AI Article Synopsis
- Allele loss at chromosome region 17p is common in lung cancer and is associated with recessive oncogenes, highlighting the importance of this area in cancer development.
- The p53 gene, located on 17p13, often shows mutations or inactivation across various human lung cancers, suggesting its role as an important tumor suppressor.
- Abnormal genetic changes to p53, including deletions and mutations, alongside significantly lower expression of p53 in lung cancer cells compared to normal cells, link its disruption to lung cancer's progression.
Article Abstract
Allele loss is a hallmark of chromosome regions harboring recessive oncogenes. Lung cancer frequently demonstrates loss of heterozygosity on 17p. Recent evidence suggests that the p53 gene located on 17p13 has many features of such an antioncogene. The p53 gene was frequently mutated or inactivated in all types of human lung cancer. The genetic abnormalities of p53 include gross changes such as homozygous deletions and abnormally sized messenger RNAs along with a variety of point or small mutations, which map to the p53 open reading frame and change amino acid sequence in a region highly conserved between mouse and man. In addition, very low or absent expression of p53 messenger RNA in lung cancer cell lines compared to normal lung was seen. These findings, coupled with the previous demonstration of 17p allele loss in lung cancer, strongly implicate p53 as an anti-oncogene whose disruption is involved in the pathogenesis of human lung cancer.
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| http://dx.doi.org/10.1126/science.2554494 | DOI Listing |
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