Journal
VIRUSES-BASEL
Volume 3, Issue 6, Pages 714-749Publisher
MDPI
DOI: 10.3390/v3060714
Keywords
ATL; IKK; HTLV; immune escape; NF-kappa B; PDLIM2; Tax; transformation; tumorigenesis; virus-host interaction; WWOX
Categories
Funding
- National Institutes of Health/National Cancer Institute (NIH/NCI) [R01 CA116616]
- American Cancer Society (ACS) [RSG-06-066-01-MGO]
- Hillman Innovative Cancer Research Award
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Human T-cell lymphotropic virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma (ATL), whereas the highly related HTLV-2 is not associated with ATL or other cancers. In addition to ATL leukemogenesis, studies of the HTLV viruses also provide an exceptional model for understanding basic pathogenic mechanisms of virus-host interactions and human oncogenesis. Accumulating evidence suggests that the viral regulatory protein Tax and host inflammatory transcription factor NF-kappa B are largely responsible for the different pathogenic potentials of HTLV-1 and HTLV-2. Here, we discuss the molecular mechanisms of HTLV-1 oncogenic pathogenesis with a focus on the interplay between the Tax oncoprotein and NF-kappa B pro-oncogenic signaling. We also outline some of the most intriguing and outstanding questions in the fields of HTLV and NF-kappa B. Answers to those questions will greatly advance our understanding of ATL leukemogenesis and other NF-kappa B-associated tumorigenesis and will help us design personalized cancer therapies.
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