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Your search keyword '"K. Harashima"' showing total 3 results
Start Over Author "K. Harashima" Journal anticancer research
3 results on '"K. Harashima"'

1. Cytotoxic enhancement of low dose-rate irradiation in human lung cancer cells by mild hyperthermia

Author

H, Sakurai, N, Mitsuhashi, Y, Kitamoto, T, Nonaka, K, Harashima, K, Higuchi, H, Muramatsu, T, Ebara, H, Ishikawa, and H, Niibe

Subjects
Hot Temperature, Lung Neoplasms, Time Factors, Cell Survival, Dose-Response Relationship, Radiation, DNA, Neoplasm, Hyperthermia, Induced, Flow Cytometry, Polymerase Chain Reaction, Cesium Radioisotopes, Tumor Cells, Cultured, Humans, Polymorphism, Single-Stranded Conformational, Tumor Stem Cell Assay
Abstract

The aim of this study was to investigate the cell killing induced by low dose-rate irradiation (LDRI) simultaneously combined with long duration mild hyperthermia in LK87 human lung cancer cells. Cell cycle alteration due to this combined treatment was also observed.Human lung adenocarcinoma cells, LK87, were treated with concurrent LDRI (50 cGy/hr) and mild hyperthermia (38 to 42 degrees C). Cell survival was estimated by clonogenic assay. Flow cytometry was performed with FACScan. The treatments were simultaneously performed for up to 48 hr (24 Gy).Survival curves of mild hyperthermia alone revealed development of chronic thermotolerance up to 48 hr, whereas LDRI plus hyperthermia caused an exponential decrease in survival. The LDRI cytotoxicities were enhanced by mild hyperthermia over a non-lethal temperature range. The Do values calculated from dose response curves at 37, 38, 39, 40, 41 41.5 and 42 degrees C were 6.55, 5.25, 4.24, 3.99, 3.46, 1.83 and 0.70 Gy, respectively. Cell cycle analysis demonstrated a remarkable G2 and a mild G1 block for LDRI alone, but only a G1 block was observed for LDRI combined with 41 degrees C hyperthermia.The LDRI cytotoxicity was enhanced by long duration mild temperature hyperthermia. The suppression of chronic thermotolerance was considered to be a mechanism involved in this sensitization.

Published
1998

2. Selective inhibition of survival signal transduction pathways enhanced radiosensitivity in human esophageal cancer cell lines in vitro.

Author

Akimoto T, Nonaka T, Harashima K, Ishikawa H, Sakurai H, and Mitsuhashi N

Subjects
Caspase 3, Caspase Inhibitors, Caspases metabolism, Cell Line, Tumor, Chromones pharmacology, Combined Modality Therapy, Enzyme Activation drug effects, Enzyme Activation radiation effects, Esophageal Neoplasms drug therapy, Esophageal Neoplasms enzymology, Flavonoids pharmacology, Humans, MAP Kinase Kinase Kinases antagonists & inhibitors, Morpholines pharmacology, Phosphoinositide-3 Kinase Inhibitors, Poly(ADP-ribose) Polymerases metabolism, Quinazolines, Radiation Tolerance physiology, Radiation-Sensitizing Agents pharmacology, Radiography, Signal Transduction drug effects, Signal Transduction radiation effects, Tyrphostins pharmacology, Enzyme Inhibitors pharmacology, Esophageal Neoplasms diagnostic imaging, MAP Kinase Kinase Kinase 1, Protein Kinase Inhibitors, Radiation Tolerance drug effects
Abstract

Purpose: The purpose of this study was to examine how selective inhibition of the survival signal transduction pathways affects radiosensitivity in human cancer cell lines., Materials and Methods: Two human esophageal cancer cell lines, TE-1 (mutant p53) and TE2 (wild-type p53), were used. To inhibit the pathways selectively, 3 specific kinase inhibitors, AG1478 (an inhibitor of EGFR), PD98059 (an inhibitor of MEK) and LY294002 (an inhibitor of PI3K), were combined with radiation., Results: Radiation in combination with these kinase inhibitors potentiated radiation-induced cell killing synergistically. Enhancement ratios were greater in TE-2 than those in TE-1. Radiation in combination with kinase inhibitors increased the expression of the active form of caspase-3 and the PARP cleavage only in TE-2 that has wild-type p53., Conclusion: Targeting the key molecules of the survival signal transduction pathway resulted in potentiation of radiation-induced cell killing. The results of this study suggest that the survival signal transduction pathways would be a molecular target in enhancing radiosensitivity.

Published
2004

3. Cytotoxic enhancement of low dose-rate irradiation in human lung cancer cells by mild hyperthermia.

Author

Sakurai H, Mitsuhashi N, Kitamoto Y, Nonaka T, Harashima K, Higuchi K, Muramatsu H, Ebara T, Ishikawa H, and Niibe H

Subjects
Cell Survival radiation effects, Cesium Radioisotopes, DNA, Neoplasm analysis, DNA, Neoplasm radiation effects, Dose-Response Relationship, Radiation, Flow Cytometry, Hot Temperature, Humans, Lung Neoplasms, Polymerase Chain Reaction, Polymorphism, Single-Stranded Conformational, Time Factors, Tumor Cells, Cultured, Tumor Stem Cell Assay, Cell Survival physiology, Hyperthermia, Induced
Abstract

Purpose: The aim of this study was to investigate the cell killing induced by low dose-rate irradiation (LDRI) simultaneously combined with long duration mild hyperthermia in LK87 human lung cancer cells. Cell cycle alteration due to this combined treatment was also observed., Materials and Methods: Human lung adenocarcinoma cells, LK87, were treated with concurrent LDRI (50 cGy/hr) and mild hyperthermia (38 to 42 degrees C). Cell survival was estimated by clonogenic assay. Flow cytometry was performed with FACScan. The treatments were simultaneously performed for up to 48 hr (24 Gy)., Results: Survival curves of mild hyperthermia alone revealed development of chronic thermotolerance up to 48 hr, whereas LDRI plus hyperthermia caused an exponential decrease in survival. The LDRI cytotoxicities were enhanced by mild hyperthermia over a non-lethal temperature range. The Do values calculated from dose response curves at 37, 38, 39, 40, 41 41.5 and 42 degrees C were 6.55, 5.25, 4.24, 3.99, 3.46, 1.83 and 0.70 Gy, respectively. Cell cycle analysis demonstrated a remarkable G2 and a mild G1 block for LDRI alone, but only a G1 block was observed for LDRI combined with 41 degrees C hyperthermia., Conclusion: The LDRI cytotoxicity was enhanced by long duration mild temperature hyperthermia. The suppression of chronic thermotolerance was considered to be a mechanism involved in this sensitization.

Published
1998

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