Dorothea Nagel — Page 2

PubMed2002

Magnetic resonance imaging as a supplement for the clinical staging system of Durie and Salmon?

BACKGROUND: This study evaluated the prognostic value of a three-grade staging system of spinal involvement using magnetic resonance imaging (MRI) in patients with multiple myeloma and determined its usefulness as an independent parameter in the staging system of Durie and Salmon. METHODS: Seventy-seven previously untreated patients with multiple myeloma underwent MRI of the thoracic and lumbar spine with unenhanced T1-weighted spin echo and short-tau inversion time inversion recovery sequences. The patients were evaluated according to their infiltration patterns and the extent of bone marrow involvement was staged using a three-grade scale: Stage I, no focal or diffuse infiltration; Stage II, 1-10 foci or mild diffuse infiltration; Stage III, more than 10 foci or strong diffuse infiltration. RESULTS: The infiltration patterns had no significant effect on survival. Of 77 patients, 25 would have been understaged using the standard staging system of Durie and Salmon without the findings of MRI and 8 patients would have been understaged if the staging was based only on MRI. The combination of the staging system of Durie and Salmon and MRI was highly significant with respect to survival (P < 0.0001, log rank analysis). MRI staging I-III was independent of the staging system of Durie and Salmon (Cox regression model). CONCLUSIONS: A three-grade staging of spinal MRI provides a significant prognostic tool for patients with multiple myeloma. The authors propose including it in the staging system of Durie and Salmon.

Aged↗

PubMedDate not supplied

Nucleosomes indicate the in vitro radiosensitivity of irradiated bronchoepithelial and lung cancer cells.

Nucleosomes, which are typical cell death products, are elevated in the serum of cancer patients and are known to rapidly increase during radiotherapy. As both normal and malignant cells are damaged by irradiation, we investigated to which extent both cell types contribute to the release of nucleosomes. We cultured monolayers of normal bronchoepithelial lung cells (BEAS-2B, n = 18) and epithelial lung cancer cells (EPLC, n = 18), exposed them to various radiation doses (0, 10 and 30 Gy) and observed them for 5 days. Culture medium was changed every 24 h. Subsequently, nucleosomes were determined in the supernatant by the Cell Death Detection-ELISA(plus) (Roche Diagnostics). Additionally, the cell number was estimated after harvesting the cells in a second preparation. After 5 days, the cell number of BEAS-2B cultures in the irradiated groups (10 Gy: median 0.03 x 10(6) cells/culture, range 0.02-0.08 x 10(6) cells/culture; 30 Gy: median 0.08 x 10(6) cells/culture, range 0.02-0.14 x 10(6) cells/culture) decreased significantly (10 Gy: p = 0.005; 30 Gy p = 0.005; Wilcoxon test) compared to the non-irradiated control group (median 4.81 x 10(6) cells/culture, range 1.50-9.54 x 10(6) cells/culture). Consistently, nucleosomes remained low in the supernatant of non-irradiated BEAS-2B. However, at 10 Gy, BEAS-2B showed a considerably increasing release of nucleosomes, with a maximum at 72 h (before irradiation: 0.24 x 10(3) arbitrary units, AU, range 0.13-4.09 x 10(3) AU, and after 72 h: 1.94 x 10(3) AU, range 0.11-5.70 x 10(3) AU). At 30 Gy, the release was even stronger, reaching the maximum earlier (at 48 h, 11.09 x 10(3) AU, range 6.89-18.28 x 10(3) AU). In non-irradiated EPLC, nucleosomes constantly increased slightly. At 10 Gy, we observed a considerably higher release of nucleosomes in EPLC, with a maximum at 72 h (before irradiation: 2.79 x 10(3) AU, range 2.42-3.80 x 10(3) AU, and after 72 h: 7.16 x 10(3) AU, range 4.30-16.20 x 10(3) AU), which was more than 3.5 times higher than in BEAS-2B. At 30 Gy, the maximum (6.22 x 10(3) AU, range 5.13-9.71 x 10(3) AU) was observed already after 24 h. These results indicate that normal bronchoepithelial and malignant lung cancer cells contribute to the release of nucleosomes during irradiation in a dose- and time-dependent manner with cancer cells having a stronger impact at low doses.

Cell Death↗