Abstract
The FHIT gene is considered to be a tumor suppressor gene, its role and inactivation mechanism remain unclear. We analyzed FHIT gene aberrations in 64 lung cancer tissues and found that the appearance of the aberrant FHIT transcripts depends on the condition of RT-PCR and high telomerase activity, shortened telomere length, and advanced pathological stage were likely associated with the prevalence of aberrant FHIT transcripts, but not with allelic loss of the FHIT gene. These observations would indicate that an additional unknown gene may exist, which is more responsible for the allelic loss around the FHIT gene locus.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acid Anhydride Hydrolases*
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Alleles
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Carcinoma, Non-Small-Cell Lung / genetics*
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Carcinoma, Non-Small-Cell Lung / metabolism
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Carcinoma, Small Cell / genetics*
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Carcinoma, Small Cell / metabolism
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Chromosomes, Human / ultrastructure
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Gene Expression Regulation, Neoplastic*
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Genes, Tumor Suppressor*
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Humans
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Loss of Heterozygosity
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Lung Neoplasms / genetics*
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Lung Neoplasms / pathology
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Neoplasm Proteins / biosynthesis
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Neoplasm Proteins / genetics*
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Protein Biosynthesis
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Proteins / genetics*
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RNA Splicing*
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RNA, Messenger / genetics
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RNA, Messenger / metabolism*
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RNA, Neoplasm / genetics
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RNA, Neoplasm / metabolism*
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Reverse Transcriptase Polymerase Chain Reaction
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Telomerase / metabolism
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Telomere / ultrastructure
Substances
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Neoplasm Proteins
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Proteins
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RNA, Messenger
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RNA, Neoplasm
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fragile histidine triad protein
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Telomerase
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Acid Anhydride Hydrolases