To provide baseline information for the "local" therapy of the glioblastoma multiforme (GBM), whole-brain histological sections of 15 untreated GBM's were studied to determine the distribution of neoplastic cells. These findings were then compared with the computerized tomography (CT) scans in 11 cases in order to determine the extent to which the peripheral portion of the neoplasm can be estimated by the presence of a low-density area without contrast enhancement. The results of the histological study confirmed the marked heterogeneity of GBM's and disclosed a great variability in the geometry, extent, and character of the peripheral "infiltrating" margin. In spite of the widely held concept that glioblastomas are localized within 2 cm of the contrast-enhanced rim, there were three cases in this two-dimensional study in which this distance was exceeded, and it seems likely that three-dimensional reconstructions would have detected additional cases in which neoplastic cells extended beyond this arbitrary limit. Only three of the 15 GBM's were restricted to the distribution of one internal carotid or one vertebral artery. To the extent that the neoplasms in the present series are representative, this suggests that glioblastomas will be difficult to treat successfully by intra-arterial therapy using existing therapeutic agents. Correlations of histological sections with the CT scans revealed that the vast majority of the neoplastic tissue was contained within the contrast-enhancing and "peritumoral" areas of low density, but that in five cases fingers of neoplasm extended for short distances beyond the outer margin of the latter region. This indicates that the distribution of cells of a GBM cannot be inferred from CT images since the "peritumoral" area of low density can over- or underestimate the extent of the lesion.
There are a few reports suggesting that rituximab (RTX) might be a risk for interstitial pneumonitis (IP). We also experienced such patients in the era of RTX. Here, we reviewed all the patients with non-Hodgkin lymphoma who were treated with RTX-CHOP-like regimen (R-CHOP) to determine the risk of developing IP. One of 59 (1.7%) patients who received CHOP alone and 8 of 129 (6.2%) patients who were treated with R-CHOP experienced IP (p = 0.28). Furthermore, three of eight patients who have had IP during R-CHOP were confirmed having Pneumocystis jirovecii pneumonia (PCP). PCP occurred during the fourth, sixth, and seventh cycle of chemotherapy, respectively. Among the patients treated by R-CHOP, 3 of 32 (9%) patients whose lymphocyte counts were <1000/microL before chemotherapy developed PCP, while 70 patients whose lymphocyte counts were >1000/microL did not (p = 0.03). In four of eight patients, IP occurred during the administration of granulocyte-colony stimulating factor. RTX seems to have a certain risk to induce IP including PCP. Patients with lymphoma who were treated by R-CHOP regimen, might be considered as PCP prophylactic, especially if the number of lymphocytes is low at the beginning of chemotherapy.
Hodgkin and Reed-Sternberg (H & RS) cells are generally considered to be the neoplastic cells of Hodgkin's disease (HD), however such cells are only found in a minority of the lesions. Recently in a few studies on HD, the clonality of H & RS cells was examined, using a single-cell polymerase chain reaction (PCR) examination. To clarify the lineage and clonality of H & RS cells, we performed single cell PCR and in situ hybridization (ISH), and nine cases of classical HD were thus studied. By ISH, the immunoglobulin J chain, and the kappa and lambda light chain were rarely expressed in the H & RS cells, however, no T-cell markers could be detected. The expression of the recombination activating genes (RAG-1, 2) could be determined in the H & RS cells. We isolated CD30+ H & RS cells, CD3 + T cells and CD20 + B cells from suspended materials using a mechanical sorter. We performed single cell PCR in a sorted individual cell, to amplify the complementarity determining region of the Ig heavy chain (IgH) gene and T-cell receptor gamma chain (TCR gamma) gene. In all cases, TCR gamma could be frequently amplified in the T cells, but was only rarely amplified in the H & RS and B cells. In contrast, the IgH was frequently amplified in the H & RS and B cells, but not in the T cells. In addition, the PCR production of the H & RS cells all showed different lengths. The results therefore support the polyclonal nature and immature B lymphoid cell origin of H & RS cells.
Background: Paclitaxel has been approved for 3-weekly administration in Japan. Recent reports suggest that weekly paclitaxel can achieve a higher tumor response and lower toxicity. Methods: This study was designed to investigate the usefulness and tolerability of weekly paclitaxel by 1-hour infusion in patients with metastatic breast cancer who were previously treated with docetaxel or other anticancer agents. Results: Thirty-five patients were enrolled. The overall response rate was 41.2% (14/34, 95% confidence interval: 24.6–59.3%). The median time to progression and the median survival time were 218.5 and 624 days, respectively. One patient developed dyspnea, probably induced by a hypersensitivity reaction. The most common hematological toxicities were leukopenia and neutropenia, although no patients developed grade 4 leukopenia or neutropenia and G-CSF support was not required. Conclusions: Weekly paclitaxel could be safely administered and achieved a relatively high response rate. Weekly paclitaxel would be a good candidate second-line therapy for recurrent or advanced breast cancer.
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