Human T‐cell leukemia virus type I (HTLV‐1) is the etiologic agent for adult T‐cell leukemia (ATL). Among the X region products of HTLV‐1, the p42 kDa protein Tax was identified, as responsible for cell immortalization and transformation. However, the observations that only a low percentage of individuals infected with HTLV‐1 eventually progress to leukemia and that leukemic transformation of HTLV‐1‐infected cells is associated with aberrant karyotype suggest that additional genetic events are required for HTLV‐1‐induced malignant transformation. Results of our study demonstrate that expression of the Tax protein of HTLV‐1 increased the radiosensitivity of a mouse fibroblast cell line. These data are consistent with a previous report indicating a negative regulatory control by Tax on DNA repair. Unrepaired DNA damage and karyotypic instability could represent a common factor in both the initiation and progression of HTLV‐1‐related diseases. © 1993 Wiley‐Liss, Inc.
- ionizing irradiation
- radiation repair
- tumor progression
ASJC Scopus subject areas
- Radiological and Ultrasound Technology
- Radiology Nuclear Medicine and imaging