Linked Life Data

10229497

Source:http://linkedlifedata.com/resource/pubmed/id/10229497

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-6-11
pubmed:abstractText
Max interacting protein 1 (MXI1), a negative regulator of myc oncoprotein with tumor suppressor properties, has been mapped to chromosome 10q24-25. MXI1 gene loss, demonstrated by loss of heterozygosity (LOH) analysis (allelic imbalance), is a frequent event in astrocytomas and other forms of glial neoplasia. Development and progression of malignant melanoma likely involves several cooperative oncogene/tumor suppressor gene alterations, many of which remain to be elucidated. We sought to discover whether desmoplastic melanoma (DM) exhibited MXI1 LOH. Archival fixative treated tissue was used for genotyping; this necessitated a microdissection-based molecular approach uniquely designed for minute tissue samples. Nineteen formalin-fixed tissue samples from 11 patients representing primary, locally recurrent, and metastatic DM were available for study. In each case, normal and neoplastic tissue was microdissected under stereomicroscopic observation as a basis for genetic analysis. We identified MXI1 LOH in neoplastic tissue by observing allelic imbalance for a microsatellite repeat polymorphism in the 3' nontranslated region of the MXI1 gene in subjects shown to be informative. Colorectal adenocarcinoma (n = 21) and astrocytomas (n = 19) were similarly analyzed, serving as negative and positive controls, respectively, for MXI1 LOH. Five of 11 DMs in subjects informative for the MXI1 microsatellite manifested MXI1 allelic imbalance consistent with tumor suppressor LOH. Genotype fidelity with respect to MXI1 status was present in two patients from whom primary and recurrent tumor was available for comparative analysis. We found that MXI1 LOH was independent of tumor stage and survival. MXI1 LOH seems to be a relatively frequent and early event in DM development and progression, consistent with neuroectodermal histogenesis of the neoplasm.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0893-3952
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
344-50
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10229497-Adult, pubmed-meshheading:10229497-Aged, pubmed-meshheading:10229497-Basic Helix-Loop-Helix Transcription Factors, pubmed-meshheading:10229497-DNA, Neoplasm, pubmed-meshheading:10229497-DNA-Binding Proteins, pubmed-meshheading:10229497-Female, pubmed-meshheading:10229497-Genotype, pubmed-meshheading:10229497-Humans, pubmed-meshheading:10229497-Immunohistochemistry, pubmed-meshheading:10229497-Loss of Heterozygosity, pubmed-meshheading:10229497-Male, pubmed-meshheading:10229497-Melanoma, pubmed-meshheading:10229497-Microsatellite Repeats, pubmed-meshheading:10229497-Middle Aged, pubmed-meshheading:10229497-Polymorphism, Genetic, pubmed-meshheading:10229497-S100 Proteins, pubmed-meshheading:10229497-Transcription Factors, pubmed-meshheading:10229497-Tumor Suppressor Proteins
pubmed:year
1999
pubmed:articleTitle
Max interacting protein 1: loss of heterozygosity is frequent in desmoplastic melanoma.
pubmed:affiliation
Department of Pathology, Presbyterian University Hospital, University of Pittsburgh Medical Center, Pennsylvania 15213-2582, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't