No abstract

Summary:with acute myelogenous leukemia (AML). 1,2 However, most will relapse despite consolidation and maintenance chemotherapy. Therefore, post-remission therapy is one of The safety and efficacy of myeloablative therapy followed by autologous peripheral blood stem cell transthe most important issues in the treatment of AML. An increasing number of AML patients have been treated with plantation (ABSCT) for acute myelogenous leukemia (AML) were evaluated in 60 patients. Peripheral blood intensified consolidation chemotherapy, autologous bone marrow transplantation (BMT), or allogeneic BMT. ditioning regimen and graft-versus-leukemia (GVL) effects. 5 Nevertheless, in addition to the requirement of was used for pretransplant conditioning in 13 patients. For the remaining 47 patients, granulocyte colony-HLA-identical marrow donors, transplant-related morbidity and mortality remain the major obstacles to improving stimulating factor (G-CSF) was administered concurrently with the BEA regimen during conditioning.clinical results of allogeneic BMT. In autologous BMT, regimen-related toxicities are fewer, although a GVL effect Unpurged, cryopreserved PBSC containing a median number of 5.4 × 10 8 MNC/kg or 12 × 10 4 CFU-GM/kg cannot be obtained. One randomized study has demonstrated that patients treated with autologous BMT have were reinfused at transplantation. The median number of days to granulocytes exceeding 500/l and last platesuperior disease-free survivals (DFS) to those receiving intensive chemotherapy alone.3 let transfusion were 15 (8-44) and 24 (0-Ͼ180), respectively. The 3-year probabilities of disease-free survival Recently, autologous peripheral blood stem cell transplantation (ABSCT) has begun to replace autologous BMT (DFS) and relapse were 78.6 and 21.4% for patients transplanted in first remission, 29.6 and 64.4% for those because of rapid engraftment and low transplant-related mortality. 6-11 However, high relapse rates have been in second or third remission, and 11.1 and 77.8% for those in relapse, respectively. There were no transplantreported after ABSCT for AML. from all patients or responsible family members.

No abstract

Glioblastoma (GB) often has loss of heterozygosity on the chromosomes, 1p, 10p, 10q, 11p, 17p, 19q, 22q, and several others. In the case of chromosome 12q; however, it remains to be seen whether LOH occurs. Apaf‐1, the apoptotic protease activating factor‐1, located at chromosome 12q22‐23, is a major effecter of the p53 mediated apoptosis pathway, and Apaf‐1 inactivation due to chromosome 12q22‐23 LOH and hypermethylation may be involved in some of the neoplasms in malignancy. However, little is known about the frequency of the 12q22‐23 LOH or the state of Apaf‐1 in GB. To elucidate their involvement in GB, we analyzed a series of 33 GBs for chromosome 12q22‐23 LOH, Apaf‐1 mRNA expression, and Apaf‐1 protein expression, using microsatellite analysis, reverse transcription (RT) ‐PCR analysis, and immunohistochemical (IHC) analysis, respectively. We also evaluated if and how the 12q22‐23 LOH correlated with the p53 gene mutation and EGFR gene amplification. Chromosome 12q22‐23 LOH was detected in 14 (42%) of 33 cases. Among the examined cases with LOH at 12q22‐23, a low expression of Apaf‐1 mRNA was detected in 9 (69%) of 13 cases, and a low expression of Apaf‐1 protein was detected in 12 (86%) of 14 cases. The 12q22‐23 LOH was significantly correlated with low expression of mRNA and protein (p<0.05, p<0.001 respectively). The p53 gene mutation and EGFR gene amplification were found in 13 cases (39%) and 8 cases (24%), respectively, and these gene alterations were inversely correlated. However, 12q22‐23 LOH had no correlations with the p53 gene mutation or EGFR gene amplification. Six of 9 GBs (67%) with neither p53 gene mutation nor EGFR gene amplification tested positive for 12q22‐23 LOH. These GBs are likely to belong to another subset independent from the 2 common genetic subsets in GB (one with p53 gene mutation and without EGFR gene amplification, and the other with EGFR gene amplification and without p53 gene mutation). Twenty‐three (70%) out of the 33 GBs with the 12q22‐23 LOH also tested positive for Apaf‐1 inactivation or p53 gene mutation. This high frequency of alterations in the apoptosis‐associated factors prompts a speculation that abrogation of the Apaf‐1 and p53 mediated apoptosis pathway may play an important role in the tumorigenesis of GB.

Quantitative and qualitative tissue characterization of carotid plaques using MDCT might be a useful predictor for silent ischemic lesions after CAS.