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Wilms' tumor gene expression by normal and malignant human B lymphocytes
P Spinsanti1, U de Grazia, A Faggioni
1Dipartimento di Medicina Sperimentale e Patologia, Università di Roma La Sapienza, Rome, Italy.
Leukemia & Lymphoma
|August 23, 2000
Summary
Wilms' tumor gene (WT1) is activated in Epstein-Barr virus (EBV)-immortalized B cells but absent in normal B lymphocytes and Burkitt tumors. This WT1 expression pattern suggests gene inactivation may contribute to B-cell growth dysregulation.
Area of Science:
- Immunology
- Molecular Biology
- Oncology
Background:
- Wilms' tumor gene (WT1) role in B-cell growth and differentiation is largely unknown.
- WT1 expression patterns in normal and malignant B cells require further investigation.
Purpose of the Study:
- To investigate WT1 gene expression in various B-cell types, including normal lymphocytes and B-cell lines.
- To determine the significance of WT1 expression in B-cell growth regulation and differentiation, particularly in relation to Epstein-Barr virus (EBV) infection.
Main Methods:
- RT-PCR was used to detect and analyze WT1 transcript isoforms in fresh B lymphocytes and B-cell lines.
- Expression levels were compared between normal B lymphocytes, EBV-immortalized lymphoblastoid cell lines (LCLs), and Burkitt tumor-derived cell lines.
Main Results:
- WT1 was constitutively activated in all EBV-immortalized LCLs, irrespective of EBV status.
- WT1 expression was abrogated in normal B lymphocytes and all Burkitt tumor cell lines.
- Balanced expression of WT1 isoforms was observed in LCLs, similar to non-tumorous tissues.
Conclusions:
- WT1 gene inactivation, alongside alternative splicing, may contribute to growth control abnormalities in B-cell malignancies.
- WT1 expression serves as a potential marker differentiating EBV-associated lymphoblastoid cell lines from normal B cells and Burkitt tumors.