[1] Hall E. Protons for radiotherapy:a 1946 proposal[J]. Lancet Oncol, 2009, 10(2):196. DOI:10.1016/s1470-2045(09)70022-1.
[2] Tobias CA, Lyman JT, Chatterjee A, et al. Radiological physics characteristics of the extracted heavy ion beams of the bevatron[J].Science, 1971, 174(4014):1131-1134. DOI:10.1126/science.174.4014.1131.
[3] Okayasu R. Repair of DNA damage induced by accelerated heavy ions-a mini review[J]. Inter J Cancer, 2012, 130(5):991-1000. DOI:10.1002/ijc.26445.
[4] Matsumoto Y, Matsuura T, Wada M, et al. Enhanced radiobiological effects at the distal end of a clinical proton beam:in vitro study[J]. J Radiat Res, 2014, 55(4):816-822.DOI:10.1093/jrr/rrt230.
[5] Loeffler JS, D urante M. Charged particle therapy-optimization, challenges and future directions[J]. Nat Rev Clin Oncol, 2013, 10(7):411-424. DOI:10.1038/nrclinonc.2013.79.
[6] Yoo SH, Cho I, Cho S, et al. Effective Generation of the spread-out-Bragg peak from the laser accelerated proton beams using a carbon-proton mixed target[J]. Australas Phys Eng Sci Med, 2014, 37(4):635-644. DOI:10.1007/s13246-014-0292-7.
[7] Paganetti H.Relative biological effectiveness (RBE) values for proton beam therapy. Variations as a function of biological endpoint, dose, and linear energy transfer[J]. Phys Med Biol, 2014, 59(22):R419-R472. DOI:10.1088/0031-9155/59/22/R419.
[8]

Held KD, Kawamura H, Kaminuma T, et al. Effects of charged particles on human tumor cells[J/OL]. Front Oncol, 2016, 6: 23[2017-11-10]. https://www.frontiersin.org/articles/10.3389/fonc.2016.00023/full. DOI: 10.3389/fonc.2016.00023.
[9] Tsujii H, Kamada T. A review of update clinical results of Carbon ion radiotherapy[J]. Jpn J Clin Oncol, 2012, 42(8):670-685. DOI:10.1093/jjco/hys104.
[10] Alexander BM, Pinnell N, Wen PY, et al.Targeting DNA repair and the cell cycle in glioblastoma[J]. J Neurooncol, 2012, 107(3):463-477.DOI:10.1007/s11060-011-0765-4.
[11]

Suetens A, Konings K, Moreels M, et al. Higher initial DNA damage and persistent cell cycle arrest after Carbon ion irradiation compared to X-irradiation in prostate and colon cancer cells[J/OL]. Front Oncol, 2016, 6: 87[2017-11-10]. https://www.frontiersin.org/articles/10.3389/fonc.2016.00087/full. DOI: 10.3389/fonc.2016.00087.
[12] Wang H, Liu S, Zhang P, et al. S-phase cells are more sensitive to high-linear energy transfer radiation[J]. Int J Radiat Oncol Biol Phys, 2009, 74(4):1236-1241. DOI:10.1016/j.ijrobp.2008.12.089.
[13] Hirayama R, Uzawa A, Obara M, et al. Determination of the relative biological effectiveness and Oxygen enhancement ratio for micronuclei formation using high-LET radiation in solid tumor cells:An in vitro and in vivo study[J]. Mut Res Genet Toxicol Environ Mutagen, 2015, 793:41-47. DOI:10.1016/j.mrgentox.2015.08.003.
[14] Lin BR, Li D, Zhang L. Oxymatrine mediates Bax and Bcl-2 expression in human breast cancer MCF-7 cells[J]. Pharmazie, 2016, 71(3):154-157. DOI:10.1691/ph.2016.5765.
[15] Li C, Wu X, Sun R, et al.Croton tiglium extract induces apoptosis via Bax/Bcl-2 pathways in human lung cancer a549 cells[J]. Asian Pac J Cancer Prev, 2016, 17(11):4893-4898. DOI:10.22034/APJCP.2016.17.11.4893.
[16] Khodapasand E, Jafarzadeh N, Farrokhi F, et al. Is Bax/Bcl-2 ratio considered as a prognostic marker with age and tumor location in colorectal cancer?[J]. Iran Biomed J, 2015, 19(2):69-75. DOI:10. 6091/ibj.1366.2015.
[17] Delbridge AR, Grabow S, Strasser A, et al.Thirty years of Bcl-2:translating cell death discoveries into novel cancer therapies[J]. Nat Rev Cancer, 2016, 16(2):99-109. DOI:10.1038/nrc.2015.17.
[18] Hamada N, Hara T, Omura-Minamisawa MA, et al. Energetic heavy ions overcome tumor radioresistance caused by overexpression of Bcl-2[J]. Radiother Oncol, 2008, 89(2):231-236. DOI:10.1016/j.radonc.2008.02.013.
[19]

