Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-4-2
pubmed:abstractText
For prostate cancer, allelic deletions from the long arm of chromosome 10 (#10q23-25), the locus of the putative tumor suppressor gene MXI1 (#10q24-25), have been identified as a frequently occurring genetic event. During the development of several human malignancies, the c-myc proto-oncogene has been identified to enhance cellular transformation, mitogenesis and cell proliferation. The MXI1 gene, belonging to the helix-loop-helix (bHLH) gene family, was demonstrated to display tumor suppressor function by antagonizing c-myc induced transcriptional activities. Due to the detection of point mutations in the retained alleles of four primary adenocarcinomas of the prostate, MXI1 gene alterations have been suggested to be involved in the development and/or the progression of prostate cancer. To evaluate the role of MXI1 gene alterations for the development of adenocarcinoma of the prostate, 42 primary prostate cancers of different stage (T1-4) and histological grade (G1-3) were investigated for alterations within exons 4 and 5 of the MXI1 gene (spanning 6 exons in total), encoding for the functional HLH-Zip domain, by RNA-SSCP analysis and direct PCR-DNA-sequencing following the microscopically guided tumor cell dissection from 5 microm fresh-frozen buffer-soaked tissue sections. Even by application of this highly elaborated technical approach, MXI1 gene alterations could not be deleted in any of the tumor specimens investigated. Therefore, a substantial involvement of MXI1 gene alterations in the development of prostate cancer appears unlikely. The newly identified putative tumor suppressor gene PTEN, located at #10q23, might be responsible for the frequently observed allelic deletions from #10q23-25 in prostate cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1021-335X
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
213-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9458379-Adenocarcinoma, pubmed-meshheading:9458379-Alleles, pubmed-meshheading:9458379-Basic Helix-Loop-Helix Transcription Factors, pubmed-meshheading:9458379-Chromosome Mapping, pubmed-meshheading:9458379-Chromosomes, Human, Pair 10, pubmed-meshheading:9458379-DNA Primers, pubmed-meshheading:9458379-DNA-Binding Proteins, pubmed-meshheading:9458379-Exons, pubmed-meshheading:9458379-Gene Deletion, pubmed-meshheading:9458379-Genes, Tumor Suppressor, pubmed-meshheading:9458379-Helix-Loop-Helix Motifs, pubmed-meshheading:9458379-Humans, pubmed-meshheading:9458379-Male, pubmed-meshheading:9458379-Mutation, pubmed-meshheading:9458379-Neoplasm Staging, pubmed-meshheading:9458379-Polymerase Chain Reaction, pubmed-meshheading:9458379-Prostatic Neoplasms, pubmed-meshheading:9458379-Transcription Factors, pubmed-meshheading:9458379-Tumor Suppressor Proteins
pubmed:articleTitle
The MXI1 tumor suppressor gene is not mutated in primary prostate cancer.
pubmed:affiliation
Department of Urology, Hannover University Medical School, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't