Abstract:
:We previously reported the presence of mitotic check-point 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.
journal_name
Oncogenejournal_title
Oncogeneauthors
Nomoto S,Haruki N,Takahashi T,Masuda A,Koshikawa T,Takahashi T,Fujii Y,Osada H,Takahashi Tdoi
10.1038/sj.onc.1203141subject
Has Abstractpub_date
1999-11-25 00:00:00pages
7180-3issue
50eissn
0950-9232issn
1476-5594journal_volume
18pub_type
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