Document Detail


HTLV-1 and apoptosis: role in cellular transformation and recent advances in therapeutic approaches.
MedLine Citation:
PMID:  18421579     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A universal cellular defense mechanism against viral invasion is the elimination of infected cells through apoptotic cell death. To counteract host defenses many viruses have evolved complex apoptosis evasion strategies. The oncogenic human retrovirus HTLV-1 is the etiological agent of adult-T-cell leukemia/lymphoma (ATLL) and the neurodegenerative disease known as HTLV-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The poor prognosis in HTLV-1-induced ATLL is linked to the resistance of neoplastic T cells against conventional therapies and the immuno-compromised state of patients. Nevertheless, several studies have shown that the apoptotic pathway is largely intact and can be reactivated in ATLL tumor cells to induce specific killing. A better understanding of the molecular mechanisms employed by HTLV-1 to counteract cellular death pathways remains an important challenge for future therapies and the treatment of HTLV-1-associated diseases.
Authors:
John M Taylor; Christophe Nicot
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Apoptosis : an international journal on programmed cell death     Volume:  13     ISSN:  1573-675X     ISO Abbreviation:  Apoptosis     Publication Date:  2008 Jun 
Date Detail:
Created Date:  2008-05-16     Completed Date:  2008-07-09     Revised Date:  2012-03-20    
Medline Journal Info:
Nlm Unique ID:  9712129     Medline TA:  Apoptosis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  733-47     Citation Subset:  IM    
Affiliation:
Department of Microbiology, Immunology, and Molecular Genetics, University of Kansas Medical Center, 3025 Wahl Hall West, 3901 Rainbow Blvd., Kansas City, KS 66160, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects,  physiology*
Cell Transformation, Viral / physiology*
Gene Products, tax / physiology
Human T-lymphotropic virus 1 / drug effects,  physiology*
Humans
I-kappa B Kinase / physiology
Janus Kinases / physiology
Leukemia-Lymphoma, Adult T-Cell / drug therapy*,  virology*
NF-kappa B / antagonists & inhibitors,  physiology
Paraparesis, Tropical Spastic / drug therapy,  virology
Proto-Oncogene Proteins c-akt / physiology
Receptors, Interleukin-2 / physiology
Retroviridae Proteins / physiology
STAT Transcription Factors / physiology
Tretinoin / pharmacology
Tumor Suppressor Protein p53 / physiology
Viral Regulatory and Accessory Proteins / physiology
Grant Support
ID/Acronym/Agency:
CA106258/CA/NCI NIH HHS; CA115398/CA/NCI NIH HHS; R01 CA106258-05/CA/NCI NIH HHS; R01 CA106258-08/CA/NCI NIH HHS; R01 CA115398-01A2/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Gene Products, tax; 0/NF-kappa B; 0/Receptors, Interleukin-2; 0/Retroviridae Proteins; 0/STAT Transcription Factors; 0/Tumor Suppressor Protein p53; 0/Viral Regulatory and Accessory Proteins; 0/p12I protein, Human T-lymphotropic virus 1; 0/rof protein, Human T-lymphotropic virus 1; 0/tof protein, Human T-lymphotropic virus 1; 302-79-4/Tretinoin; EC 2.7.10.2/Janus Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.10/I-kappa B Kinase
Comments/Corrections

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