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• W2000778518 abstract "Purpose/Objective(s)Whole abdominal radiation therapy (WART) has been used in cases of GI cancer with disseminated intra-abdominal disease. However, the main shortcoming of WART is the inability to combine it with full-dose chemotherapy, due to the increased toxicity to normal tissue. Recent findings have suggested the possibility of a novel treatment paradigm allowing the use of full dose systemic chemotherapy safely in combination with Low Dose Fractionated radiation therapy (LDFRT). Traditionally, the cell survival curve suggested that fractionated radiation doses of greater than 120 cGy were required to overcome the initial shoulder where low doses of radiation produced negligible effects on cell survival. However, preliminary data have shown a low-dose hyper-radiosensitivity (HRS) phenomenon in which cells die from hypersensitivity to 15 cGy of radiation. The primary goal of this study is to identify various biomarkers and cellular pathways that are responsive to low-dose radiation and determine their contribution to chemopotentiation.Materials/MethodsTreatment includes a combination of LDFRT and modified Docetaxel, Cisplatin, 5-fluorouracil (mDCF). Metastatic gastric carcinoma 5822 and gastric adenocarcinoma 1739 cells were treated with three consecutive daily doses of radiation and 5-FU and docetaxel on day 1, 5-FU on day 2 and 5-FU and cisplatin on day 3. RNA was extracted 24 h later or cells were analyzed by clonogenic survival assay 10 days later.ResultsOur data indicate that three consecutive daily fractions of 15 cGy are sufficient to induce HRS in gastric cancer cells and potentiate mDCF. RT-PCR analysis of cellular pathways suggest that the combination of mDCF with LDFRT induces HRS in gastric cancer cells by down regulating the DNA repair machinery (ATM, p53, BRCA1, MDM2) and up regulating the production of hydrogen peroxide (DUOX2).ConclusionsLDFRT can potentiate mDCF through mechanisms different than the conventional DNA damage response and could be considered for WART in combination treatments for patients with advanced and metastatic GI cancers. Purpose/Objective(s)Whole abdominal radiation therapy (WART) has been used in cases of GI cancer with disseminated intra-abdominal disease. However, the main shortcoming of WART is the inability to combine it with full-dose chemotherapy, due to the increased toxicity to normal tissue. Recent findings have suggested the possibility of a novel treatment paradigm allowing the use of full dose systemic chemotherapy safely in combination with Low Dose Fractionated radiation therapy (LDFRT). Traditionally, the cell survival curve suggested that fractionated radiation doses of greater than 120 cGy were required to overcome the initial shoulder where low doses of radiation produced negligible effects on cell survival. However, preliminary data have shown a low-dose hyper-radiosensitivity (HRS) phenomenon in which cells die from hypersensitivity to 15 cGy of radiation. The primary goal of this study is to identify various biomarkers and cellular pathways that are responsive to low-dose radiation and determine their contribution to chemopotentiation. Whole abdominal radiation therapy (WART) has been used in cases of GI cancer with disseminated intra-abdominal disease. However, the main shortcoming of WART is the inability to combine it with full-dose chemotherapy, due to the increased toxicity to normal tissue. Recent findings have suggested the possibility of a novel treatment paradigm allowing the use of full dose systemic chemotherapy safely in combination with Low Dose Fractionated radiation therapy (LDFRT). Traditionally, the cell survival curve suggested that fractionated radiation doses of greater than 120 cGy were required to overcome the initial shoulder where low doses of radiation produced negligible effects on cell survival. However, preliminary data have shown a low-dose hyper-radiosensitivity (HRS) phenomenon in which cells die from hypersensitivity to 15 cGy of radiation. The primary goal of this study is to identify various biomarkers and cellular pathways that are responsive to low-dose radiation and determine their contribution to chemopotentiation. Materials/MethodsTreatment includes a combination of LDFRT and modified Docetaxel, Cisplatin, 5-fluorouracil (mDCF). Metastatic gastric carcinoma 5822 and gastric adenocarcinoma 1739 cells were treated with three consecutive daily doses of radiation and 5-FU and docetaxel on day 1, 5-FU on day 2 and 5-FU and cisplatin on day 3. RNA was extracted 24 h later or cells were analyzed by clonogenic survival assay 10 days later. Treatment includes a combination of LDFRT and modified Docetaxel, Cisplatin, 5-fluorouracil (mDCF). Metastatic gastric carcinoma 5822 and gastric adenocarcinoma 1739 cells were treated with three consecutive daily doses of radiation and 5-FU and docetaxel on day 1, 5-FU on day 2 and 5-FU and cisplatin on day 3. RNA was extracted 24 h later or cells were analyzed by clonogenic survival assay 10 days later. ResultsOur data indicate that three consecutive daily fractions of 15 cGy are sufficient to induce HRS in gastric cancer cells and potentiate mDCF. RT-PCR analysis of cellular pathways suggest that the combination of mDCF with LDFRT induces HRS in gastric cancer cells by down regulating the DNA repair machinery (ATM, p53, BRCA1, MDM2) and up regulating the production of hydrogen peroxide (DUOX2). Our data indicate that three consecutive daily fractions of 15 cGy are sufficient to induce HRS in gastric cancer cells and potentiate mDCF. RT-PCR analysis of cellular pathways suggest that the combination of mDCF with LDFRT induces HRS in gastric cancer cells by down regulating the DNA repair machinery (ATM, p53, BRCA1, MDM2) and up regulating the production of hydrogen peroxide (DUOX2). ConclusionsLDFRT can potentiate mDCF through mechanisms different than the conventional DNA damage response and could be considered for WART in combination treatments for patients with advanced and metastatic GI cancers. LDFRT can potentiate mDCF through mechanisms different than the conventional DNA damage response and could be considered for WART in combination treatments for patients with advanced and metastatic GI cancers." @default.
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• W2000778518 date "2013-10-01" @default.
• W2000778518 modified "2023-09-27" @default.
• W2000778518 title "Investigation of Low-Dose Fractionated Radiation Therapy as a Chemopotentiator in Advanced/Metastatic Gastrointestinal Carcinoma" @default.
• W2000778518 doi "https://doi.org/10.1016/j.ijrobp.2013.06.1739" @default.
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