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556 Ectopic p16INK4 expression enhances the susceptibility of human non-small cell lung cancer (NSCLC) cells to CPT-11-induced apoptosis

โœ Scribed by Fukuoka, K.; Nishio, K.; Adachi, J.; Arioka, H.; Kurokawa, H.; Fukumoto, H.; Ishida, T.; Nomoto, T.; Yokote, H.; Tomonari, A.; Iwamoto, Y.; Suzuki, T.; Usuda, J.; Yokota, J.; Saijo, N.


Book ID
122613857
Publisher
Elsevier Science
Year
1997
Tongue
English
Weight
162 KB
Volume
18
Category
Article
ISSN
0169-5002

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Ectopic p16ink4 expression enhances CPT-
โœ Kazuya Fukuoka; Kazuto Nishio; Hisao Fukumoto; Hitoshi Arioka; Hirokazu Kurokawa ๐Ÿ“‚ Article ๐Ÿ“… 2000 ๐Ÿ› John Wiley and Sons ๐ŸŒ French โš– 164 KB

A tumor-suppressor gene, p16 INK4 , which is deleted or mutated in tumors, regulates cell-cycle progression through a G 1 -S restriction point by inhibiting CDK4(CDK6)/cyclin-Dmediated phosphorylation of pRb. We have found that ectopic p16 INK4 expression increased cellular sensitivity of human non-