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| Article |
| Alterations of Fas (Apo-1/CD95) gene in non-small cell lung cancer |
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| Sug Hyung Lee1,4,a, Min Sun Shin1,a, Won Sang Park1,4, Su Young Kim1, Ho Sik Kim2, Ji Youn Han3, Gyeong Sin Park1, Seung Myung Dong1, Jae Ho Pi1, Choo Soung Kim1, Sang Ho Kim1, Jung Young Lee1,4 and Nam Jin Yoo1,4 |
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1Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea
2Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea
3Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea
4Cancer Research Institute, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul 137-701, Korea
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Correspondence to: Nam Jin Yoo, Department of Pathology, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Socho-gu, Seoul 137-701, Korea
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aSH Lee and MS Shin contributed equally to this study |
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| Abstract |
| Fas (Apo-1/CD95) is a cell-surface receptor involved in cell death signaling. The key role of the Fas system in negative growth regulation has been studied mostly within the immune system, and somatic mutations of Fas gene in cancer patients have been described solely in lymphoid-lineage malignancies. However, many non-lymphoid tumor cells have been found to be resistant to Fas-mediated apoptosis, which suggests that Fas mutations, one of the possible mechanisms for Fas-resistance, may be involved in the pathogenesis of non-lymphoid malignancies as well. In this study, we have analysed the entire coding region and all splice sites of the Fas gene for the detection of the gene mutations in 65 human non-small cell lung cancers by polymerase chain reaction, single strand conformation polymorphism and DNA sequencing. Overall, five tumors (7.7%) were found to have the Fas mutations, which were all missense mutations. Four of the five mutations identified were located in the cytoplasmic region (death domain) known to be involved in the transduction of an apoptotic signal and one mutation was located in the transmembrane domain. This is the first report on the Fas gene mutations in non-lymphoid malignancies, and the data presented here suggests that alterations of the Fas gene might lead to the loss of its apoptotic function and contribute to the pathogenesis of some human lung cancers. |
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| Keywords |
| lung cancer; apoptosis; Fas; mutation; loss of heterozygosity |
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| Received 27 November 1998; revised 9 February 1999; accepted 26 February 1999 |
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| 24 June 1999, Volume 18, Number 25, Pages 3754-3760 |
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