PubMed Health⌕ Search

Biomedical subjects

C Tanimoto

Publications and source records attributed to C Tanimoto.

4 recordsLinked to original sources

Apoptosis in thyroid diseases: a histochemical study.

Recent studies demonstrate that apoptosis is an important process in physiological and pathological cell death. We examined the apoptotic phenomena in thyroid tissues by two methods: immunohistological and in situ end-labeling of fragmented DNA (ISEL). In thyroid tissues from patients with Hashimoto's thyroiditis and thyroid cancer, fragmented nuclear DNA and LeY (apoptosis associated antigen) were observed. In tissues from patients with Graves' disease, LeY and bcl-2 oncoprotein were expressed, but no ISEL positive cells were observed. In contrast, thyrocytes in normal thyroid tissues were not stained with ISEL or anti-LeY antibodies (Abs). Fas antigen (Ag) was expressed in various thyroid tissues, including normal subjects. The clinical meaning of this was not determined. These results suggest that the apoptotic process takes place in Hashimoto's thyroiditis and thyroid cancer, and is overcome in Graves' disease by bcl-2 expression.

Apoptosis↗

ICRF-193 modifies etoposide-induced apoptosis in thymocytes.

Etoposide (VP-16), one of the topoisomerase II (TopoII) inhibitors, interferes with TopoII by inducing the formation of and stabilizing a cleavable enzyme-DNA complex. VP-16 has been demonstrated to induce apoptosis in murine thymocytes. To clarify the mechanism of action of VP-16, we examined the in vitro effect of a non-cleavable-complex-forming type TopoII inhibitor, ICRF-193 which inhibits the DNA strand breakage induced by VP-16, on murine thymocytes in which apoptosis had been induced with VP-16. DNA fragmentation is characteristic of apoptosis. In the early stages, ICRF-193 decreased DNA fragmentation induced by VP-16, although this inhibitory effect decreased in the later. These data suggest that TopoII inhibitors induce apoptosis in murine thymocytes in two ways: with DNA-strand breaks in the early stage or without them. ICRF-193 itself induced apoptosis in murine thymocytes. The time course of DNA fragmentation caused by ICRF-193 was different from that of VP-16.

Animals↗