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S.J. Kim
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P1.03 - Chemotherapy/Targeted Therapy (ID 689)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Chemotherapy/Targeted Therapy
- Presentations: 1
- Moderators:
- Coordinates: 10/16/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P1.03-025 - Combination Therapy with Carboplatin and Hyperoxia Synergistically Enhances Suppression of Benzo[a]Pyrene Induced Lung Cancer (ID 8432)
09:30 - 09:30 | Author(s): S.J. Kim
- Abstract
Background:
We explored the effects of intermittent normobaric hyperoxia alone or combined with chemotherapy on the growth, general morphology, oxidative stress, and apoptosis of benzo[a]pyrene (B[a]P)-induced lung tumors in mice.
Method:
Female A/J mice were given a single dose of B[a]P and randomized into four groups: (1) control, (2) carboplatin (50 mg/kg intraperitoneally), (3) hyperoxia (95% fraction of inspired oxygen), and (4) carboplatin and hyperoxia. Normobaric hyperoxia (95%) was applied for 3 h each day from weeks 21 to 28. Tumor load was determined as the average total tumor numbers and volumes. Several markers of oxidative stress and apoptosis were evaluated.
Result:
Intermittent normobaric hyperoxia combined with chemotherapy reduced the tumor number by 59% and the load by 72% compared with the control B[a]P group. Intermittent normobaric hyperoxia, either alone or combined with chemotherapy, decreased the levels of superoxide dismutase (SOD) and glutathione (GSH) and increased the levels of catalase and 8-hydroxydeoxyguanosine (8-OHdG). The Bax/Bcl-2 mRNA ratio, caspase-3 level, and number of transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells increased following treatment with hyperoxia with or without chemotherapy.
Conclusion:
Intermittent normobaric hyperoxia was found to be tumoricidal and thus may serve as an adjuvant therapy for lung cancer. Oxidative stress and its effects on DNA are increased following exposure to hyperoxia and even more with chemotherapy, and this may lead to apoptosis of lung tumors.