Genomic Imprinting of Human p57KIP2 and Its Reduced Expression in Wilms' Tumors

p57KIP2 is a potent tight-binding inhibitor of several G1 cyclin complexes, and is a negative regulator of cell proliferation. The gene encoding human p57KIP2is located on chromosome 11p15.5, a region implicated in both sporadic cancers and Beckwith-Wiedemann syndrome (BWS), a cancer syndrome, makin...

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Bibliographic Details
Published in:Human molecular genetics 1996-06, Vol.5 (6), p.783-788
Main Authors: Hatada, Izuho, Inazawa, Johji, Abe, Tatsuo, Nakayama, Masahiro, Kaneko, Yasuhiko, Jinno, Yoshihiro, Niikawa, Norio, Ohashi, Hirofumi, Fukushima, Yoshimitsu, Iida, Kazuki, Yutani, Chikao, Takahashi, Shun-ichi, Chiba, Yoshihide, Ohishi, Sachiko, Mukai, Tsunehiro
Format: Article
Language:English
Subjects:
Alleles
Base Sequence
Biological and medical sciences
Chromosome Mapping
Cyclin-Dependent Kinase Inhibitor p57
DNA
Gene Expression
Genomic Imprinting
Humans
Kidneys
Medical sciences
Molecular Sequence Data
Nephrology. Urinary tract diseases
Nuclear Proteins - genetics
Tumors of the urinary system
Wilms Tumor - genetics
Wilms Tumor - metabolism
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Summary:p57KIP2 is a potent tight-binding inhibitor of several G1 cyclin complexes, and is a negative regulator of cell proliferation. The gene encoding human p57KIP2is located on chromosome 11p15.5, a region implicated in both sporadic cancers and Beckwith-Wiedemann syndrome (BWS), a cancer syndrome, making it a tumor suppressor candidate. Several types of childhood tumors including Wilms' tumor, adrenocortical carcinoma and rhabdomyosarcoma display a specific loss of maternal 11p15 alleles, suggesting that genomic imprinting plays an important part. Genetic analysis of the familial BWS has indicated maternal carriers and suggested a role in genomic imprinting. Previously, we demonstrated that p57KIP2is imprinted in the mouse. Here we describe the genomic imprinting of human p57KIP2and the reduction of its expression in Wilms' tumors. High resolution mapping locates p57KIP2 in the region responsible for both tumor suppressivity and BWS.
ISSN:0964-6906
1460-2083
1460-2083
DOI:10.1093/hmg/5.6.783