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Cancer is a great challenge to efficient therapy due to biological diversity. Disturbed oxidative homeostasis in cancer cells certainly contributes to differential therapy response. Further, one of the hallmarks of cancer cells is adaptation which includes fine tuning of the cellular metabolic and signalling pathways as well as transcription profiles. There are several factors which contribute to the tumor diversity and therapy response, and oxidative stress is certainly one of them. Changes in oxygen levels due to hypoxia/reoxygenation during tumor growth modulate antioxidative patterns finally supporting increased cell diversity and adaptation to stressing conditions. Additionally, cancer chemotherapy based on ROS production can also induce also adaptation. To counteract these negative effects natural products are often used for their antioxidant activities as well as photodynamic therapy supported by novel chemosensitizers. Understanding of possible pathways which can trigger antioxidant defence at a certain time during cancer development can also provide possible strategies in fighting cancer.

Technology: general issues --- NQO1 --- NQO1*2 --- polymorphism --- quinone --- breast cancer --- menadione --- lapachone --- doxorubicin --- ascorbate --- oxidative stress --- reactive oxygen species --- sperm --- cancer chemotherapy --- antioxidant therapy --- antioxidant proteins --- chemoresistance --- oxaliplatin --- 5-Fluorouracil --- myelodysplastic syndromes --- carbonylation --- deferasirox --- ovary --- calcium channel --- Trolox --- granulosa cell tumor --- cell death --- mitochondria --- photodynamic therapy --- singlet oxygen --- nitric oxide --- light --- combination therapy --- antioxidants --- bleomycin --- cancer treatment --- chemotherapy-induced toxicity --- cisplatin --- free radicals --- methotrexate --- ozone therapy --- lung cancer --- cancer metabolism --- reactive oxygen species (ROS) --- therapy resistance --- new therapeutic strategies --- breast cancer stem cells --- 4-hydroxy-2-nonenal --- extracellular matrix --- NRF2 --- bardoxolone methyl --- prostate cancer --- castration-resistant prostate cancer --- androgen receptor (AR), AR-V7 --- anti-androgen --- enzalutamide --- androgen deprivation therapy --- cancer --- antioxidant --- triphala --- ayurveda --- chemoprevention and chemotherapy --- n/a

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Cancer is a great challenge to efficient therapy due to biological diversity. Disturbed oxidative homeostasis in cancer cells certainly contributes to differential therapy response. Further, one of the hallmarks of cancer cells is adaptation which includes fine tuning of the cellular metabolic and signalling pathways as well as transcription profiles. There are several factors which contribute to the tumor diversity and therapy response, and oxidative stress is certainly one of them. Changes in oxygen levels due to hypoxia/reoxygenation during tumor growth modulate antioxidative patterns finally supporting increased cell diversity and adaptation to stressing conditions. Additionally, cancer chemotherapy based on ROS production can also induce also adaptation. To counteract these negative effects natural products are often used for their antioxidant activities as well as photodynamic therapy supported by novel chemosensitizers. Understanding of possible pathways which can trigger antioxidant defence at a certain time during cancer development can also provide possible strategies in fighting cancer.

Technology: general issues --- NQO1 --- NQO1*2 --- polymorphism --- quinone --- breast cancer --- menadione --- lapachone --- doxorubicin --- ascorbate --- oxidative stress --- reactive oxygen species --- sperm --- cancer chemotherapy --- antioxidant therapy --- antioxidant proteins --- chemoresistance --- oxaliplatin --- 5-Fluorouracil --- myelodysplastic syndromes --- carbonylation --- deferasirox --- ovary --- calcium channel --- Trolox --- granulosa cell tumor --- cell death --- mitochondria --- photodynamic therapy --- singlet oxygen --- nitric oxide --- light --- combination therapy --- antioxidants --- bleomycin --- cancer treatment --- chemotherapy-induced toxicity --- cisplatin --- free radicals --- methotrexate --- ozone therapy --- lung cancer --- cancer metabolism --- reactive oxygen species (ROS) --- therapy resistance --- new therapeutic strategies --- breast cancer stem cells --- 4-hydroxy-2-nonenal --- extracellular matrix --- NRF2 --- bardoxolone methyl --- prostate cancer --- castration-resistant prostate cancer --- androgen receptor (AR), AR-V7 --- anti-androgen --- enzalutamide --- androgen deprivation therapy --- cancer --- antioxidant --- triphala --- ayurveda --- chemoprevention and chemotherapy --- NQO1 --- NQO1*2 --- polymorphism --- quinone --- breast cancer --- menadione --- lapachone --- doxorubicin --- ascorbate --- oxidative stress --- reactive oxygen species --- sperm --- cancer chemotherapy --- antioxidant therapy --- antioxidant proteins --- chemoresistance --- oxaliplatin --- 5-Fluorouracil --- myelodysplastic syndromes --- carbonylation --- deferasirox --- ovary --- calcium channel --- Trolox --- granulosa cell tumor --- cell death --- mitochondria --- photodynamic therapy --- singlet oxygen --- nitric oxide --- light --- combination therapy --- antioxidants --- bleomycin --- cancer treatment --- chemotherapy-induced toxicity --- cisplatin --- free radicals --- methotrexate --- ozone therapy --- lung cancer --- cancer metabolism --- reactive oxygen species (ROS) --- therapy resistance --- new therapeutic strategies --- breast cancer stem cells --- 4-hydroxy-2-nonenal --- extracellular matrix --- NRF2 --- bardoxolone methyl --- prostate cancer --- castration-resistant prostate cancer --- androgen receptor (AR), AR-V7 --- anti-androgen --- enzalutamide --- androgen deprivation therapy --- cancer --- antioxidant --- triphala --- ayurveda --- chemoprevention and chemotherapy