|
|
|
|
LEADER |
02358 am a22003133u 4500 |
001 |
47933 |
042 |
|
|
|a dc
|
100 |
1 |
0 |
|a Jenner, Matthew W.
|e author
|
700 |
1 |
0 |
|a Leone, Paola E.
|e author
|
700 |
1 |
0 |
|a Walker, Brian A.
|e author
|
700 |
1 |
0 |
|a Ross, Fiona M.
|e author
|
700 |
1 |
0 |
|a Johnson, David C.
|e author
|
700 |
1 |
0 |
|a Gonzalez, David
|e author
|
700 |
1 |
0 |
|a Chiecchio, Laura
|e author
|
700 |
1 |
0 |
|a Dachs Cabanas, Elisabet
|e author
|
700 |
1 |
0 |
|a Dagrada, Gian Paolo
|e author
|
700 |
1 |
0 |
|a Nightingale, Mathew
|e author
|
700 |
1 |
0 |
|a Protheroe, Rebecca K.M.
|e author
|
700 |
1 |
0 |
|a Stockley, David
|e author
|
700 |
1 |
0 |
|a Else, Monica
|e author
|
700 |
1 |
0 |
|a Dickens, Nicholas J.
|e author
|
700 |
1 |
0 |
|a Cross, Nicholas C.P.
|e author
|
700 |
1 |
0 |
|a Davies, Faith E.
|e author
|
700 |
1 |
0 |
|a Morgan, Gareth J.
|e author
|
245 |
0 |
0 |
|a Gene mapping and expression analysis of 16q loss of heterozygosity identifies WWOX and CYLD as being important in determining clinical outcome in multiple myeloma
|
260 |
|
|
|c 2007-07-03.
|
856 |
|
|
|z Get fulltext
|u https://eprints.soton.ac.uk/47933/1/blood-2007-02-075069v1.pdf
|
520 |
|
|
|a We performed FISH for 16q23 abnormalities in 861 patients with newly diagnosed multiple myeloma and identified del(16q) in 19.5%. In 467 cases in which demographic and survival data were available, del(16q) was associated with a worse overall survival. It was an independent prognostic marker and conferred additional adverse survival impact in cases with the known poor risk cytogenetic factors t(4;14) and del(17p). Gene expression profiling and gene mapping using 500K SNP mapping arrays revealed loss of heterozygosity (LOH) involving 3 regions, the whole of 16q, a region centered on 16q12, the location of CYLD, and a region centered on 16q23, the location of WWOX. CYLD is a negative regulator of the NF-kappaB pathway and cases with low expression of CYLD were used to define a "low-CYLD signature". Cases with 16q LOH or t(14;16) had significantly reduced WWOX expression. WWOX, the site of the translocation breakpoint in t(14;16) cases, is a known tumor suppressor gene involved in apoptosis and we were able to generate a "low-WWOX signature" defined by WWOX expression. These two genes and their corresponding signatures provide an important insight in to the potential mechanisms by which 16q LOH confers poor prognosis.
|
655 |
7 |
|
|a Article
|