Synergistic antiglioma action of hyperthermia and nitric oxide

Janjetović, Kristina; Misirkić, Maja; Vučićević, Ljubica; Harhaji, Ljubica; Trajkovič, Vladimir

doi:10.1016/j.ejphar.2007.12.028

Cited by 20 publications

(21 citation statements)

References 41 publications

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“…Nitric oxide effects on autophagy are controversial and have shown a cell-dependent role for NO in the regulation of this lysosomal degradation process. 43,44 While studies using glioma cells have reported that NO inhibits the completion of autophagy, 45 other reports have demonstrated that in neurons NO increases mitophagy. 46 Interestingly, we observed that in addition to autophagy, preeclamptic placentas exhibit mitophagy.…”

Section: Discussionmentioning

confidence: 99%

Placental autophagy regulation by the BOK-MCL1 rheostat

Kalkat

Garcia²,

Ebrahimi³

et al. 2013

Autophagy

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Section: Discussionmentioning

confidence: 99%

Placental autophagy regulation by the BOK-MCL1 rheostat

Kalkat

Garcia²,

Ebrahimi³

et al. 2013

Autophagy

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“…One potential avenue, implicating cellular oxidative stress, has been suggested by the unexpected fi nding of increased coagulation when combining RF thermal ablation with blank liposomes ( 12,19 ). Indeed, it is known that the thermal dosimetry at which this increased coagulation is observed is only slightly higher than that at hyperthermia where oxidative stress has been shown to play a role at activating tumoricidal pathways involving both apoptosis and necrosis (20)(21)(22)(23)(24)(25). Hence, we hypothesized that the synergistic effects of RF ablation combined with liposomal doxorubicin are caused by cellular oxidative stress which leads to increased apoptosis and/or reduced heat-shock protein production (26)(27)(28).…”

Section: Experiments Overviewmentioning

confidence: 99%

Liposomal Doxorubicin Increases Radiofrequency Ablation–induced Tumor Destruction by Increasing Cellular Oxidative and Nitrative Stress and Accelerating Apoptotic Pathways

Solazzo

Ahmed²,

Schor-Bardach³

et al. 2010

Radiology

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Purpose:To determine if oxidative and nitrative stress and/or apoptosis contribute to increased coagulation when combining radiofrequency (RF) ablation with liposomal doxorubicin. Materials and Methods:Animal care committee approval was obtained. R3230 mammary adenocarcinomas in Fischer rats were treated with either RF ablation ( n = 43), 1 mg of intravenously injected liposomal doxorubicin ( n = 26), or combined therapy ( n = 30) and were compared with control subjects ( n = 11). A subset of animals receiving combination therapy ( n = 24) were treated in the presence or absence of N -acetylcysteine (NAC) administered 24 hours and 1 hour before RF ablation. Tumors were analyzed 2 minutes to 72 hours after treatment to determine the temporal range of response by using immunohistochemical staining of the apoptosis marker cleaved caspase-3, phosphorylated g H2AX , and Results:By 4 hours after RF ablation alone, a 0.48-mm 6 0.13 (standard deviation ) peripheral band with 57.0% 6 7.3 cleaved caspase-3 positive cells was noted at the ablation margin, whereas a 0.73-mm 6 0.18 band with 77.7% 6 6.3 positivity was seen for combination therapy ( P , .03 for both comparisons). Combination therapy caused increased and earlier staining for 4-HNE-modifi ed proteins, 8-OHdG, NT, and g H2AX with colocalization to cleaved caspase-3 staining. A rim of increased HSP70 was identifi ed peripheral to the area of cleaved caspase-3. Parameters of oxidative and nitrative stress were signifi cantly inhibited by NAC 1 hour following RF ablation, resulting in decreased cleaved caspase-3 positivity (0.28-mm 6 0.09 band of 25.9% 6 7.4 positivity vs 0.59-mm 6 0.11 band of 62.9% 6 6.0 positivity, P , .001 for both comparisons). Conclusion:Combining RF ablation with liposomal doxorubicin increases cell injury and apoptosis in the zone of increased coagulation by using a mechanism that involves oxidative and nitrative stress that leads to accelerated apoptosis.q RSNA, 2010

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“…SNP and hyperthermia caused oxidative stress and mitochondrial depolarization 8 leading to necrosis on one hand and to caspase-mediated apoptosis on the other [44]. Recent clinical trials using hyperthermia alone in recurrent glioma showed that this treatment was well tolerated and produced promising results [45,46] …”

Section: Reactive Oxygen and Nitrogenmentioning

confidence: 99%

“…While most of the results mentioned above were generated in in vitro settings, hyperthermia has shown promising results in recent clinical trials on recurrent glioma [45,46] and might be enhanced by concurrent application of a NO-releasing agent [44].…”

Section: Treatment Optionmentioning

confidence: 99%

Hypoxia Helps Glioma to Fight Therapy

Amberger-Murphy

2009

CCDT

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Abstract:Despite major improvements in the surgical management the prognosis for patients bearing malignant gliomas is still dismal. Malignant gliomas are notoriously resistant to treatment and the survival time of patients is between 3-8 years for low-grade and anaplastic gliomas and 6 -12 month for glioblastoma. Increasing malignancy of gliomas correlates with an increase in cellularity and a poorly organized tumour vasculature leading to insufficient blood supply, hypoxic areas and ultimately to the formation of necrosis, a characteristic of glioblastoma. Hypoxic/necrotic tumours are more resistant to chemotherapy and radiation. Hypoxia induces either directly or indirectly (through the activation of transcription factors) changes in the biology of a tumour and its microenvironment leading to increased aggressiveness and tumour resistance to chemotherapy and radiation. This review is focused on hypoxia-induced molecular changes affecting glioma biology and therapy.3

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Synergistic antiglioma action of hyperthermia and nitric oxide

Cited by 20 publications

References 41 publications

Placental autophagy regulation by the BOK-MCL1 rheostat

Placental autophagy regulation by the BOK-MCL1 rheostat

Liposomal Doxorubicin Increases Radiofrequency Ablation–induced Tumor Destruction by Increasing Cellular Oxidative and Nitrative Stress and Accelerating Apoptotic Pathways

Hypoxia Helps Glioma to Fight Therapy

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