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5. Stereotactic radiotherapy for locally recurrent nasopharyngeal carcinoma.

Author

Mitsuhashi N, Sakurai H, Katano S, Kurosaki H, Hasegawa M, Akimoto T, Nozaki M, Hayakawa K, Niibe H, Mitsuhashi, N, Sakurai, H, Katano, S, Kurosaki, H, Hasegawa, M, Akimoto, T, Nozaki, M, Hayakawa, K, and Niibe, H

Abstract

Objective: To determine the efficacy of stereotactic radiotherapy (SRT) in the treatment of recurrent nasopharyngeal carcinoma.Study Design: A retrospective review of the outcome of SRT for patients with recurrent nasopharyngeal carcinomas following definitive conventional radiation therapy.Methods: Five patients were treated with daily static multiportal irradiation. Two Gy was administered with eight isocentric portals in a single plane 5 days a week, and the plane was changed for every 20 to 30 Gy. Of these patients, three had poorly differentiated squamous cell carcinoma. Tumor sizes ranged from 1 to 15 cm3, with a median size 3.2 cm3. Median follow-up time from SRT was 34 months (range, 4-61 mo).Results: Four of five recurrent tumors responded well and achieved complete regression. Three patients have survived without evidence of local recurrence with a median follow-up time of 34 months. Marginal recurrence was observed at the posterosuperior wall in a patient with adenoid cystic carcinoma at 30 months after SRT. One patient who received SRT after the two complete courses of radiation therapy died 6 months after SRT as a result of rupture of a branch of the left carotid artery, but autopsy revealed no local residual tumor.Conclusions: Stereotactic radiotherapy with isocentric multiportals in one plane, which is changed at every 20 to 30 Gy, can provide local control with acceptable toxicity in patients with recurrent nasopharyngeal carcinoma, but increased clinical experience and longer follow-up will be necessary to evaluate the overall role of this technique in nasopharyngeal carcinoma. [ABSTRACT FROM AUTHOR]

Published
1999

17. Patterns of Care Study of Radiation Therapy for Esophageal Cancer in Japan: Influence of the Stratification of Institution on the Process

Author

Teshima, T., primary, Abe, M., additional, Ikeda, H., additional, Hanks, G. E., additional, Owen, J. B., additional, Hiraoka, M., additional, Hirokawa, Y., additional, Oguchi, M., additional, Nishio, M., additional, Yamashita, T., additional, Niibe, H., additional, Masuda, K., additional, Watanabe, S., additional, and Inoue, T., additional

Published
1998
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38. Interaction between low dose-rate irradiation, mild hyperthermia and low-dose caffeine in a human lung cancer cell line.

Author

Sakurai, H., Mitsuhashi, N., Tamaki, Y., Akimoto, T., Murata, O., Kitamoto, Y., Maebayashi, K., Ishikawa, H., Hayakawa, K., and Niibe, H.

Subjects
PHYSIOLOGICAL effects of radiation, FEVER, CAFFEINE
Abstract

Purpose: To investigate cell killing by means of low dose-rate irradiation (LDRI) combined with concurrent mild hyperthermia and to determine the effect of low-dose caffeine on this combination treatment. Materials and methods: Human lung adenocarcinoma cells, LK87, were treated with LDRI (50cGy/h) in combination with mild hyperthermia at 41 C and low-dose caffeine (1mm). Cell survival was estimated by clonogenic assay. Flow-cytometry was performed with PI staining using FACScan. Heat-shock protein (HSP72/73) was measured by the Western blotting method. All treatments were simultaneously performed for up to 48h (24Gy). Results: LDRI cytotoxicities were enhanced by hyperthermia at 41 C. D0 calculated from the dose-response curve for LDRI combined with 41 C was 3.46Gy whereas it was 6.55Gy for LDRI alone. The survival curve for LDRI+41 C demonstrated no chronic thermotolerance up to 48h. For LDRI+simultaneous low-dose caffeine, cell killing was also enhanced, where D0 was 3.38Gy at 37 C. Radiosensitization caused by caffeine was enhanced by combination with simultaneous mild hyperthermia at 41 C, where D0=1.78Gy. Cell cycle analysis demonstrated remarkable G2 and mild G1 arrest for LDRI alone, but only G arrest was observed for L1DRI combined with 41 C and for LDRI combined with caffeine. Strong and early G1 arrest was observed in the treatment with LDRI+caffeine at 41 C. The amount of HSP72/73 in the combination of LDRI with caffeine at 41 C was less than that at 41 C alone. Conclusion: LDRI cytotoxicity was enhanced by non-lethal hyperthermia. Low dose caffeine produced further cell killing in the combination of LDRI with mild hyperthermia. [ABSTRACT FROM AUTHOR]

Published
1999
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39. Cytotoxic effect of paclitaxel (taxol) either alone or in combination with irradiation in two rat yolk sac tumour cell lines with different radiosensitivities in vitro.

Author

Saito, Y., Mitsuhashi, N., Takahashi, T., Sakurai, H., Nozaki, M., Ishikawa, H., Nasu, S., Hayakawa, K., and Niibe, H.

Subjects
PACLITAXEL, RADIOBIOLOGY
Abstract

Abstract. Purpose: To investigate the differences between two rat yolk sac tumour cell lines with different radiosensitivities in paclitaxel sensitivity and in the sensitizing effects of paclitaxel in combination with irradiation. Materials and methods: NMT-1 is a parent radiosensitive cell line and NMT-1R is a variant radioresistant cell line. Results: Clonogenic assay demonstrated almost the same paclitaxel sensitivity with D of 5.15 nm in NMT-1 and 5.02 nm in NMT-1R. o Many apoptotic cells and DNA ladder formations were observed at 24 h after exposure to paclitaxel in both cell lines. The incidence of DNA fragmentation after 24 h exposure to 20 nm paclitaxel was 12.4 3.3% for NMT-1, and 13.0 1.9% for NMT-1R. Paclitaxel showed a supra-additive effect in combination with irradiation in both cell lines at 12 h after paclitaxel treatment only when the accumulation of cells in the G /M phase reached 2 its peak. Conclusions: Paclitaxel had the same cytotoxic effect in two cell lines with different radiosensitivity due to the induction of apoptosis. A supra-additive effect to radiation was observed with 12 h pretreatment in both cell lines. Paclitaxel may be effective for tumours with a component of different radiosensitivity in combination with irradiation. [ABSTRACT FROM AUTHOR]

Published
1998
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