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Relaxation of insulin‐like growth factor 2 gene imprinting in esophageal cancer
Author(s) -
Mori Masaki,
Inoue Hiroshi,
Shiraishi Takeshi,
Mimori Koshi,
Shibuta Kenji,
Nakashima Hideaki,
Mafune Kenichi,
Tanaka Youichi,
Ueo Hiroaki,
Barnard Graham F.,
Sugimachi Keizo,
Akiyoshi Tsuyoshi
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19961115)68:4<441::aid-ijc7>3.0.co;2-0
Subject(s) - loss of heterozygosity , insulin like growth factor 2 , imprinting (psychology) , genomic imprinting , biology , exon , esophageal cancer , esophagus , gene expression , microbiology and biotechnology , gene , allele , cancer research , cancer , genetics , dna methylation , anatomy
Paternal allele‐specific expression is identified for the insulin‐like growth factor 2 ( IGF2 ) gene. Relaxation or loss of IGF2 imprinting, however, has been reported in several neoplasms. We studied the expression of IGF2 mRNA in 35 squamous cancers of the esophagus and searched for the presence or absence of relaxation of IGF2 imprinting. In 28 (80%) cases, IGF2 mRNA was overexpressed in the tumor tissues (T) compared to the normal tissues (N). The patients whose tumor invaded the adventitia showed a higher T/N ratio than those whose tumor was restricted to the musculi propria layer. Heterozygosity was determined by using the Apa 1 polymorphism in exon 9. Thirteen of 35 cases showed heterozygosity. In these 13 cases, a similar analysis was performed on cDNA obtained by reverse transcriptase‐polymerase chain reaction. Consequently, 7 cases disclosed relaxation of IGF2 imprinting in the tumor tissue. The cases of esophageal cancer with relaxation of IGF2 imprinting showed a higher T/N ratio and deeper invasion than those without relaxation. The results suggest that overexpression of IGF2 mRNA plays an important role in esophageal cancer and, in certain cases, is associated with relaxation of IGF2 imprinting. © 1996 Wiley‐Liss, Inc.