PMID- 9669667
OWN - NLM
STAT- MEDLINE
DCOM- 19990304
LR  - 20220311
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 22
IP  - 4
DP  - 1998 Aug
TI  - Commonly occurring loss and mutation of the MXI1 gene in prostate cancer.
PG  - 295-304
AB  - One of the most common chromosomal abnormalities in prostate cancer involves loss 
      of 10q22-qter. Rarely, a smaller deletion, involving 10q24-q25, has been 
      observed, suggesting the presence of a tumor suppressor gene at this site. We 
      previously demonstrated that the MXI1 gene maps to 10q24-q25 and is mutated in 
      some tumors with cytogenetically detectable deletions of this locus. MXI1 encodes 
      a basic-helix-loop-helix protein that suppresses the transcriptional activity of 
      the MYC oncoprotein by competing for the common dimerization partner, MAX, and 
      binding to identical DNA sites. Because more than 90% of prostate tumors contain 
      no cytogenetic abnormality of 10q, the relevance of MXI1 loss and/or mutation to 
      the vast majority of cases remains unclear. We prospectively evaluated prostate 
      tumors for loss of MXI1 by fluorescence in situ hybridization (FISH) and 
      cytogenetic techniques. Twenty-one of 40 tumors (53%) demonstrated loss of a 
      single MXI1 allele as determined by FISH. Ten cases with cytogenetically normal 
      10qs, but with FISH-documented deletion of MXI1, were examined at the molecular 
      level, and eight mutations were identified, albeit at low frequency. Five of the 
      mutant proteins were unable to bind DNA in association with MAX. We conclude that 
      MXI1 gene loss in prostate cancer is common and most frequently involves a 
      cytogenetically undetectable deletion.
FAU - Prochownik, E V
AU  - Prochownik EV
AD  - Section of Hematology/Oncology, Children's Hospital of Pittsburgh, Pennsylvania 
      15213, USA.
FAU - Eagle Grove, L
AU  - Eagle Grove L
FAU - Deubler, D
AU  - Deubler D
FAU - Zhu, X L
AU  - Zhu XL
FAU - Stephenson, R A
AU  - Stephenson RA
FAU - Rohr, L R
AU  - Rohr LR
FAU - Yin, X
AU  - Yin X
FAU - Brothman, A R
AU  - Brothman AR
LA  - eng
GR  - MO1 RR00064/RR/NCRR NIH HHS/United States
GR  - R01 CA46269/CA/NCI NIH HHS/United States
GR  - R01 HL33741/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (Basic Helix-Loop-Helix Transcription Factors)
RN  - 0 (DNA, Neoplasm)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (MXI1 protein, human)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Suppressor Proteins)
SB  - IM
MH  - Basic Helix-Loop-Helix Transcription Factors
MH  - Chromosome Deletion
MH  - DNA, Neoplasm/analysis
MH  - DNA-Binding Proteins/*genetics/physiology
MH  - *Gene Deletion
MH  - Helix-Loop-Helix Motifs/*genetics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Male
MH  - Mutation/*genetics
MH  - Neoplasm Recurrence, Local
MH  - Prostatic Neoplasms/*genetics
MH  - Transcription Factors/*genetics/physiology
MH  - Tumor Suppressor Proteins
EDAT- 1998/07/21 02:16
MHDA- 2000/06/20 09:00
CRDT- 1998/07/21 02:16
PHST- 1998/07/21 02:16 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1998/07/21 02:16 [entrez]
AID - 10.1002/(SICI)1098-2264(199808)22:4<295::AID-GCC5>3.0.CO;2-Q [pii]
PST - ppublish
SO  - Genes Chromosomes Cancer. 1998 Aug;22(4):295-304.