Ontology type: schema:ScholarlyArticle Open Access: True
1999-11-25
AUTHORSShuji Nomoto, Nobuhiro Haruki, Takao Takahashi, Akira Masuda, Takashi Koshikawa, Toshitada Takahashi, Yoshitaka Fujii, Hirotaka Osada, Takashi Takahashi
ABSTRACTWe previously reported the presence of mitotic checkpoint impairment in about 40% of lung cancer cell lines. To gain an insight into the molecular basis of this impairment, we examined 49 lung cancer specimens for alterations in the hMAD1 mitotic checkpoint gene and identified a somatic, non-conservative missense mutation, which substitutes alanine (GCG) for threonine (ACG) at codon 299, together with a number of amino acid substituting, single nucleotide polymorphisms. This is the first demonstration of hMAD1 mutation in any type of human cancers. The present finding marks hMAD1 as a potential target, although with low frequency, for genetic alterations in lung cancer. Thus, further studies of hMAD1 dysfunction caused by other mechanisms appear to be warranted, as well as potential involvement of other components of the mitotic checkpoint. More... »
PAGES7180-7183
http://scigraph.springernature.com/pub.10.1038/sj.onc.1203141
DOIhttp://dx.doi.org/10.1038/sj.onc.1203141
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PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/10597320
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