Early effects of boron neutron capture therapy on rat glioma models

Nakagawa, Nobuhiro; Akai, Fumiharu; Fukawa, Norihito; Fujita, Yoshihiko; Suzuki, Minoru; Ono, Koji; Taneda, Mamoru

doi:10.1007/s10014-007-0214-4

Cited by 9 publications

(14 citation statements)

References 30 publications

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“…Among these changed genes, tumour suppression gene, BRCA1, is a known negative regulators of cell growth [29,30]. In accordance with these observations, we found down-regulation of some proliferation-related genes, such as E2F2 and Ki67, which are used as proliferation markers in a variety of tumour types [31][32][33][34][35]. Some cell cycle-related genes, including ATM, ATR, were also increased by MSP58 shRNA treatment, all of which are known to either arrest the cell cycle or inhibit the growth of different cancer cells [36,37].…”

Section: Discussionsupporting

confidence: 84%

RNAi‐mediated inhibition of MSP58 decreases tumour growth, migration and invasion in a human glioma cell line

Lin

Zhang

et al. 2009

J Cellular Molecular Medi

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MSP58, a 58-kD nuclear microspherule protein, is an evolutionarily conserved nuclear protein implicated in the regulation of gene transcription as well as in malignant transformation. An analysis of mRNA expression by real-time PCR revealed that MSP58 was significantly up-regulated in 29% of high-grade glioblastoma tissues as well as in four glioblastoma cell lines. In the present study, we further evaluated the biological functions of MSP58 in U251 glioma cell proliferation, migration, invasion and tumour growth in vivo by specific MSP58 knockdown using short hairpin RNA (shRNA). We found that MSP58 depletion inhibited glioma cell growth, primarily by inducing cell cycle arrest rather than apoptosis. MSP58 depletion also decreased the invasive capability of glioma cells and anchorage-independent colony formation in soft agar. Moreover, suppression of MSP58 expression significantly impaired the growth of glioma xenografts in nude mice. Finally, a cell cycle-associated gene array revealed potential molecular mechanisms contributing to cell cycle arrest in MSP58-depleted glioma cells. In summary, our data highlight the importance of MSP58 in glioma progression and provided a biological basis for MSP58 as a novel candidate target for treatment of glioma.

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Section: Discussionsupporting

confidence: 84%

RNAi‐mediated inhibition of MSP58 decreases tumour growth, migration and invasion in a human glioma cell line

Lin

Zhang

et al. 2009

J Cellular Molecular Medi

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“…They compared a BNCT group with an untreated group using pathological analysis at 4days after BNCT. Compared to the untreated group, C6 rat glioma cell in the BNCT group showed cell swelling on the H & E stained rat brain sections [37]. …”

Section: Discussionmentioning

confidence: 99%

Identification of early and distinct glioblastoma response patterns treated by boron neutron capture therapy not predicted by standard radiographic assessment using functional diffusion map

et al. 2013

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BackgroundRadiologic response of brain tumors is traditionally assessed according to the Macdonald criteria 10 weeks from the start of therapy. Because glioblastoma (GB) responds in days rather than weeks after boron neutron capture therapy (BNCT) that is a form of tumor-selective particle radiation, it is inconvenient to use the Macdonald criteria to assess the therapeutic efficacy of BNCT by gadolinium-magnetic resonance imaging (Gd-MRI). Our study assessed the utility of functional diffusion map (fDM) for evaluating response patterns in GB treated by BNCT.MethodsThe fDM is an image assessment using time-dependent changes of apparent diffusion coefficient (ADC) in tumors on a voxel-by-voxel approach. Other than time-dependent changes of ADC, fDM can automatically assess minimum/maximum ADC, Response Evaluation Criteria In Solid Tumors (RECIST), and the volume of enhanced lesions on Gd-MRI over time. We assessed 17 GB patients treated by BNCT using fDM. Additionally, in order to verify our results, we performed a histopathological examination using F98 rat glioma models.ResultsOnly the volume of tumor with decreased ADC by fDM at 2 days after BNCT was a good predictor for GB patients treated by BNCT (P value = 0.022 by log-rank test and 0.033 by wilcoxon test). In a histopathological examination, brain sections of F98 rat glioma models treated by BNCT showed cell swelling of both the nuclei and the cytoplasm compared with untreated rat glioma models.ConclusionsThe fDM could identify response patterns in BNCT-treated GB earlier than a standard radiographic assessment. Early detection of treatment failure can allow a change or supplementation before tumor progression and might lead to an improvement of GB patients’ prognosis.

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“…Typical indices and radiological measures used to evaluate the tumor response to treatment are the variation in tumor volume, the enhancement area on Gd-MRI and the intensity on T2w-MRI [16,17]. With this method, treatment effects were assessed in pre-clinical rat models [18]. In patients, BNCT treatment effects were assessed in patients treated for high grade gliomas [16,17,19,20], in patients suffering from head and neck cancer (HNC) [21] and for the evaluation of adverse effects in patients treated for brain tumor [22,23].…”

Section: Medical Imaging For Bnct Response Evaluation: Current Use and Future Perspectivesmentioning

confidence: 99%

“…Other radioisotopes than 18 F might be coupled to boron-containing compounds, allowing their tracking and quantification in preclinical studies. Several gold nanoparticles were labeled with iodine ( 123 I [48] or 124 I [49,50]) for mice investigations.…”

Section: Bpa and [ 18 F]fbpa: An Existing First Theranostic Approach In Bnctmentioning

confidence: 99%

Theranostics in Boron Neutron Capture Therapy

Sauerwein

Sancey

Hey‐Hawkins

et al. 2021

Life

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Boron neutron capture therapy (BNCT) has the potential to specifically destroy tumor cells without damaging the tissues infiltrated by the tumor. BNCT is a binary treatment method based on the combination of two agents that have no effect when applied individually: 10B and thermal neutrons. Exclusively, the combination of both produces an effect, whose extent depends on the amount of 10B in the tumor but also on the organs at risk. It is not yet possible to determine the 10B concentration in a specific tissue using non-invasive methods. At present, it is only possible to measure the 10B concentration in blood and to estimate the boron concentration in tissues based on the assumption that there is a fixed uptake of 10B from the blood into tissues. On this imprecise assumption, BNCT can hardly be developed further. A therapeutic approach, combining the boron carrier for therapeutic purposes with an imaging tool, might allow us to determine the 10B concentration in a specific tissue using a non-invasive method. This review provides an overview of the current clinical protocols and preclinical experiments and results on how innovative drug development for boron delivery systems can also incorporate concurrent imaging. The last section focuses on the importance of proteomics for further optimization of BNCT, a highly precise and personalized therapeutic approach.

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Early effects of boron neutron capture therapy on rat glioma models

Cited by 9 publications

References 30 publications

RNAi‐mediated inhibition of MSP58 decreases tumour growth, migration and invasion in a human glioma cell line

RNAi‐mediated inhibition of MSP58 decreases tumour growth, migration and invasion in a human glioma cell line

Identification of early and distinct glioblastoma response patterns treated by boron neutron capture therapy not predicted by standard radiographic assessment using functional diffusion map

Theranostics in Boron Neutron Capture Therapy

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