PMID- 21176360
OWN - NLM
STAT- MEDLINE
DCOM- 20111006
LR  - 20161018
IS  - 1009-2137 (Print)
IS  - 1009-2137 (Linking)
VI  - 18
IP  - 6
DP  - 2010 Dec
TI  - [Comparative study of genetic aberrations in human multiple myeloma cell lines 
      and newly diagnosed MM by fluorescence in situ hybridization].
PG  - 1505-10
AB  - Multiple myeloma (MM) is a neoplasm of a terminally differentiated B-cell. Human 
      myeloma cell lines were shown to be suitable model systems for use in various 
      fields of the biological sciences. This study was aimed to investigate the 
      genetic aberrations in human multiple myeloma cell lines. Interphase fluorescence 
      in situ hybridization (FISH) with probes for the regions containing 13q14 (RB-1), 
      13q14.3 (D13S19), 14q32 (IGHC/IGHV) , 1q12 (CEP1), 17p13 (TP53) were was used to 
      detect 7 HMCL and 85 cases of newly diagnosed MM. FISH with LSI IGH/CCND1 , LSI 
      IGH/FGFR3 and LSI IGH/MAF probes were used to detect t(11;14) (q13;q32) , t(4;14) 
      (p16;q32) and t(14;16) (q32;q23) in HMCL and MM with 14q32 rearrangement. The 
      results showed that molecular cytogenetic aberrations were found in all 7 HMCL, 
      six (85.7%) HMCL simultaneously had 13q14, 13q14.3 deletion. Chromosome 1q21 
      abnormality was found in six (33.3%) HMCL with at least 3 copies amplifications. 
      Illegitimate 14q32 rearrangement was found in five (71.4%) HMCL, including one 
      with t(11;14), two with t(4;14) and three with t(14;16). 17p13 deletion was 
      detected in 5 HMCL. Chromosomal changes were observed in 85.9% of the 85 cases of 
      newly diagnosed MM. The del(13), 1q12 amplification, del(17p), 14q32 
      rearrangement, t(11;14), t(4;14), t(14;16) were present in 44.7%, 52.9%, 20%, 
      62.4%, 27.1%, 24.7% and 3.5% of the patients respectively. There was no 
      significant difference in the prevalence of genetic abnormalities of del(13q), 
      14q32 rearrangement, 1q12 amplification, t(11;14), t(4;14) except del(17p) and 
      t(14;16). It is concluded that HMCL representative of the most aggressive phase 
      of plasma cell neoplasms accumulated a large amount of genetic aberrations. Loss 
      of p53 are strikingly common in HMCL suggesting that the impairment of the P53 
      tumor suppressor pathway is an important contributor to extramedullary tumor 
      expansion.
FAU - An, Gang
AU  - An G
AD  - Chinese Academy of Medical Sciences, Tianjin 300020, China.
FAU - Xie, Zhen-Qing
AU  - Xie ZQ
FAU - Li, Chang-Hong
AU  - Li CH
FAU - Li, Qian
AU  - Li Q
FAU - Yi, Shu-Hua
AU  - Yi SH
FAU - Qiu, Lu-Gui
AU  - Qiu LG
LA  - chi
PT  - Comparative Study
PT  - English Abstract
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Zhongguo Shi Yan Xue Ye Xue Za Zhi
JT  - Zhongguo shi yan xue ye xue za zhi
JID - 101084424
RN  - 0 (TP53 protein, human)
RN  - 0 (Tumor Suppressor Protein p53)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Bone Marrow/pathology
MH  - Cell Line, Tumor
MH  - *Chromosome Aberrations
MH  - Female
MH  - Humans
MH  - In Situ Hybridization, Fluorescence/methods
MH  - Male
MH  - Middle Aged
MH  - Multiple Myeloma/*genetics/pathology
MH  - Translocation, Genetic
MH  - Tumor Suppressor Protein p53/genetics
EDAT- 2010/12/24 06:00
MHDA- 2011/10/07 06:00
CRDT- 2010/12/24 06:00
PHST- 2010/12/24 06:00 [entrez]
PHST- 2010/12/24 06:00 [pubmed]
PHST- 2011/10/07 06:00 [medline]
AID - 1009-2137(2010)06-1505-06 [pii]
PST - ppublish
SO  - Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2010 Dec;18(6):1505-10.