Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-4-20
pubmed:abstractText
The genetic events underlying the development of prostate cancer are poorly defined. c-Myc is often activated in tumors that have progressed to metastatic status, so events that promote this process may be important. Bin1 is a nucleocytoplasmic adaptor protein with features of a tumor suppressor that was identified through its ability to interact with and inhibit malignant transformation by c-Myc. We investigated a role for Bin1 loss or inactivation in prostate cancer because the human Bin1 gene is located at chromosome 2q14 within a region that is frequently deleted in metastatic prostate cancer but where no tumor suppressor candidate has been located. A novel polymorphic microsatellite marker located within intron 5 of the human Bin1 gene was used to demonstrate loss of heterozygosity and coding alteration in 40% of informative cases of prostate neoplasia examined. RNA and immunohistochemical analyses indicated that Bin1 was expressed in most primary tumors, even at slightly elevated levels relative to benign tissues, but that it was frequently missing or inactivated by aberrant splicing in metastatic tumors and androgen-independent tumor cell lines. Ectopic expression of Bin1 suppressed the growth of prostate cancer lines in vitro. Our findings support the candidacy of Bin1 as the chromosome 2q prostate tumor suppressor gene.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
86
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
155-61
pubmed:dateRevised
2007-7-24
pubmed:meshHeading
pubmed-meshheading:10738240-Adaptor Proteins, Signal Transducing, pubmed-meshheading:10738240-Adenocarcinoma, pubmed-meshheading:10738240-Alternative Splicing, pubmed-meshheading:10738240-Blotting, Northern, pubmed-meshheading:10738240-Carrier Proteins, pubmed-meshheading:10738240-Genes, Tumor Suppressor, pubmed-meshheading:10738240-Genes, myc, pubmed-meshheading:10738240-Humans, pubmed-meshheading:10738240-Immunohistochemistry, pubmed-meshheading:10738240-Introns, pubmed-meshheading:10738240-Loss of Heterozygosity, pubmed-meshheading:10738240-Male, pubmed-meshheading:10738240-Microsatellite Repeats, pubmed-meshheading:10738240-Nuclear Proteins, pubmed-meshheading:10738240-Prostatic Intraepithelial Neoplasia, pubmed-meshheading:10738240-Prostatic Neoplasms, pubmed-meshheading:10738240-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:10738240-Tumor Cells, Cultured, pubmed-meshheading:10738240-Tumor Suppressor Proteins
pubmed:year
2000
pubmed:articleTitle
Loss of heterozygosity and tumor suppressor activity of Bin1 in prostate carcinoma.
pubmed:affiliation
The Wistar Institute, Philadelphia, Pennsylvania, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't