In conclusion, PTEN contributes in maintaining normal cell homeostasis, and the numerous alterations found in several sporadic tumor types emphasize the significance of this tumor suppressor gene. Somatic PTEN mutations appear to play an important role in the development of a subgroup of sporadic co
Integrating mutation data and structural analysis of the TP53 tumor-suppressor protein
β Scribed by Andrew C.R. Martin; Angelo M. Facchiano; Alison L. Cuff; Tina Hernandez-Boussard; Magali Olivier; Pierre Hainaut; Janet M. Thornton
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 678 KB
- Volume
- 19
- Category
- Article
- ISSN
- 1059-7794
No coin nor oath required. For personal study only.
β¦ Synopsis
Communicated by
π SIMILAR VOLUMES
## Communicated by Albert de la Chapelle PTEN regulates cell homeostasis by inhibiting growth signals transduced through PI3kinases. The gene is mutated in several cancer types, but so far, only a limited number of mutations have been reported in colorectal cancer. In the present study, direct seq
The tumor suppressor gene TP53 is frequently mutated in human cancers. More than 75% of all mutations are missense substitutions that have been extensively analyzed in various yeast and human cell assays. The International Agency for Research on Cancer (IARC) TP53 database (www-p53.iarc.fr) compiles
## Detection of mutations and polymorphisms in the p53 tumor suppressor gene by single-strand conformation polymorphism analysis Deciphering the genetic mechanisms in cancer development requires analysis of a large number of tumors for consistent genetic alterations. Single-strand conformational p
## Abstract Chronic lymphocytic leukemia (CLL) cells show constitutive nuclear factor kappa B (NFβΞΊB) activation, which may have a pathogenetic role. The mechanisms causing this NFβΞΊB activity are poorly understood. A20, encoded by the __TNFAIP3__ gene, is a repressor of the NFβΞΊB pathway and was r
The p53 protein is an ubiquitous multifunction, zinc-binding transcription factor that is activated in response to multiple forms of stress and that controls proliferation, survival, DNA repair, and differentiation of cells exposed to potentially genotoxic DNA-damage. Loss of p53 function by mutatio