Hiroko Suzuki — Page 2

PubMed2002

[Anti-allergic drugs inhibit the proliferation of human Tenon's capsule fibroblast and maintain the experimental filtering blebs on rabbit eyes].

PURPOSE: To examine whether tranilast and ketotifen fumarate inhibit the growth of human Tenon's capsule fibroblasts and maintain experimental filtering blebs on rabbit eyes. METHODS: Human Tenon's capsule fibroblasts were grown in Dulbecco's modified Eagle's medium with 10% fetal calf serum and growth was measured with 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and direct counting of cell number. Production of collagen and transforming growth factor-beta 1 (TGF-beta 1) was measured with corresponding enzyme-linked immunosorbent assay (ELISA). In experimental filtering surgery performed on rabbit eyes, the effects of the topical drugs on intraocular pressure and on maintenance of the filtering blebs were observed. RESULTS: Both tranilast and ketotifen inhibited the growth of the fibroblasts and half-inhibitory concentrations were 200 microM and 70 microM, respectively. Low concentration (10 microM) of tranilast and ketotifen decreased the synthesis of collagen but neither drug had any obvious effect on TGF-beta 1 production. Both drugs prolonged the life of the experimental filtering bleb significantly [12.5 +/- 3.2 (mean +/- standard deviation) days, 13.9 +/- 3.4 days, respectively; control, 10.5 +/- 2.4 days]. CONCLUSION: Tranilast and ketotifen inhibited the growth of human Tenon's capsule proliferation and are capable of maintaining experimental filtering blebs in rabbit eyes.

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PubMedDate not supplied

Mutational analysis of the ST7 gene in human myeloid tumor cell lines.

The recently described ST7 (for suppression of tumorigenicity 7) gene has been suggested to be a major target gene on chromosome 7q31 for inactivation in a variety of human neoplasias. Loss of heterozygosity (LOH) in chromosome 7q31 is frequently observed in a variety of human neoplasias including malignant myeloid tumors. We, therefore, sought to examine a total of 22 human malignant myeloid tumor cell lines comprising 17 of acute myelogenous leukemia (AML) cell lines and 5 chronic myelogenous leukemia (CML) cell lines for somatic mutations of the ST7 gene by means of bidirectional direct DNA sequencing analysis. As a result, no mutations were detected in any of these cell lines examined. In addition, our analysis of two breast tumor cell lines, which had been reported to harbour ST7 mutations, provided no evidence for such mutations. Thus, our results strongly suggest that somatic mutations of ST7 do not commonly contribute to the molecular pathogenesis of human malignant myeloid tumors and further raise questions regarding the pathological role of ST7 as a tumor suppressor gene (TSG) in a variety of human neoplasias.

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