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Point Mutations of the Mxil Gene are Rare in Prostate Cancers
Author(s) -
Kawamata Norihiko,
Park Dorothy,
Wilczynski Sharon,
Yokota Jun,
Koeffler H. Phillip
Publication year - 1996
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/1097-0045(199609)29:3<191::aid-pros2990290305>3.0.co;2-1
Subject(s) - point mutation , gene , biology , single strand conformation polymorphism , prostate , leucine zipper , cancer research , locus (genetics) , prostate cancer , genetics , tumor suppressor gene , chromoplexy , exon , mutation , carcinogenesis , transcription factor , pca3 , cancer
Overexpression of the Myc genes promote cellular transformation. Max protein exerts a pivotal function with the Myc family, and Mxil/Mad proteins play a positive and negative activity, respectively, on transcription. The function of Mxil suggests that it might be a tumor suppressor protein. The Mxil gene map to 1Op24‐25 and deletions of this locus are frequently observed in prostate cancers. The N‐terminal helical motif, helix‐loop‐helix (HLH) and leucine zipper (ZIP) regions of the Mxil gene are functionally important. We analyzed most of the coding region of the Mxil gene, including these three important regions in 32 prostate cancers and three cell lines by PCR‐single strand conformational polymorphism (SSCP). To enrich neoplastic cells, the microdissection was performed on clinical samples. We detected a silent mutation in the HLH region, but no point mutations reflecting the functional change of Mxil were found in human prostate cancers. Point mutations of the Mxil gene, if they occur, must be minor events in primary prostate cancers. © 1996 Wiley‐Liss, Inc.