BRCA2 is required for neurogenesis and suppression of medulloblastoma. Downregulation of BRCA1-BRCA2-containing complex subunit 3 sensitizes glioma cells to temozolomide. Breast and ovarian cancer predisposition due to de novo BRCA1 and BRCA2 mutations. The BRCA1 and BRCA2 genes in early-onset breast cancer patients. Role of BRCA1 and BRCA2 as regulators of DNA repair, transcription, and cell cycle in response to DNA damage. PARP inhibitor resistance: the underlying mechanisms and clinical implications. Clinical assays for assessment of homologous recombination DNA repair deficiency. Stover EH, Fuh K, Konstantinopoulos PA, Matulonis UA, Liu JF. Repair of strand breaks by homologous recombination. Knockdown of BRCA2 causes DNA damage repair by regulating RAD51-mediated signaling pathway in Daoy cells. Knockdown of BRCA2 increases the sensitivity of medulloblastoma cells to Olaparib and strengthens the efficacy of Olaparib in vitro and in vivo. In addition, the level of RAD51, RAD50, MRE11, and NBS was increased by Olaparib alone but decreased reversely after knockdown of BRCA2 in Daoy cells. In xenograft mice model, tumor volume in Olaparib and Olaparib/shBRCA2 group was 376.12 and 84.95mm 3 when tumor weight was 0.46 g and 0.12 g. However, it was 33.4% after RAD51 was overexpressed. In Daoy cells, apoptotic rate was 26.9% in Olaparib group and 58.9% in Olaparib/shBRCA2 group. Overexpression of RAD51 partially reversed the effect of shBRCA2. The inhibition rate of Olaparib on Daoy or LN229 cells was 61.1%, 66.03% in shBRCA2 group, while it was 42.9%, 41.1% in shNC group. Knockdown of BRCA2 enhanced the inhibitory effect of Olaparib on proliferation of Daoy and LN229 cells. Western blotting technology was used to explore the mechanism of BRCA2. Cell apoptosis was determined by FACS analysis when the in vivo role of BRCA2 was explored with xenograft mice model. MethodsīRCA2 was knocked down by RNAi technology and cell proliferation was detected by CCK-8 assay. To investigate the effects of BRCA2 deficiency combined with Olaparib in medulloblastoma and the mechanism. However, its role in medulloblastoma and the mechanism is not known. All rights reserved.BRCA2 defect exists in glioma and regulates drug resistance of glioma to chemotherapy. Nevertheless, partial arc plans could not offer a statistically significant dose reduction for delineated organs compared to full arc plans, except for bilateral kidneys.ģDCRT CSI Conformity Medulloblastoma PNET Short arc VMAT.Ĭopyright © 2019 American Association of Medical Dosimetrists. However, the VMAT_PA plan exhibited a lower D Body-PTV compared to VMAT_FA plans (0.007 ≤ p < 0.05) in the 1 to 5 Gy range. D95%, V110% and CI did not exhibit a statistically significant difference between partial and full-arc VMAT plans. Average CI shows a similar value for VMAT_FA (0.84 ± 0.04) and VMAT_PA (0.82 ± 0.05) plans. The conformity index (CI) was averaged over both prescription doses. Mean D95% difference between the two VMAT plans did not exceed 1.3% for cranial and spinal targets for both prescription levels. In addition to these VMAT plans, a 3-dimensional conformal radiotherapy plan was also created for all these patients to compare the D Body-PTV and target volume related dose constraints. Spillage dose (D Body-PTV) to Body-PTV (D Body-PTV: dose to body excluding planning target volume) was compared with VMAT_FA and VMAT_PA plans. In both the plans, 360° arc fields were employed for treating cranial volume. For a cohort of 10 patients, 2 VMAT CSI plans were created for each patient, one using the conventional full 360° arc (VMAT_FA) for the spine and the other using 100° posterior arc (VMAT_PA) for 23.4 Gy and 35 Gy prescriptions. This study was aimed to do a dosimetric comparison between the large and shorter spinal arc for CSI. Since 2011 when it was first described, the volumetric-modulated arc therapy (VMAT) technique for craniospinal irradiation (CSI) has always seen the use of large arc lengths for the spine fields ranging from 200° to 360°.
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