Combining sonodynamic therapy with chemoradiation for the treatment of pancreatic cancer

声动力疗法 吉西他滨 医学 光动力疗法 胰腺癌 放射治疗 抗代谢物 联合疗法 肿瘤科 放射增敏剂 内科学 癌症 癌症研究 超声波 放射科 化学 有机化学
作者
Richard Browning,Sarah Able,Jia‐Ling Ruan,Luca Baù,Paul Allen,Veerle Kersemans,Sheena Wallington,Paul Kinchesh,Sean Smart,Christiana Kartsonaki,Sukanta Kamila,Keiran Logan,Mark A. Taylor,Anthony P. McHale,John F. Callan,Eleanor Stride,Katherine A. Vallis
出处
期刊:Journal of Controlled Release [Elsevier]
卷期号:337: 371-377 被引量:21
标识
DOI:10.1016/j.jconrel.2021.07.020
摘要

Treatment options for patients with pancreatic cancer are limited and survival prospects have barely changed over the past 4 decades. Chemoradiation treatment (CRT) has been used as neoadjuvant therapy in patients with borderline resectable disease to reduce tumour burden and increase the proportion of patients eligible for surgery. Antimetabolite drugs such as gemcitabine and 5-fluorouracil are known to sensitise pancreatic tumours to radiation treatment. Likewise, photodynamic therapy (PDT) has also been shown to enhance the effect of radiation therapy. However, PDT is limited to treating superficial lesions due to the attenuation of light by tissue. The ability of the related technique, sonodynamic therapy (SDT), to enhance CRT was investigated in two murine models of pancreatic cancer (PSN-1 and BxPC-3) in this study. SDT uses low intensity ultrasound to activate an otherwise non-toxic sensitiser, generating toxic levels of reactive oxygen species (ROS) locally. It is applicable to greater target depths than PDT due to the ability of ultrasound to propagate further than light in tissue. Both CRT and the combination of CRT plus SDT delayed tumour growth in the two tumour models. In the PSN-1 model, but not the BxPC-3 model, the combination treatment caused an increase in survival relative to CRT alone (p = 0.038). The improvement in survival conferred by the addition of SDT in this model may be related to differences in tumour architecture between the two models. MRI and US images showed that PSN-1 tumours were less well perfused and vascularised than BxPC-3 tumours. This poor vascularisation may explain why PSN-1 tumours were more susceptible to the effects of vascular damage exerted by SDT treatment.
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