๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

Mechanisms of p16INK4A inactivation in non small-cell lung cancers

โœ Scribed by Gazzeri, Sylvie; Gouyer, Valerie; Vour'ch, Clair; Brambilla, Christian; Brambilla, Elisabeth

Book ID
110061119
Publisher
Nature Publishing Group
Year
1998
Tongue
English
Weight
560 KB
Volume
16
Category
Article
ISSN
0950-9232

No coin nor oath required. For personal study only.

๐Ÿ“œ SIMILAR VOLUMES

Intragenic mutations of the p16INK4, p15
Intragenic mutations of the p16INK4, p15INK4B and p18 genes in primary non-small-cell lung cancers
โœ Marek R. Rusin; Aikou Okamoto; Mieczyslaw Chorazy; Kazimierz Czyzewski; Jolanta ๐Ÿ“‚ Article ๐Ÿ“… 1996 ๐Ÿ› John Wiley and Sons ๐ŸŒ French โš– 721 KB

The p p ! 6INK4 and p I8 genes are members of the gene famil coding for inhibitors of cyclin-dependent kinases 4 and 6. frequently deleted in many human neoplasms. To examine the role of these 3 genes in lung carcinogenesis, somatic mutations within the genes were analyzed by single-strand conformat

p16INK4A and CDH13 hypermethylation in t
p16INK4A and CDH13 hypermethylation in tumor and serum of non-small cell lung cancer patients
โœ Paola Ulivi; Wainer Zoli; Daniele Calistri; Francesco Fabbri; Anna Tesei; Marco ๐Ÿ“‚ Article ๐Ÿ“… 2005 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 131 KB

## Abstract Aberrant promoter hypermethylation of several known or putative tumor suppressor genes occurs frequently during the etiopathogenesis of lung cancer and is a promising tool for cancer detection. In the present study, promoter hypermethylation of __p16^INK4A^__ and __CDH13__ genes was inv