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Biomedical subjects

K Hamajima

Publications and source records attributed to K Hamajima.

62 records · Page 4Linked to original sources

Application of double staining technique and incident light fluorescence microscopy to immunofluorescence studies on renal diseases.

A method, by which the more precise localization of immunofluorescent deposits in the glomerulus is easily demonstrated with the fluorescence microscopy, was described. By means of this method, the deposits even in the Bowman's space could be identified, as well as the deposits in the subepithelial, subendothlial and mesangial regions. From this result, it was suggested that this method should be widely used for the immunofluorescence studies on human renal biopsied sections, in order to elucidate the relationship between the localization of deposits and renal diseases.

Animals↗

Alteration of the Bcl-2/Bax status of head and neck cancer cell lines by chemotherapeutic agents.

The Bcl-2 family of genes includes some important regulators of apoptosis. Among these genes, Bcl-2 and Bax control cell death, thus contributing to both tumor growth and drug sensitivity. We determined the levels of protein and RNA expression of Bcl-2 family in 21 head and neck cancer cell lines. Then using four cell lines, which were KB (Bcl-2+/Bax+), KCC-L871 (Bcl-2+/Bax-), YCU-T891 (Bcl-2-/Bax+) and TC901 (Bcl-2-/Bax-), we investigated the impact of Bcl-2/Bax status on sensitivity to the following chemotherapeutic agents; paclitaxel, cisplatin, vincristine and 5-fluorouracil. Immunohistochemistry and RT-PCR showed that 71% of the cell lines were Bcl-2 positive, 62% were Bax positive, 38% were Bcl-XL positive and 62% were Bcl-XS positive. After treatment with all the chemotherapeutic agents, Bax expression changed from negative to positive in TC901 cells. In KB cells, Bcl-2 expression decreased only after treatment with paclitaxel. YCU-T891 cells were sensitive to all of the drugs. In conclusion, Bcl-2/Bax status was correlated with drug sensitivity and treatment with chemotherapeutic agents induced apoptosis in these cancer cells.

Antimetabolites, Antineoplastic↗