Feasibility and effectiveness of treatment strategy of tandem high-dose chemotherapy and autologous stem cell transplantation in combination with 131 I-MIBG therapy for high-risk neuroblastoma.

This study was performed to evaluate the safety and effectiveness of tandem HDCT/ASCT combined with targeted radiotherapy using 131 I-MIBG for high-risk neuroblastoma. Patients with high-risk neuroblastoma were treated with 8 to 10 cycles of induction chemotherapy before tandem HDCT/ASCT. Patients received 131 I-MIBG treatment before the second HDCT/ASCT. Local radiotherapy and maintenance therapy were performed after tandem HDCT/ASCT. Between 2012 and 2016, 19 patients were diagnosed with high-risk neuroblastoma in our institution and 18 of them received tandem HDCT/ASCT combined with 131 I-MIBG therapy. For the first HDCT/ASCT regimen, 12 patients received busulfan/melphalan and six patients received melphalan/etoposide/carboplatin. The second HDCT included ThioCy. The median dose of 131 I-MIBG was 17.2 mCi/kg for the first eight patients, while 12 patients in the latter period of the study received reduced dose of 10.7 mCi/kg. The 5-year OS and EFS rates were 79% and 61%, respectively, for all 19 patients with high-risk neuroblastoma, and 83% and 64%, respectively, for 18 patients who completed tandem HDCT/ASCT combined with 131 I-MIBG therapy. Six patients experienced disease relapse and five patients died. Treatment-related mortality was not observed. Among 15 evaluable patients, 11 patients (73%) developed hypothyroidism, six patients (40%) had CKD, and six patients (40%) had growth failure. Hypothyroidism and growth failure were less frequent in patients who received reduced doses of 131 I-MIBG therapy. Tandem HDCT/ASCT combined with HD 131 I-MIBG therapy could be feasible for patients with high-risk neuroblastoma with acceptable toxicity profiles and favorable outcomes.

Radiation therapy is a treatment to be considered for recurrent epithelial ovarian cancer after chemotherapy.

AIMS AND BACKGROUND: Radiation therapy provides a safe and effective alternative treatment option for recurrent epithelial ovarian cancer, although it has not been a treatment of choice. We evaluated the efficacy and toxicity of radiation therapy for recurrent epithelial ovarian cancer after chemotherapy according to the disease status. METHODS: This was a retrospective study of 38 patients with recurrent epithelial ovarian cancer treated with radiation therapy at the Asan Medical Center, Seoul, Korea, between January 1997 and December 2007. We analyzed their clinical characteristics and the outcome of radiation therapy. RESULTS: Thirty-eight patients were treated with radiation therapy. Their median age was 51.5 years. Most patients were FIGO stage III (27/38) with serous adenocarcinoma (26/38). All patients had received at least one regimen of platinum-based chemotherapy; 24 patients were sensitive to the first chemotherapy and the others were resistant. Lymph node and abdominopelvic wall were the most common sites of radiation therapy. The response rate was 65.0% (16 complete remissions and 10 partial remissions), and the median regression rate was 78.8% (range, -66.6 to 100.0). Median progression-free survival was 7.2 months (range, 1.0-66.6). In 28 patients who had a solitary relapsed site from the radiographic finding at the time of radiation therapy, it was 10.7 months (range, 1.8-66.6). Neither hematologic nor intestinal toxicity of grade 3-4 was observed. Prognostic factors were sensitivity to platinum and the site treated with radiation therapy. CONCLUSIONS: Radiation therapy is a treatment that should be considered for recurrent epithelial ovarian cancer, especially in good responders to platinum or patients with solitary relapsed lesions.

Functional characterization of pectin methylesterase inhibitor (PMEI) in wheat.

Pectin, one of the main components of plant cell wall, is deesterified by the pectin methylesterase (PME). PME activity is regulated by inhibitor proteins known as the pectin methylesterase inhibitor (PMEI), which plays a key role in wounding, osmotic stress, senescence and seed development. However, the role of PMEI in many plant species still remains to be elucidated, especially in wheat. To facilitate the expression analysis of the TaPMEI gene, RT-PCR was performed using leaf, stem and root tissues that were treated with exogeneous application of phytohormones and abiotic stresses. High transcription was detected in salicylic acid (SA) and hydrogen peroxide treatments. To elucidate the subcellular localization of the TaPMEI protein, the TaPMEI:GFP fusion construct was transformed into onion epidermal cells by particle bombardment. The fluorescence signal was exclusively detected in the cell wall. Using an enzyme assay, we confirmed that PME was completely inhibited by TaPMEI. These results indicated that TaPMEI was involved in inhibition of pectin methylesterification and may play a role in the plant defense mechanism via cell wall fortification.