Abstract
Human T-cell leukemia virus type I (HTLV-I) is the etiologic agent of adult T-cell leukemia, an acute and often fatal T-cell malignancy. A key step in HTLV-I-induced leukemigenesis is induction of abnormal T-cell growth and survival. Unlike antigen-stimulated T cells, which cease proliferation after a finite number of cell division, HTLV-I-infected T cells proliferate indefinitely (immortalized), thus facilitating occurrence of secondary genetic changes leading to malignant transformation. To explore the molecular basis of HTLV-I-induced abnormal T-cell survival, we compared the gene expression profiles of normal and HTLV-I-immortalized T cells using 'gene array', These studies revealed a strikingly altered expression pattern of a large number of genes along with HTLV-I-mediated T-cell immortalization. Interestingly, many of these deregulated genes are involved in the control of programmed cell death or apoptosis. These findings indicate that disruption of the cellular apoptosis-regulatory network may play a role in the HTLV-I-mediated oncogenesis.
Original language | English (US) |
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Pages (from-to) | 1341-1349 |
Number of pages | 9 |
Journal | Oncogene |
Volume | 18 |
Issue number | 6 |
DOIs | |
State | Published - Feb 11 1999 |
Externally published | Yes |
Keywords
- Adult T-cell leukemia
- Gene array
- Gene expression profile
- HTLV-I
- T-cell immortalization
ASJC Scopus subject areas
- Molecular Biology
- Genetics
- Cancer Research