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The amount of potentially lethal damage repair (PLDR) is a significant factor in the process of modeling the survival curves of cells irradiated with fractionated carbon beams. Because the amount of PLDR generally depends on the features of the cells and the linear energy transfer (LET), the amount of PLDR of cells irradiated with fractionated carbon beams shows distinct differences from that of cells irradiated with X-rays. This study considered a new parameter dependent on the correlation between the PLDR trait (T) of the cells over a time interval (Δ) at the fractionated carbon beam irradiation. The survival curves of the cells irradiated with fractionated carbon beams n times were predicted using the ζ and the Ψ values from the delay assay. This study aims to overcome the barriers of traditional methods by developing a new survival curve model with new parameters based on an analysis of the PLDR traits of cells over time interval in fractionated carbon beam irradiation and to suggest a model that produces results significantly closer to the experimental data.

Tumor-treating fields (TTFs) - a type of electromagnetic field-based therapy using low-intensity electrical fields - has recently been characterized as a potential anticancer therapy for glioblastoma multiforme (GBM). However, the molecular mechanisms involved remain poorly understood. Our results show that the activation of autophagy contributes to the TTF-induced anti-GBM activity in vitro or in vivo and GBM patient stem cells or primary in vivo culture systems. TTF-treatment upregulated several autophagy-related genes (~2-fold) and induced cytomorphological changes. TTF-induced autophagy in GBM was associated with decreased Akt2 expression, not Akt1 or Akt3, via the mTOR/p70S6K pathway. An Affymetrix GeneChip miRNA 4.0 Array analysis revealed that TTFs altered the expression of many microRNAs (miRNAs). TTF-induced autophagy upregulated miR-29b, which subsequently suppressed the Akt signaling pathway. A luciferase reporter assay confirmed that TTFs induced miR-29b to target Akt2, negatively affecting Akt2 expression thereby triggering autophagy. TTF-induced autophagy suppressed tumor growth in GBM mouse models subjected to TTFs as determined by positron emission tomography and computed tomography (PET-CT). GBM patient stem cells and a primary in vivo culture system with high Akt2 levels also showed TTF-induced inhibition. Taken together, our results identified autophagy as a critical cell death pathway triggered by TTFs in GBM and indicate that TTF is a potential treatment option for GBM.

The purpose of this study was to investigate the potential of gold nanoparticles as radiosensitizer for use in neutron therapy against hepatocellular carcinoma. The hepatocellular carcinoma cells lines Huh7 and HepG2 were irradiated with γ and neutron radiation in the presence or absence of gold nanoparticles. Effects were evaluated by transmission electron microscopy, cell survival, cell cycle, DNA damage, migration, and invasiveness. Gold nanoparticles significantly enhanced the radiosensitivity of Huh7 and HepG2 cells to γ-rays by 1.41- and 1.16-fold, respectively, and by 1.80- and 1.35-fold to neutron radiation, which has high linear energy transfer. Accordingly, exposure to neutron radiation in the presence of gold nanoparticles induced cell cycle arrest, DNA damage, and cell death to a significantly higher extent, and suppressed cell migration and invasiveness more robustly. These effects are presumably due to the ability of gold nanoparticles to amplify the effective dose from neutron radiation more efficiently. The data suggest that gold nanoparticles may be clinically useful in combination therapy against hepatocellular carcinoma by enhancing the toxicity of radiation with high linear energy transfer.

Glioblastoma, the most common primary brain tumor in adults, is an incurable malignancy with poor short-term survival and is typically treated with radiotherapy along with temozolomide. While the development of tumor-treating fields (TTFields), electric fields with alternating low and intermediate intensity has facilitated glioblastoma treatment, clinical outcomes of TTFields are reportedly inconsistent. However, combinatorial administration of chemotherapy with TTFields has proven effective for glioblastoma patients. Sorafenib, an anti-proliferative and apoptogenic agent, is used as first-line treatment for glioblastoma. This study aimed to investigate the effect of sorafenib on TTFields-induced anti-tumor and anti-angiogenesis responses in glioblastoma cells in vitro and in vivo. Sorafenib sensitized glioblastoma cells to TTFields, as evident from significantly decreased post-TTFields cell viability ( < 0.05), and combinatorial treatment with sorafenib and TTFields accelerated apoptosis via reactive oxygen species (ROS) generation, as evident from Poly (ADP-ribose) polymerase (PARP) cleavage. Furthermore, use of sorafenib plus TTFields increased autophagy, as evident from LC3 upregulation and autophagic vacuole formation. Cell cycle markers accumulated, and cells underwent a G2/M arrest, with an increased G0/G1 cell ratio. In addition, the combinatorial treatment significantly inhibited tumor cell motility and invasiveness, and angiogenesis. Our results suggest that combination therapy with sorafenib and TTFields is slightly better than each individual therapy and could potentially be used to treat glioblastoma in clinic, which requires further studies.

This study estimated the planning quality of intensity-modulated radiotherapy in 42 lung cancer cases to provide preliminary data for the development of a planning quality assurance algorithm. Organs in or near the thoracic cavity (ipsilateral lung, contralateral lung, heart, liver, esophagus, spinal cord, and bronchus) were selected as organs at risk (OARs). Radiotherapy plans were compared using the conformity index (CI), coverage index (CVI), and homogeneity index (HI) of the planning target volume (PTV), OAR-PTV distance and OAR-PTV overlap volume, and the V10Gy, V20Gy, and equivalent uniform dose (EUD) of the OARs. The CI, CVI, and HI of the PTV were 0.54 - 0.89 , 0.90 - 1.00 , and 0.11 - 0.41, respectively. The mean EUDs (V10Gy, V20Gy) of the ipsilateral lung, contralateral lung, esophagus, cord, liver, heart, and bronchus were 8.07 Gy (28.06, 13.17), 2.59 Gy (6.53, 1.18), 7.02 Gy (26.17, 12.32), 3.56 Gy (13.56, 4.48), 0.72 Gy (2.15, 0.91), 5.14 Gy (19.68, 8.62), and 10.56 Gy (36.08, 19.79), respectively. EUDs tended to decrease as OAR-PTV distance increased and OAR-PTV overlap volume decreased. Because the plans in this study were from a single department, relatively few people were involved in treatment planning. Differences in treatment results for a given patient would be much more pronounced if many departments were involved.

In these days, 3D-printer is on the rise in various fields including radiation therapy. This preliminary study aimed to estimate the dose characteristics of the 3D-printer materials which could be used as the compensator or immobilizer in radiation treatment. The cubes which have 5cm length and different densities as 50%, 75% and 100% were printed by 3D-printer. A planning CT scans for cubes were performed using a CT simulator (Brilliance CT, Philips Medical System, Netherlands). Dose distributions behind the cube were calculated when 6MV photon beam passed through cube. The dose response for 3D-printed cube, air and water were measured by using EBT3 film and 2D array detector. When results of air case were normalized to 100, dose calculated by TPS and measured dose of 50% and 75% cube were 96~99. Measured and calculated doses of water and 100% cube were 82~84. HU values of 50%, 75% and 100% were -910, -860 and -10, respectively. From these results, 3D-printer in radiotherapy could be used for medical purpose accurately.