Promoter hypermethylation and homozygous deletion of P16INK4A in biliary tract cancer
โ Scribed by Karel Caca; Juergen Faisthammel; Andrea Tannapfel; Joachim Moessner; Frieder Berr
- Book ID
- 119425374
- Publisher
- Elsevier Science
- Year
- 2000
- Tongue
- English
- Weight
- 167 KB
- Volume
- 118
- Category
- Article
- ISSN
- 0016-5085
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We have studied p16(INK4) mutation (by PCR-SSCP) and deletion (by Southern blotting and/or multiplex PCR) in a series of 47 bilharziasis-associated tumors from Egypt and compared the results with those obtained on a series of 17 established bladder cell lines and non-bilharziasis-associated bladder
Inactivation of p16(INK4a) in the Rb pathway is among the most common somatic alterations observed in nonsmall cell lung cancers (NSCLCs). While epigenetic inactivation of the p16(INK4a) gene promoter has been shown to be associated with increased tobacco carcinogen exposure, little investigation of
## Abstract Inactivation of p16INK4a gene through promoter hypermethylation has been frequently observed in non small cell lung cancer; however, various studies have shown a controversial correlation between p16INK4a hypermethylation and cigarette smoking. Our recent report showed that human papill