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Radiation therapy has been used in the treatment of a wide variety of cancers for nearly a century and is one of the most effective ways to treat cancer. Low-dose ionizing radiation (IR) can interfere with cell division of cancer and normal cells by introducing oxidative stress and injury to DNA. The differences in the response to IR-induced DNA damage and increased reactive oxygen species between normal human fibroblasts (NHFs) and cancerous SHSY-5Y cells were considered. H2AX staining and comet assays revealed that NHF cells responded by initiating a DNA repair sequence whereas SHSY-5Y cells did not. In addition, NHF cells appeared to quench the oxidative stress induced by IR, and after 24 h no DNA damage was present. SHSY-5Y cells, however, did not repair their DNA, did not quench the oxidative stress, and showed characteristic signs that they were beginning to undergo apoptosis. These results indicate that there is a differential response between this cancerous and normal cell line in their ability to respond to low-dose IR, and these differences need to be exploited in order to treat cancer effectively. Further study is needed in order to elucidate the mechanism by which SHSY-5Y cells undergo apoptosis following radiation and why these normal cells are better equipped to deal with IR-induced double-strand breaks and oxidative stress.
Radiation therapy has been used in the treatment of a wide variety of cancers for nearly a century and is one of the most effective ways to treat cancer. Low-dose ionizing radiation (IR) can interfere with cell division of cancer and normal cells by introducing oxidative stress and injury to DNA. The differences in the response to IR-induced DNA damage and increased reactive oxygen species between normal human fibroblasts (NHFs) and cancerous SHSY-5Y cells were considered. H2AX staining and comet assays revealed that NHF cells responded by initiating a DNA repair sequence whereas SHSY-5Y cells did not. In addition, NHF cells appeared to quench the oxidative stress induced by IR, and after 24 h no DNA damage was present. SHSY-5Y cells, however, did not repair their DNA, did not quench the oxidative stress, and showed characteristic signs that they were beginning to undergo apoptosis. These results indicate that there is a differential response between this cancerous and normal cell line in their ability to respond to low-dose IR, and these differences need to be exploited in order to treat cancer effectively. Further study is needed in order to elucidate the mechanism by which SHSY-5Y cells undergo apoptosis following radiation and why these normal cells are better equipped to deal with IR-induced double-strand breaks and oxidative stress.
Introduction: Despite small-cell lung cancer often being very sensitive to chemotherapy treatment, duration of response is often short-lived in patients who are diagnosed with extensive disease at the onset. To improve survival in these patients and provide alternative treatment options, new chemotherapeutic agents have been evaluated, including amrubicin, a recent second-line treatment for patients with relapsed small-cell lung cancer. Areas covered: The authors reviewed the pharmacodynamics and pharmacokinetics of amrubicin and evaluated it versus other currently available chemotherapeutic agents. Existing Phases I, II, and III clinical data were reviewed. In Phase I trials, amrubicin was shown to be a safe and tolerable agent. Results from Phase II studies appeared promising, suggesting that patients treated with amrubicin had a better overall response rate and a longer progressionfree survival versus topotecan. Unfortunately, the randomized Phase III trial, designed to definitively compare amrubicin to topotecan as second-line treatment for relapsed small-cell lung cancer, failed to show an improvement in overall survival. Expert opinion: Options for second-line therapy in relapsed small-cell lung cancer continue to be limited. The current role of amrubicin remains uncertain, and predictive biomarkers may be necessary to better establish its role. Further basic and clinical research studies are needed to expand treatment options and improve overall survival in patients with relapsed small-cell lung cancer.
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