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Mutational analysis of the ST7 gene in human myeloid tumor cell lines
Karnan Sivasundaram1, Hiroko Suzuki, Masao Seto
1Division of Molecular Medicine, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan.
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.
Insights
The ST7 gene, a potential tumor suppressor, was investigated for mutations in malignant myeloid tumors. Researchers found no evidence of ST7 gene mutations in these cancers, questioning its role in their development.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The ST7 (suppression of tumorigenicity 7) gene, located on chromosome 7q31, is implicated in various human cancers.
- Loss of heterozygosity (LOH) at 7q31 is common in malignant myeloid tumors, suggesting ST7 as a potential tumor suppressor gene (TSG).
Purpose of the Study:
- To investigate the presence of somatic mutations in the ST7 gene within human malignant myeloid tumor cell lines.
- To evaluate the role of ST7 gene mutations in the molecular pathogenesis of acute myelogenous leukemia (AML) and chronic myelogenous leukemia (CML).
Main Methods:
- Analysis of 22 human malignant myeloid tumor cell lines (17 AML, 5 CML) using bidirectional direct DNA sequencing.
- Re-examination of two breast tumor cell lines previously reported to have ST7 mutations.
Main Results:
- No somatic mutations of the ST7 gene were detected in any of the examined malignant myeloid tumor cell lines.
- Analysis of two breast tumor cell lines did not confirm previously reported ST7 mutations.
Conclusions:
- Somatic mutations in the ST7 gene do not appear to be a common factor in the development of human malignant myeloid tumors.
- The findings challenge the proposed role of ST7 as a frequently inactivated tumor suppressor gene in these cancers and other neoplasias.
