PMID- 15796964
OWN - NLM
STAT- MEDLINE
DCOM- 20050509
LR  - 20140515
IS  - 0165-4608 (Print)
IS  - 0165-4608 (Linking)
VI  - 158
IP  - 2
DP  - 2005 Apr 15
TI  - Alterations of loci encoding PU.1, BOB1, and OCT2 transcription regulators do not 
      correlate with their suppressed expression in Hodgkin lymphoma.
PG  - 167-71
AB  - Neoplastic cells of Hodgkin lymphoma (HL) originating from germinal or 
      postgerminal center B cells lose their capacity to transcribe and to express 
      surface immunoglobulins (Ig). This defect correlates with the absence of 
      expression of B-cell-specific transcription regulators, including PU.1, BOB1, and 
      OCT2. These findings suggest that Ig impairment in HL is caused by the defective 
      transcription machinery. The mechanism or mechanisms underlying failure of 
      Hodgkin cells to express PU.1, BOB1, and OCT2 remain unclear. The genes encoding 
      for these three respective transcription factors have been mapped at 11p11.2 
      (SPI1), 11q23.1 (POU2AF1), and 19q13.2 (POU2F2); these are chromosomes 
      recurrently affected in HL. To check the genomic status of PU.1, BOB1, and OCT2 
      in HL, we performed metaphase fluorescence in situ hybridization (FISH) analysis 
      of 10 HL cases using locus-specific bacterial artificial chromosome clones. FISH 
      signal pattern was correlated with the ploidy level of each analyzed cell and 
      showed recurrent imbalances of the studied loci. The underrepresentation of one 
      or two analyzed regions was detected in five cases; the remaining five cases 
      showed either random losses, a ploidy-equivalent FISH pattern, or overrepresented 
      signals. Neither a constant loss nor genomic aberration of at least one of these 
      genes could be observed in studied cases. These findings indicate that genomic 
      imbalances or rearrangements are not a cause of PU.1, BOB1, and OCT2 deficiency 
      in cHL and argue for another mechanism underlying this phenomenon.
FAU - Cavazzini, Francesco
AU  - Cavazzini F
AD  - Center for Human Genetics, Katholieke Universiteit Leuven, Leuven, Belgium.
FAU - De Wolf-Peeters, Chris
AU  - De Wolf-Peeters C
FAU - Wlodarska, Iwona
AU  - Wlodarska I
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Cancer Genet Cytogenet
JT  - Cancer genetics and cytogenetics
JID - 7909240
RN  - 0 (Octamer Transcription Factor-2)
RN  - 0 (POU2AF1 protein, human)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Trans-Activators)
RN  - 0 (Transcription Factors)
RN  - 0 (proto-oncogene protein Spi-1)
SB  - IM
MH  - Chromosome Aberrations
MH  - Chromosome Banding
MH  - Chromosomes, Artificial, Bacterial/genetics
MH  - Cytogenetic Analysis
MH  - Hodgkin Disease/*genetics/pathology
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Metaphase
MH  - Octamer Transcription Factor-2/*genetics
MH  - Ploidies
MH  - Proto-Oncogene Proteins/*genetics
MH  - Trans-Activators/*genetics
MH  - Transcription Factors/*genetics
MH  - *Transcription, Genetic
EDAT- 2005/03/31 09:00
MHDA- 2005/05/10 09:00
CRDT- 2005/03/31 09:00
PHST- 2004/08/23 00:00 [received]
PHST- 2004/09/13 00:00 [accepted]
PHST- 2005/03/31 09:00 [pubmed]
PHST- 2005/05/10 09:00 [medline]
PHST- 2005/03/31 09:00 [entrez]
AID - S0165-4608(04)00423-6 [pii]
AID - 10.1016/j.cancergencyto.2004.09.005 [doi]
PST - ppublish
SO  - Cancer Genet Cytogenet. 2005 Apr 15;158(2):167-71. doi: 
      10.1016/j.cancergencyto.2004.09.005.