Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1998-4-16
pubmed:abstractText
We examined 61 lung cancer cases to determine whether alterations of p73, a novel monoallelically expressed p53-like molecule, may be involved in the pathogenesis of lung cancer. Allelic loss at the p73 locus at 1p36.33 was observed in 42% (11 of 26 informative cases), and squamous cell carcinoma tended to carry this lesion most frequently. Somatic mutations in the p73 gene itself, however, were not detected, despite our extensive search. We found interindividual difference in the allelic expression of p73 in normal lung, as well as intertissue variance, even within the same individual, but preferential loss of the expressed allele appeared to be an unlikely mechanism for p73 inactivation. This study, consequently, suggests the presence of an as yet unidentified tumor suppressor gene or genes within the subtelomeric region of 1p, warranting further studies aimed at its isolation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1380-3
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Search for mutations and examination of allelic expression imbalance of the p73 gene at 1p36.33 in human lung cancers.
pubmed:affiliation
Laboratory of Ultrastructure Research, Aichi Cancer Center Research Institute, Nagoya, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't