Loss of chromosome arms 3p and 9p and inactivation ofP16INK4a in normal epithelium of patients with primary lung cancer
- 8 August 2001
- journal article
- research article
- Published by Wiley in Genes, Chromosomes and Cancer
- Vol. 32 (2), 119-125
- https://doi.org/10.1002/gcc.1173
Abstract
No abstract availableKeywords
This publication has 20 references indexed in Scilit:
- Epigenetic inactivation of a RAS association domain family protein from the lung tumour suppressor locus 3p21.3Nature Genetics, 2000
- Mechanisms of p16INK4A inactivation in non small-cell lung cancersOncogene, 1998
- Detailed deletion mapping at chromosome 9p21 in non-small cell lung cancer by microsatellite analysis and fluorescencein situ hybridizationInternational Journal of Cancer, 1997
- Clonal Genetic Alterations in the Lungs of Current and Former SmokersJNCI Journal of the National Cancer Institute, 1997
- Detection of chromosome instability of tissue fields at risk: In situ hybridizationJournal of Cellular Biochemistry, 1996
- Frequency of homozygous deletion at p16/CDKN2 in primary human tumoursNature Genetics, 1995
- Allele-Specific Loss in Chromosome 9p Loci in Preneoplastic Lesions Accompanying Non-Small-Cell Lung CancersJNCI Journal of the National Cancer Institute, 1995
- 5′ CpG island methylation is associated with transcriptional silencing of the tumour suppressor p16/CDKN2/MTS1 in human cancersNature Medicine, 1995
- Rates of p16 ( MTS1 ) Mutations in Primary Tumors with 9p LossScience, 1994
- Development of carcinoma of the lung as reflected in exfoliated cellsCancer, 1974