PMID- 10602435
OWN - NLM
STAT- MEDLINE
DCOM- 20000106
LR  - 20201113
IS  - 0887-6924 (Print)
IS  - 0887-6924 (Linking)
VI  - 13
IP  - 12
DP  - 1999 Dec
TI  - Analysis of p73 and p53 gene deletions in multiple myeloma.
PG  - 2099-103
AB  - Recently, p73, a protein with structural and functional similarities to p53, an 
      extensively studied tumor suppressor gene, has been cloned. After being mapped to 
      the chromosomal region 1p35-1p36, it has been postulated to act as a tumor 
      suppressor gene, too, as this region is altered in several human malignancies. 
      Deletions of the short arm of chromosome 1 have frequently been described in 
      multiple myeloma (MM) whereas structural abnormalities of the 17p13 region 
      including p53 are rare events in this disease. Since it has been proposed that 
      especially neoplasias lacking p53 alterations might show a loss of heterozygosity 
      at 1p35-1p36, we studied the frequency of p53 and p73 deletions in bone marrow 
      mononuclear cells of 68 patients with MM, two patients with monoclonal gammopathy 
      of undetermined significance and four patients with plasma cell leukemia. 
      Dual-color fluorescence in situ hybridization (FISH) for p53 and p73 was 
      performed using commercially available DNA probes for 17p13.3 and the 
      microsatellite marker D1Z2, respectively. Centromeric DNA probes served to 
      distinguish gene deletions from whole chromosome losses. In contrast to recently 
      published FISH results, we only detected heterozygous p53 deletions in eight out 
      of the 74 patients, three of them showing a monosomy 17. Heterozygous deletions 
      of the D1Z2 region at 1p36 were found in six cases with one patient having a 
      monosomy 1. Neither homozygous deletions of either chromosomal region nor 
      nullisomies 1 or 17 could be detected. These results argue against a major role 
      of p73 deletions in MM. As MM patients with 1p structural abnormalities have a 
      significantly poorer survival rate than those with normal karyotypes, the role of 
      other putative tumor suppressor genes located at the chromosomal region 1p36 in 
      the pathogenesis of MM has to be determined.
FAU - Schultheis, B
AU  - Schultheis B
AD  - III Medizinische Klinik, Klinikum Mannheim, Universitat Heidelberg, Mannheim, 
      Germany.
FAU - Kramer, A
AU  - Kramer A
FAU - Willer, A
AU  - Willer A
FAU - Hegenbart, U
AU  - Hegenbart U
FAU - Goldschmidt, H
AU  - Goldschmidt H
FAU - Hehlmann, R
AU  - Hehlmann R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Leukemia
JT  - Leukemia
JID - 8704895
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Nuclear Proteins)
RN  - 0 (TP73 protein, human)
RN  - 0 (Tumor Protein p73)
RN  - 0 (Tumor Suppressor Proteins)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Chromosome Aberrations
MH  - Chromosomes, Human, Pair 1
MH  - Chromosomes, Human, Pair 17
MH  - DNA-Binding Proteins/*genetics
MH  - Female
MH  - *Gene Deletion
MH  - *Genes, Tumor Suppressor
MH  - *Genes, p53
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Male
MH  - Middle Aged
MH  - Multiple Myeloma/*genetics
MH  - Nuclear Proteins/*genetics
MH  - Tumor Protein p73
MH  - Tumor Suppressor Proteins
EDAT- 1999/12/22 00:00
MHDA- 1999/12/22 00:01
CRDT- 1999/12/22 00:00
PHST- 1999/12/22 00:00 [pubmed]
PHST- 1999/12/22 00:01 [medline]
PHST- 1999/12/22 00:00 [entrez]
AID - 10.1038/sj.leu.2401609 [doi]
PST - ppublish
SO  - Leukemia. 1999 Dec;13(12):2099-103. doi: 10.1038/sj.leu.2401609.