Abstract
Simple SummaryUltra-high dose rate radiation, widely nicknamed FLASH-RT, kills tumors without significantly damaging nearby normal tissues. This selective sparing of normal tissue by FLASH-RT tissue is called the FLASH effect. This review explores some of the proposed mechanisms of the FLASH effect and the current data that might support its use in pancreatic cancer. Since radiation for pancreatic cancer treatment is limited by GI toxicity issues and is a disease with one of the lowest five-year survival rates, FLASH-RT could have a large impact in the treatment of this disease with further study.Recent preclinical evidence has shown that ionizing radiation given at an ultra-high dose rate (UHDR), also known as FLASH radiation therapy (FLASH-RT), can selectively reduce radiation injury to normal tissue while remaining isoeffective to conventional radiation therapy (CONV-RT) with respect to tumor killing. Unresectable pancreatic cancer is challenging to control without ablative doses of radiation, but this is difficult to achieve without significant gastrointestinal toxicity. In this review article, we explore the propsed mechanisms of FLASH-RT and its tissue-sparing effect, as well as its relevance and suitability for the treatment of pancreatic cancer. We also briefly discuss the challenges with regard to dosimetry, dose rate, and fractionation for using FLASH-RT to treat this disease.
Highlights
External beam radiation therapy uses ionizing radiation to induce double strand DNA breaks in cancer cells and is thought to selectively kill tumors by exploiting differences in DNA repair between tumors and normal tissues
FLASH-RT is a relatively novel form of radiation therapy that involves the use of ionizing radiation at ultra-high dose rate (UHDR), which distinguishes FLASH-RT from conventional radiation therapy (CONV-RT), which involves much lower dose rates
Preclinical studies have shown that FLASH-RT can confer healthy tissue sparing through a phenomenon known as the FLASH effect
Summary
External beam radiation therapy uses ionizing radiation to induce double strand DNA breaks in cancer cells and is thought to selectively kill tumors by exploiting differences in DNA repair between tumors and normal tissues. The doses of radiation used in modern oncology have generally been derived empirically, usually as the maximum permitted by normal tissue toxicity [1]. Many tumors in the abdomen cannot be sufficiently treated with only radiation and chemotherapy, since the maximum dose of radiation that the intestines can receive over a lifetime is about 50 Gy [7]. Radiation can be a useful preparative treatment before surgery, but it is often insufficient to achieve oncologic control on its own. Surgery is limited as a treatment option and poses risks such as pain and infection. Chemotherapy shares similar risks of pain as surgery and improvements are limited. Without advancements in radiation protection or radiosensitization, the curative potential of radiation therapy alone for gastrointestinal tumors will be limited
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