Eficacia del oxígeno hiperbárico en el tratamiento de la radionecrosis y el edema cerebral sintomáticos tras radiocirugía con acelerador lineal

Pérez-Espejo, M.A.; Felipe-Murcia, M.; Martínez‐Lage, Juan F.; García-Fernández, R.; Fuente-Muñoz, I. de la; Salinas-Ramos, Juan; Fernández-Pérez, Juan José; Tobarra-González, B.M.; Palma-Copete, J.D.; González‐López, Antonio; Romero, José María

doi:10.1016/s1130-1473(09)70142-3

Cited by 6 publications

(1 citation statement)

References 19 publications

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“…Hyperoxia may also promote a reversion from anaerobic metabolism to non-tumorigenic oxidative metabolism [39]. Reported studies on HBO for brain tumors focused mainly on its role as a radiation sensitizer [40, 41] and in the prevention of radiation-induced brain injury [42]. The potential use of hyerpoxia as a chemotherapy adjunct remains unexplored.…”

Section: Discussionmentioning

confidence: 99%

Hyperoxia resensitizes chemoresistant human glioblastoma cells to temozolomide

Sun

Lee

et al. 2012

J Neurooncol

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Temozolomide (TMZ) is standard chemotherapy for glioblastoma multiforme (GBM). Intratumoral hypoxia is common in GBM and may be associated with the development of TMZ resistance. Oxygen therapy has previously been reported to potentiate the effect of chemotherapy in cancer. In this study, we investigated whether hyperoxia can enhance the TMZ-induced cytotoxicity of human GBM cells, and whether and how it would resensitize TMZ-resistant GBM cells to TMZ. TMZ-sensitive human GBM cells (D54-S and U87-S) were treated with TMZ to develop isogenic subclones of TMZ-resistant cells (D54-R and U87-R). All cell lines were then exposed to different oxygen levels (1, 21, 40, or 80 %), with or without concomitant TMZ treatment, before assessment of cell cytotoxicity and morphology. Cell death and survival pathways elicited by TMZ and/or hyperoxia were elucidated by western blotting. Our results showed that TMZ sensitivity of both chemo-sensitive and resistant cells was enhanced significantly under hyperoxia. At the cell line-specific optimum oxygen concentration (D54-R, 80 %; U87-R, 40 %), resistant cells had the same response to TMZ as the parent chemosensitive cells under normoxia via the caspase-dependent pathway. Both TMZ and hyperoxia were associated with increased phosphorylation of ERK p44/42 MAPK (Erk1/2), but to a lesser extent in D54-R cells, suggesting that Erk1/2 activity may be involved in regulation of hyperoxia and TMZ-mediated cell death. Overall, hyperoxia enhanced TMZ toxicity in GBM cells by induction of apoptosis, possibly via MAPK-related pathways. Induced hyperoxia is a potentially promising approach for treatment of TMZ-resistant GBM.

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Section: Discussionmentioning

confidence: 99%

Hyperoxia resensitizes chemoresistant human glioblastoma cells to temozolomide

Sun

Lee

et al. 2012

J Neurooncol

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Conventional MRI does not reliably distinguish radiation necrosis from tumor recurrence after stereotactic radiosurgery

Stockham¹,

Tievsky

Koyfman³

et al. 2012

J Neurooncol

145

103

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Distinguishing radiation necrosis (RN) from tumor recurrence after stereotactic radiosurgery (SRS) for brain metastases is challenging. This study assesses the sensitivity (SN) and specificity (SP) of an MRI-based parameter, the "lesion quotient" (LQ), in characterizing tumor progression from RN. Records of patients treated with SRS for brain metastases between 01/01/1999 and 12/31/2009 and with histopathologic analysis of a subsequent contrast enhancing enlarging lesion at the treated site at a single institution were examined. The LQ, the ratio of maximal nodular cross sectional area on T2-weighted imaging to the corresponding maximal cross sectional area of T1-contrast enhancement, was calculated by a neuroradiologist blinded to the histopathological outcome. Cutoffs of <0.3, 0.3-0.6, and >0.6 have been previously suggested to have correlated with RN, mixed findings and tumor recurrence, respectively. These cutoff values were evaluated for SN, SP, positive predictive value (PPV) and negative predictive value (NPV). Logistic regression analysis evaluated for associated clinical factors. For the 51 patients evaluated, the SN, SP, PPV and NPV for identifying RN (LQ < 0.3) were 8, 91, 25 and 73 %, respectively. For the combination of recurrent tumor and RN (LQ 0.3-0.6) the SN, SP, PPV and NPV were 0, 64, 0 and 83 %. The SN, SP, PPV and NPV of the LQ for recurrent tumor (LQ > 0.6) were 59, 41, 62 and 39 %, respectively. Standard MRI techniques do not reliably discriminate between tumor progression and RN after treatment with SRS for brain metastases. Additional imaging modalities are warranted to aid in distinguishing between these diagnoses.

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An analysis of radiation necrosis of the central nervous system treated with bevacizumab

et al. 2014

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Radiation necrosis is a devastating complication following radiation to the central nervous system. The purpose of this study was to perform a comprehensive analysis of cases in the literature using bevacizumab, a monoclonal antibody against vascular endothelial growth factor, as treatment for radiation necrosis. A MEDLINE/PubMed search of articles about the use of bevacizumab for radionecrosis treatment yielded 16 studies published between 2007 and 2012. Data was summarized according to patient characteristics, treatment received and outcomes measured. A total of 71 unique cases were identified that met the inclusion criteria. The median age at the time of treatment with bevacizumab was 47 years. The most common tumors treated were glioblastoma (31 %), anaplastic glioma (14 %), and metastatic brain tumors (15 %). The median time from ending radiotherapy to starting treatment with bevacizumab was 11 months and the median follow up time after bevacizumab treatment was 8 months. The median number of cycles of bevacizumab was administered was 4, and the median dosage of bevacizumab was 7.5 mg/kg. The median time elapsed between cycles of bevacizumab was 2 weeks. Overall, pre and post treatment imaging revealed a median decrease in T1 contrast enhancement of 63 %, and a 59 % median decrease in T2/FLAIR signal abnormality. Treatment with bevacizumab resulted in a significant radiographic response for patients with radionecrosis. The median dosage of bevacizumab of 7.5 mg/kg for four cycles every 2 weeks should be considered as a treatment option in this patient population.

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Eficacia del oxígeno hiperbárico en el tratamiento de la radionecrosis y el edema cerebral sintomáticos tras radiocirugía con acelerador lineal

Cited by 6 publications

References 19 publications

Hyperoxia resensitizes chemoresistant human glioblastoma cells to temozolomide

Hyperoxia resensitizes chemoresistant human glioblastoma cells to temozolomide

Conventional MRI does not reliably distinguish radiation necrosis from tumor recurrence after stereotactic radiosurgery

An analysis of radiation necrosis of the central nervous system treated with bevacizumab

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