PMID- 15305377
OWN - NLM
STAT- MEDLINE
DCOM- 20041019
LR  - 20160303
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 112
IP  - 1
DP  - 2004 Oct 20
TI  - Cyclin D3 immunoreactivity in follicular lymphoma is independent of the 
      t(6;14)(p21.1;q32.3) translocation or cyclin D3 gene amplification and is 
      correlated with histologic grade and Ki-67 labeling index.
PG  - 71-7
AB  - An abnormal expression of cyclin D3, a key regulator of the cell cycle, has been 
      documented in a variety of human malignancies, and the cyclin D3 gene, mapping to 
      6p21, may be deregulated in plasma cell myeloma and non-Hodgkin's lymphoma as a 
      result of the t(6;14)(p21.1;q32.3) translocation and/or gene amplification. In 
      the current study, we for the first time investigated by immunohistochemistry and 
      fluorescence in situ hybridization (FISH) the prevalence of cyclin D3 
      abnormalities in follicular lymphomas (FLs), comparing the results with 
      traditional clinicopathologic characteristics, p27 and skp2 immunoreactivity (IR) 
      and Ki-67 labeling index (LI). Cyclin D3, skp2 and Ki-67 IR significantly 
      increased from grade I to grade III FL (p = 0.0003, p = 0.0001 and p < 0.0001, 
      respectively), while p27 IR was significantly (p < 0.0001) more prevalent in 
      low-grade tumors. Cyclin D3 IR was directly correlated with the Ki-67 LI (p < 
      0.0001) and inversely correlated with p27 IR (p = 0.050). None of the 13 cases 
      analyzed by FISH showed the t(6;14) translocation, but in 2 (15.3%) grade I FLs 3 
      cyclin D3 signals were detected. Cohybridization with probes specific for the 
      centromeric region and the long arm of the chromosome 6 indicated trisomy in one 
      case and a pattern highly suggestive for the presence of an isochromosome 6p in 
      the other case. Our data suggest that the t(6;14) translocation may be extremely 
      uncommon in FL and that a deregulated expression of cyclin D3, possibly due to 
      epigenetic mechanisms, may be involved in the pathogenesis of high-grade tumors.
FAU - Pruneri, Giancarlo
AU  - Pruneri G
AD  - Division of Pathology and Laboratory Medicine, European Institute of Oncology, 
      Milan, Italy. giancarlo.pruneri@ieo.it
FAU - Valentini, Stefano
AU  - Valentini S
FAU - Fabris, Sonia
AU  - Fabris S
FAU - Del Curto, Barbara
AU  - Del Curto B
FAU - Laszlo, Daniele
AU  - Laszlo D
FAU - Bertolini, Francesco
AU  - Bertolini F
FAU - Martinelli, Giovanni
AU  - Martinelli G
FAU - Leocata, Pietro
AU  - Leocata P
FAU - Viale, Giuseppe
AU  - Viale G
FAU - Neri, Antonino
AU  - Neri A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (CCND3 protein, human)
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Cyclin D3)
RN  - 0 (Cyclins)
RN  - 0 (Ki-67 Antigen)
RN  - 0 (S-Phase Kinase-Associated Proteins)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Cell Cycle Proteins/genetics/metabolism
MH  - Chromosomes, Human, Pair 14/*genetics
MH  - Chromosomes, Human, Pair 6/*genetics
MH  - Cyclin D3
MH  - Cyclin-Dependent Kinase Inhibitor p27
MH  - Cyclins/genetics/*metabolism
MH  - Female
MH  - Gene Amplification
MH  - Humans
MH  - Immunoenzyme Techniques
MH  - In Situ Hybridization, Fluorescence
MH  - Ki-67 Antigen/*metabolism
MH  - Lymphoma, Follicular/genetics/*metabolism/pathology
MH  - Male
MH  - Middle Aged
MH  - Neoplasm Staging
MH  - S-Phase Kinase-Associated Proteins/genetics/metabolism
MH  - Translocation, Genetic/*physiology
MH  - Trisomy
MH  - Tumor Suppressor Proteins/genetics/metabolism
EDAT- 2004/08/12 05:00
MHDA- 2004/10/20 09:00
CRDT- 2004/08/12 05:00
PHST- 2004/08/12 05:00 [pubmed]
PHST- 2004/10/20 09:00 [medline]
PHST- 2004/08/12 05:00 [entrez]
AID - 10.1002/ijc.20354 [doi]
PST - ppublish
SO  - Int J Cancer. 2004 Oct 20;112(1):71-7. doi: 10.1002/ijc.20354.