Brachytherapy is an invasive therapy with placement of radiation source into or near the tumor. The difference between planning target volume and clinical target volume is minimal, and the dose out of the tumor reduces rapidly due to the inverse-square law. High-dose-rate brachytherapy enables three-dimensional image guidance, and currently, tumor dose as well as doses of the surrounding normal structures can be evaluated accurately. High-dose-rate brachytherapy is the utmost precision radiation therapy even surpassing carbon ion therapy. Biological disadvantages of high-dose rate have been overcome by the fractional irradiation. High-dose-rate brachytherapy is indispensable in the definitive radiation therapy of cervical cancer. Also in prostate cancer and breast cancer, high-dose-rate brachytherapy plays a significant role. Brachytherapy requires techniques and skills of radiation oncologists at the time of invasive placement of the radiation source into the tumor area. Education of young radiation oncologists is most urgent and important.
We report a case of post-operative local recurrence of castration-resistant prostate cancer with multiple bulky bladder invasions treated using external beam radiotherapy (EBRT) followed by a high-dose-rate brachytherapy (HDR-BT) boost. The EBRT dose was 46 Gy delivered in 23 fractions with intensity-modulated radiotherapy to the entire pelvis. The HDR-BT dose was 15 Gy delivered in 1 fraction using ultrasound, CT, and MRI-guided brachytherapy with 18 interstitial needles. We achieved excellent local control of cancer in the prostate bed and multiple bulky bladder invasions. EBRT plus HDR-BT boost can allow higher doses to be delivered than EBRT alone for locally recurrent bulky prostate cancer following prostatectomy.
Purpose: In defining the biological effects of the 10B(n, α)7Li neutron capture reaction, we have proposed a deterministic parsing model (ISHIYAMA-IMAHORI model) to determine the Compound Biological Effectiveness (CBE) factor in Borono-Phenyl-Alanine (BPA)-mediated Boron Neutron Capture Therapy (BNCT). In present paper, we demonstrate a specific method of how the application of the case of application to actual patient data, which is founded on this model for tissues and tumor. Method: To determine the CBE factor, we derived the following new calculation formula founded on the deterministic parsing model with three constants, CBE0, F, n and the eigen value Nth/Nmax. (1), where, Nth and Nmax are the threshold value of boron concentration of N and saturation boron density and CBE0, F and n are given as 0.5, 8 and 3, respectively. In order to determine Nth and Nmax in the formula, sigmoid logistic function was employed for 10B concentration data, Db(t) obtained by dynamic PET technique. (2), where, A, a and t0 are constants. Results and Conclusion: From the application of sigmoid function to dynamic PET data, it is concluded that the Nth and Nmax for tissue and tumor are identified with the parameter constants in the sigmoid function in Equation (2) as: (3). And the calculated CBE factor values obtained from Equation (1), with Nth/Nmax.
Abstract Background Recent improvement of machinery evaluation for the skin changes in various therapies enabled us to evaluate fine changes quantitatively. In this study, we performed evaluation of the changes in radiation dermatitis (RD) using quantitative and qualitative methods, and verified the validity of the conventional qualitative assessment for clinical use. Methods Forty-three breast cancer patients received conventional fractionated radiotherapy to whole breast after breast-conserving surgery. Erythema, pigmentation and skin dryness were evaluated qualitatively, and biophysical parameters of RD were measured using a Multi-Display Device MDD4 with a Corneometer for capacitance, a Tewameter for transepidermal water loss (TEWL), a Mexameter for erythema index and melanin index. Measurements were performed periodically until 1 year. Results The quantitative manifestations developed serially from skin erythema followed by dryness and pigmentation. Quantitative measurements detected the effects of irradiation earlier than that of qualitative indices. However, the grades of the domains in RD by qualitative and quantitative assessment showed similar time courses and peak periods. However, no significant correlation was observed between the skin dryness grade and skin barrier function. In contrast to serial increase in pigmentation grades, melanin index showed initial decrease followed by marked increase with significant correlation with pigmentation grades. Conclusion Subjectively and objectively measured results of RD were almost similar course and peak points through the study. Therefore, validity of the conventional qualitative scoring for RD is confirmed by the present quantitative assessments. Instrumental evaluations revealed the presence of modest inflammatory changes before radiotherapy and long-lasting skin dryness, suggesting indication of intervention for RD.
PolyADP-ribosylation is a post-translational modification of proteins, and poly(ADP-ribose) (PAR) polymerase (PARP) family proteins synthesize PAR using NAD as a substrate. Poly(ADP-ribose) glycohydrolase (PARG) functions as the main enzyme for the degradation of PAR. In this study, we investigated the effects of Parg deficiency on tumorigenesis and therapeutic efficacy of DNA damaging agents, using mouse ES cell-derived tumor models. To examine the effects of Parg deficiency on tumorigenesis, Parg+/+ and Parg-/- ES cells were subcutaneously injected into nude mice. The results showed that Parg deficiency delays early onset of tumorigenesis from ES cells. All the tumors were phenotypically similar to teratocarcinoma and microscopic findings indicated that differentiation spectrum was similar between the Parg genotypes. The augmented anti-tumor therapeutic effects of X-irradiation were observed under Parg deficiency. These results suggest that Parg deficiency suppresses early stages of tumorigenesis and that Parg inhibition, in combination with DNA damaging agents, may efficiently control tumor growth in particular types of germ cell tumors.