PMID- 8547659
OWN - NLM
STAT- MEDLINE
DCOM- 19960216
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 87
IP  - 1
DP  - 1996 Jan 1
TI  - Molecular characterization of 12p abnormalities in hematologic malignancies: 
      deletion of KIP1, rearrangement of TEL, and amplification of CCND2.
PG  - 324-30
AB  - Twenty patients with hematologic malignancies with 12p abnormalities were 
      investigated by fluorescence in situ hybridization (FISH) using probes mapped to 
      specific regions in 12p. The initial analysis using the YAC 964c10 (D12S736) 
      revealed that all four cases with cytogenetically identified del(12p) had lost 
      one copy of this YAC and that submicroscopic deletions had occurred in 10 of the 
      16 neoplasms with other 12p abnormalities, ie, translocations, additions, and 
      insertions. The deletions were partially mapped with cosmids localized to 
      subregions of 12p. One copy of the gene for p27kip1 (KIP1), involved in cell 
      cycle entrance, was found to be lost in all cases in which deletions could be 
      detected by other probes and in one case with a translocation as the only 
      detectable change. This implicates KIP1 as a possible tumor suppressor gene 
      affected by del(12p). Four translocations with no apparent concomitant deletions 
      were detected. All four breakpoints resulted in a split D12S736 signal. In two of 
      these cases, we showed that TEL was disrupted as a result of a 
      t(5;12)(q32-33;p12) and a t(12;22)(p12;q12), respectively. Two lymphoid 
      neoplasm--one non-Hodgkin's lymphoma and one Burkitt's lymphoma--with 12p 
      amplifications were detected. In both cases cyclin D2 (CCND2) was within the 
      amplified region. Thus, cytogenetic abnormalities of 12p in hematologic 
      malignancies result in at least three different molecular changes: deletions of 
      KIP1, amplifications of CCND2, and structural rearrangements of TEL.
FAU - Hoglund, M
AU  - Hoglund M
AD  - Department of Clinical Genetics, University Hospital, Lund, Sweden.
FAU - Johansson, B
AU  - Johansson B
FAU - Pedersen-Bjergaard, J
AU  - Pedersen-Bjergaard J
FAU - Marynen, P
AU  - Marynen P
FAU - Mitelman, F
AU  - Mitelman F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Aneuploidy
MH  - Burkitt Lymphoma/genetics/pathology
MH  - Cell Cycle Proteins
MH  - Child
MH  - Chromosome Aberrations
MH  - Chromosomes, Artificial, Yeast
MH  - Chromosomes, Human, Pair 12/*ultrastructure
MH  - Cyclin-Dependent Kinase Inhibitor p27
MH  - Female
MH  - *Genes, Tumor Suppressor
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Karyotyping
MH  - Leukemia/*genetics/pathology
MH  - Lymphoma, Non-Hodgkin/genetics/pathology
MH  - Male
MH  - Middle Aged
MH  - Myelodysplastic Syndromes/*genetics/pathology
MH  - *Oncogenes
MH  - *Translocation, Genetic
MH  - *Tumor Suppressor Proteins
EDAT- 1996/01/01 00:00
MHDA- 1996/01/01 00:01
CRDT- 1996/01/01 00:00
PHST- 1996/01/01 00:00 [pubmed]
PHST- 1996/01/01 00:01 [medline]
PHST- 1996/01/01 00:00 [entrez]
AID - S0006-4971(20)66223-1 [pii]
PST - ppublish
SO  - Blood. 1996 Jan 1;87(1):324-30.