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

作者信息

Sivasundaram Karnan, Suzuki Hiroko, Seto Masao, Hosokawa Yoshitaka

机构信息

Division of Molecular Medicine, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan.

出版信息

Oncol Rep. 2003 Nov-Dec;10(6):1737-9.

Abstract

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.

摘要

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