Complementary information from magnetic resonance imaging and 18F-fluoromisonidazole positron emission tomography in the assessment of the response to an antiangiogenic treatment in a rat brain tumor model

Valable, Samuel; Petit, Edwige; Roussel, Simon; Marteau, Léna; Toutain, Jérôme; Divoux, Didier; Sobrio, Franck; Delamare, Jérôme; Barré, Louisa; Bernaudin, Myriam

doi:10.1016/j.nucmedbio.2011.01.010

Cited by 37 publications

(55 citation statements)

References 39 publications

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“…All animal experiments were carried out under the previous European directive (86/609/EEC) as enacted in the national legislation. Individual licenses to investigate SR (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26), MB (14-71), JT , EP (14-79), OT (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) and SV are held and the study was approved by the regional ethical committee for animal research and health-care 'Comité Régional d'Éthique en matière d'Expérimentation Animale pour la Normandie' (CEEAN, agreement no. 0507-02).…”

Section: Methods Animalsmentioning

confidence: 99%

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Chronic arterial hypertension impedes glioma growth: a multiparametric MRI study in the rat

et al. 2015

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Glioblastoma is the most aggressive brain tumor and is almost always fatal. These tumors are highly vascularized and angiogenesis is one of the pre-eminent mechanisms underlying their growth. Chronic arterial hypertension (CAH) is a common and worldwide pathology that markedlly alters the structure and function of the vasculature. Yet, essential hypertension is associated in the brain with potential locally impaired vasoreactivity, disturbed perfusion supply and hypoxia phenomena. Even though CAH is a global burden and has an important impact on brain function, nothing is known about the way this frequent pathology would interact with the evolution of glioma. We sought to determine if arterial hypertension influences gliobastoma growth. In the present study, rat glioma C6 tumor cells were implanted in the caudate-putamen of spontaneously hypertensive rats (SHR) or their normotensive controls, the Wistar-Kyoto (WKY) rats. The evolution of the tumor was sequentially analyzed by multiparametric magnetic resonance imaging and the inflammatory response was examined by histochemistry. We found that CAH significantly attenuates the growth of the tumor as, at 21 days, the volume of the tumor was 85.4±34.7 and 126.1±28.8 mm(3), respectively, in hypertensive and normotensive rats (P<0.02). Moreover, cerebral blood volume and cerebral blood flow were greater in the tumors of hypertensive rats (P<0.05). The lesser growth of the tumor observed in normotensive animals was not due to an enhanced rejection of the tumor cells in WKY rats, the inflammatory response being similar in both groups. For the first time, these results show that CAH impedes the growth of glioblastoma and illustrate the need to further study the impact of hypertension on the evolution of brain tumors.

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Section: Methods Animalsmentioning

confidence: 99%

“…25 The C6 glioma is remarkably similar to human GBM with respect to vascularization, morphology, necrosis and hypoxia. [26][27][28] The growth of the tumor and its hemodynamic status were studied by sequential multiparametric magnetic resonance imaging (MRI) and inflammation was analyzed by histochemistry.…”

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confidence: 99%

Chronic arterial hypertension impedes glioma growth: a multiparametric MRI study in the rat

et al. 2015

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“…Across several different human tumor cell lines, including gliomas, mammary ovary, and melanoma carcinomas, VEGF-targeting therapies, including antibodies (e.g., DC-101, bevacizumab) and kinase inhibitors (e.g., sunitinib and semaxanib), create a transient vessel normalization window, leading to improvements in vessel function and a concomitant decrease in hypoxia as assessed by PIMO, PET imaging, or pO 2 electrode measurements (69,78,271,290). In addition, supplemental radiation therapy administered during this normalization window decreases in tumor growth compared with radiation administered outside the normalization window ( P < 0.05), ascribable to a transient decrease of hypoxia.…”

Section: A Use Of Hypoxia Information In Radiation Therapy Planningmentioning

confidence: 99%

The Clinical Importance of Assessing Tumor Hypoxia: Relationship of Tumor Hypoxia to Prognosis and Therapeutic Opportunities

Walsh

Lebedev

Aten³

et al. 2014

Antioxidants & Redox Signaling

348

317

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Tumor hypoxia is a well-established biological phenomenon that affects the curability of solid tumors, regardless of treatment modality. Especially for head and neck cancer patients, tumor hypoxia is linked to poor patient outcomes. Given the biological problems associated with tumor hypoxia, the goal for clinicians has been to identify moderately to severely hypoxic tumors for differential treatment strategies. The ''gold standard'' for detecting and characterizing of tumor hypoxia are the invasive polarographic electrodes. Several less invasive hypoxia assessment techniques have also shown promise for hypoxia assessment. The widespread incorporation of hypoxia information in clinical tumor assessment is severely impeded by several factors, including regulatory hurdles and unclear correlation with potential treatment decisions. There is now an acute need for approved diagnostic technologies for determining the hypoxia status of cancer lesions, as it would enable clinical development of personalized, hypoxia-based therapies, which will ultimately improve outcomes. A number of different techniques for assessing tumor hypoxia have evolved to replace polarographic pO 2 measurements for assessing tumor hypoxia. Several of these modalities, either individually or in combination with other imaging techniques, provide functional and physiological information of tumor hypoxia that can significantly improve the course of treatment. The assessment of tumor hypoxia will be valuable to radiation oncologists, surgeons, and biotechnology and pharmaceutical companies who are engaged in developing hypoxia-based therapies or treatment strategies. Antioxid. Redox Signal. 21, 1516-1554.

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“…No significant difference of SUV (or T/B ratio) was observed between different histopathological subtypes both in 18 PET/CT considered T/B ratio threshold of a fixed value as a parameter to discriminate hypoxic from normoxic tissues [6,10].…”

Section: Hypoxia Detection For Tumormentioning

confidence: 99%

A Comparative Study of Noninvasive Hypoxia Imaging With 18F-Fluoroerythronitroimidazole and 18F-Fluoromisonidazole PET/CT in Patients With Lung Cancer

Zhao

et al. 2016

International Journal of Radiation Oncology*Biology*Physics

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Complementary information from magnetic resonance imaging and 18F-fluoromisonidazole positron emission tomography in the assessment of the response to an antiangiogenic treatment in a rat brain tumor model

Cited by 37 publications

References 39 publications

Chronic arterial hypertension impedes glioma growth: a multiparametric MRI study in the rat

Chronic arterial hypertension impedes glioma growth: a multiparametric MRI study in the rat

The Clinical Importance of Assessing Tumor Hypoxia: Relationship of Tumor Hypoxia to Prognosis and Therapeutic Opportunities

A Comparative Study of Noninvasive Hypoxia Imaging With 18F-Fluoroerythronitroimidazole and 18F-Fluoromisonidazole PET/CT in Patients With Lung Cancer

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