Sato T, Hamada N. Model assembly for estimating cell surviving fraction for both targeted and nontargeted effects based on microdosimetric probability densities[J/OL]. PLoS One, 2014, 9(11): 0114056[2017-11-10]. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0114056. DOI: 10.1371/journal.pone.0114056.
[20] Xue L, Furusawa Y, Okayasu R, et al.The complexity of DNA double Strand break is a crucial factor for activating ATR signaling pathway for G2/M checkpoint regulation regardless of ATM function[J]. DNA repair, 2015, 25:72-83. DOI:10.1016/j.dnarep.2014.11.004.
[21] Di CX, Yang LN, Zhang H, et al. Effects of carbon-ion beam or X-ray irradiation on anti-apoptosisΔNp73 expression in HeLa cells[J].Gene, 515(1):208-213. DOI:10.1016/j.gene.2012.11.040.
[22] Abdelhaleem EF, Abdelhameid MK, Kassab AE, et al. Design and synthesis of thienopyrimidine urea derivatives with potential cytotoxic and pro-apoptotic activity against breast cancer cell line MCF-7[J]. Eur J Med Chem, 2018, 143:1807-1825. DOI:10.1016/j.ejmech, 2017.10.075.
[23] Moshrefi M, Spotin A, Kafil HS, et al. Tumor suppressor p53 induces apoptosis of host lymphocytes experimentally infected by Leishmania major, by activation of Bax and caspase-3:a possible survival mechanism for the parasite[J]. Parasitol Res, 2017, 116(8):2159-2166. DOI:10.1007/s00436-017-5517-8.
[24] Song HY, Deng XH, Yuan GY, et al. Expression of bcl-2 and p53 in induction of esophageal cancer cell apoptosis by ECRG2 in combination with cisplatin[J]. Asian Pa J Cancer Prev, 2014, 15(3):1397-1401.DOI:10.7314/APJCP.2014.15.3.1397.
[25] Zhao YF, Wang LX, Huang QY, et al.Radiosensitization of non-small cell lung cancer cells by inhibition of TGF-beta 1 signaling with SB431542 is dependent on p53 status[J]. Oncol Res, 2016, 24(1):1-7. DOI:10.3727/096504016X14570992647087.
[26]

Mirzayans R, Andrais B, Scott A, et al. New insights into p53 signaling and cancer cell response to DNA damage: implications for cancer therapy[J/OL]. J Biomed Biotechnol, 2012: 170325[2017-11-10]. https://www.hindawi.com/journals/bmri/2012/170325/. DOI: 10.1155/2012/170325.
[27]

Amornwichet N, Oike T, Shibata AA, et al. Carbon-Ion beam irradiation kills X-ray-resistant p53-Null cancer cells by inducing mitotic catastrophe[J/OL]. PLoS One, 2014, 9(12): 0115121[2017-11-10]. http://dx.org/10.1371/journal.pone.0115121. DOI: 10.1371/journal.pone.0115121.
[28] He M, Dong C, Konishi T, et al. Differential effects of p53 on bystander phenotypes induced by gamma ray and high LET heavy ion radiation[J]. Life Sci Space Res(Amst), 2014, 1:53-59. DOI:10.1016/j.lssr.2014.02.003.
[29] Nakagawa Y, Takahashi A, Kajihara AA, et al. Depression of p53-independent Akt survival signals in human oral cancer cells bearing mutated p53 gene after exposure to high-LET radiation[J].Biochem Biophys Res Commun, 2012, 423(4):654-660. DOI:10. 1016/j.bbrc.2012.06.004.
[30] Liu K, Zhao XK, Gu J, et al.Effects of C-12(6+) heavy ion beam irradiation on the p53 signaling pathway in HepG2 liver cancer cells[J]. Acta Biochim Biophys Sin (Shanghai), 2017, 49(11):989-998. DOI:10.1093/abbs/gmx096.
[31] Alphonse G, Maalouf M, Battiston MP, et al. p53-independent early and late apoptosis is mediated by ceramide after exposure of tumor cells to photon or Carbon ion irradiation[J]. BMC Cancer, 2013, 13:151. DOI:10.1186/1471-2407-13-151.
[32] Yamakawa N, Takahashi A, Mori E, et al. High LET radiation enhances apoptosis in mutated p53 cancer cells through Caspase-9 activation[J]. Cancer Sci, 2008, 99(7):1455-1460. DOI:10.1111/j.1349-7006.2008.00818.x.
[33]

Tomiyama A, Tachibana K, Suzuki K, et al. MEK-ERK-dependent multiple caspase activation by mitochondrial proapoptotic Bcl-2 family proteins is essential for heavy ion irradiation-induced glioma cell death[J/OL]. Cell Death Disease, 2010, 1: e60[2017-11-10]. https://www.nature.com/articles/cddis201037. DOI: 10.1038/cddis,2010.37.
[34] Xu H, Gao L, Che TJ, et al.The effects of C-12(6+) irradiation on cell cycle, apoptosis, and expression of caspase-3 in the human lung cancer cell line H1299[J]. Cancer Biotherapy Radiopharm, 2012, 27(2):113-118. DOI:10.1089/cbr.2011.1037.
[35]

Ghorai A, Bhattacharyya NP, Sarma A, et al. Radiosensitivity and induction of apoptosis by high LET Carbon ion beam and low LET gamma radiation: a comparative study[J/OL]. Scientifica (Cairo), 2014: 438030[2017-11-10]. https://www.hindawi.com/journals/scientifica/2014/438030/.DOI:10.1155/2014/438030.
[36] Ghorai A, Sarma A, Bhattacharyya NP. Carbon ion beam triggers both caspase-dependent and caspase-independent pathway of apoptosis in HeLa and status of PARP-1 controls intensity of apoptosis[J]. Apoptosis, 2015, 20(4):562-580. DOI:10.1007/s10495-015-1107-3.