Premium
Aberrant FHIT transcripts in cancerous and corresponding non‐cancerous lesions of the digestive tract
Author(s) -
Chen YiJen,
Chen PaoHuei,
Lee MengDar,
Chang JanGowth
Publication year - 1997
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(19970917)72:6<955::aid-ijc6>3.0.co;2-o
Subject(s) - fhit , biology , carcinogenesis , gene , exon , tumor suppressor gene , digestive tract , complementary dna , cancer , gene expression , microbiology and biotechnology , pathology , cancer research , genetics , medicine
The FHIT gene was recently discovered and proposed as a tumor‐suppressor gene. We examined the FHIT gene in a panel of digestive‐tract cancers along with their corresponding non‐tumorous tissues by reverse transcription of FHIT mRNA followed by PCR amplification and sequencing of the products. A normal FHIT transcript was found to be expressed at robust levels in 44 of 46 cancerous tissues and in all of 46 non‐cancerous tissues tested. Of the 46 cancerous specimens, 21 (45.7%) revealed the occurrence of aberrant transcripts. In addition, of the 46 matched normal tissues, 14 (30.4%) showed the existence of aberrant transcripts. Sequence analysis confirmed that aberrant transcripts were missing in one or more exons of the FHIT cDNA, while 8 cases displayed aberrant transcripts of the FHIT gene both in cancerous and in non‐cancerous tissues. However, sequence analysis revealed that the patterns of the aberrant transcripts were different between the corresponding paired samples. In addition, there were 6 cases displaying aberrant FHIT transcripts only in their normal‐tissue counterparts. These studies indicate that abnormalities of the FHIT gene transcripts occur at a fairly high frequency in cancerous and corresponding non‐cancerous lesions of the digestive tract. However, they might not be causally related to the tumorigenesis of the digestive tract. Int. J. Cancer 72:955–958, 1997. © 1997 Wiley‐Liss, Inc.