 2000, 96(13):4319-4327. [21] Zou HY, Li Q, Lee JH, et al. An orally available small-molecule inhibitor of c-Met, PF-2341066, exhibits cytoreductive antitumor efficacy through antiproliferative and antiangiogenic mechanisms[J]. Cancer Res, 2007, 67(9):4408-4417. [22] Lee JS, Lim SM, Rha SY, et al. Prognostic implications of anaplastic lymphoma kinase gene aberrations in rhabdomyosarcoma,an immunohistochemical and fluorescence in situ hybridisation study[J]. J Clin Pathol, 2014, 67(1):33-39. [23] van Gaal JC, Roeffen MH, Flucke UE, et al. Simultaneous targeting of insulin-like growth factor-1 receptor and anaplastic lymphoma kinase in embryonal and alveolar rhabdomyosarcoma:a rational choice[J]. Eur J Cancer, 2013, 49(16):3462-3470. [24] Hugle M, Fulda S. Dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 synergizes with chloroquine to induce apoptosis in embryonal rhabdomyosarcoma[J]. Cancer Lett, 2015, 360(1):1-9. [25] Gao CF, van de Woude GF. HGF/SF-Met signaling in tumor progression[J]. Cell Res, 2005, 15(1):49-51. [26] Kim ES, Salgia R. MET pathway as a therapeutic target[J].J Thorac Oncol, 2009, 4(4):444-447. [27] Knudsen BS, van de Woude GF. Showering c-MET-dependent cancers with drugs[J]. Curr Opin Genet Dev, 2008, 18(1):87-96. [28] Hou J, Dong J, Sun L, et al. Inhibition of phosphorylated c-Met in rhabdomyosarcoma cell lines by a small molecule inhibitor SU11274[J]. J Transl Med, 2011, 9:64. [29] Gerber HP, Kowalski J, Sherman D, et al. Complete inhibition of rhabdomyosarcoma xenograft growth and neovascularization requires blockade of both tumor and host vascular endothelial growth factor[J]. Cancer Res, 2000, 60(22):6253-6258. [30] 杨清平, 周知. 恩度对横纹肌肉瘤PLA-802细胞生长的抑制作用及其机制[J]. 中国生物制品学杂志, 2010, 23(11):1230-1234. [31] 杨明威, 杨林. 恩度对横纹肌肉瘤移植瘤放疗增敏作用的实验研究[J]. 临床肿瘤学杂志, 2013, 18(12):1066-1070. [32] Ferguson M, Hingorani P, Gupta AA, et al. Emerging molecular-targeted therapies in early-phase clinical trials and preclinical models[J]. Am Soc Clin Oncol Educ Book, 2013:420-424. DOI:10.1200/EdBook_AM.2013.33.420. [33] Keir ST, Morton CL, Wu J, et al. Initial testing of the multitargeted kinase inhibitor pazopanib by the Pediatric Preclinical Testing Program[J]. Pediatr Blood Cancer, 2012, 59(3):586-588. [34] Gerber HP, Kowalski J, Sherman D, et al. Complete inhibition of rhabdomyosarcoma xenograft growth and neovascularization requires blockade of both tumor and host vascular endothelial growth factor[J]. Cancer Res, 2000, 60(22):6253-6258. [35] Ciccarelli C, Vulcano F, Milazzo L, et al. Key role of MEK/ERK pathway in sustaining tumorigenicity and in vitroradio resistance of embryonal rhabdomyosarcoma stem-like cell population[J]. Mol Cancer, 2016, 15:16. [36] Kim KM, Moon YJ, Park SH, et al. Individual and combinedexpression of DNA damage response molecules PARP1,γH2AX,BRCA1,and BRCA2 predict shorter survival of soft tissue sarcoma patients[J]. PLoS One, 2016, 11(9):e0163193. [37] Walter K, Holcomb T, Januario T, et al. Genome-wide DNA methylation analysis in melanoma reveals the importance of CpG methylation in MITF regulation[J]. J Invest Dermatol, 2015, 135(7):1820-1828. [38] Seki M, Nishimura R, Yoshida K, et al. Distinct methylation profiles characterize fusion-positive and fusion negative rhabdomyosarcoma[J]. Mod Pathol, 2015, 28(9):1214-1224. [39] Tombolan L, Poli E, Martini P, et al. Global DNA methylation profiling uncovers distinct methylation patterns ofprotocadherin alpha4 in metastatic and non-metastatic rhabdomyosarcoma[J]. BMC Cancer, 2016, 16(1):886. [40] Aoki T, Hino M, Koh K, et al. Low frequency of programmed death ligand 1 expression in pediatric cancers[J]. Pediatr Blood Cancer, 2016, 63(8):1461-1464. [41] Kinn VG, Hilgenberg VA, MacNeill AL. Myxoma virus therapy for human embryonal rhabdomyosarcoma in a nude mouse model[J]. Oncolytic Virother, 2016, 5:59-71. [42] Monti E, Fanzani A. Uncovering metabolism in rhabdomyosarcoma[J]. Cell Cycle, 2016, 15(2):184-195. [43] Chen X, Stewart E, Shelat AA, et al. Targeting oxidativestress in embryonal rhabdomyosarcoma[J]. Cancer Cell, 2013, 24(6):710-724. |