Imperial College London
ANAT MELAMED

ANAT MELAMED

Faculty of Medicine, Department of Infectious Disease

Research Associate
 
 
 
//

Contact

 

anat.melamed07

 
 
//

Location

 

VD1Medical SchoolSt Mary's Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Cook:2014:10.1182/blood-2014-02-553602,
author = {Cook, LB and Melamed, A and Niederer, H and Valganon, M and Laydon, D and Foroni, L and Taylor, GP and Matsuoka, M and Bangham, CRM},
doi = {10.1182/blood-2014-02-553602},
journal = {Blood},
pages = {3925--3931},
title = {The role of HTLV-1 clonality, proviral structure, and genomic integration site in adult T-cell leukemia/lymphoma},
url = {http://dx.doi.org/10.1182/blood-2014-02-553602},
volume = {123},
year = {2014}
}
Download

RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Adult T-cell leukemia/lymphoma (ATL) occurs in ∼5% of human T-lymphotropic virus type 1 (HTLV-1)–infected individuals and is conventionally thought to be a monoclonal disease in which a single HTLV-1+ T-cell clone progressively outcompetes others and undergoes malignant transformation. Here, using a sensitive high-throughput method, we quantified clonality in 197 ATL cases, identified genomic characteristics of the proviral integration sites in malignant and nonmalignant clones, and investigated the proviral features (genomic structure and 5′ long terminal repeat methylation) that determine its capacity to express the HTLV-1 oncoprotein Tax. Of the dominant, presumed malignant clones, 91% contained a single provirus. The genomic characteristics of the integration sites in the ATL clones resembled those of the frequent low-abundance clones (present in both ATL cases and carriers) and not those of the intermediate-abundance clones observed in 24% of ATL cases, suggesting that oligoclonal proliferation per se does not cause malignant transformation. Gene ontology analysis revealed an association in 6% of cases between ATL and integration near host genes in 3 functional categories, including genes previously implicated in hematologic malignancies. In all cases of HTLV-1 infection, regardless of ATL, there was evidence of preferential survival of the provirus in vivo in acrocentric chromosomes (13, 14, 15, 21, and 22).
AU  - Cook,LB
AU  - Melamed,A
AU  - Niederer,H
AU  - Valganon,M
AU  - Laydon,D
AU  - Foroni,L
AU  - Taylor,GP
AU  - Matsuoka,M
AU  - Bangham,CRM
DO  - 10.1182/blood-2014-02-553602
EP  - 3931
PY  - 2014///
SN  - 0006-4971
SP  - 3925
TI  - The role of HTLV-1 clonality, proviral structure, and genomic integration site in adult T-cell leukemia/lymphoma
T2  - Blood
UR  - http://dx.doi.org/10.1182/blood-2014-02-553602
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000342617800016&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://ashpublications.org/blood/article/123/25/3925/32890/The-role-of-HTLV-1-clonality-proviral-structure
VL  - 123
ER  -
Download