p53 inactivation by point mutations and splice site mutations in human and mouse tumors

TL;DRAbstract

<p>The p53 tumor suppressor gene is frequently mutated in human tumors. p53 induces cell cycle arrest and/or apoptosis in response to cellular stress, such as DNA damage, hypoxia and certain activated oncogenes like c-myc.</p><p>The status of p53 in Burkitt's Iymphoma (BL) cell lines was investigated. The majority of BL lines expressed mutated p53 protein. Functional reconstitution with exogenous wild type (wt) p53 induced apoptosis in a BL line that carried a mutated p53 gene. These results substantiate the findings that c-myc induced apoptosis is p53 mediated, since all BLs carry activated c-myc by a c- myc/Ig translocation.</p><p>Established ascites tumor cells grow under highly crowded, virtually anoxic conditions. Hypoxia is a powerful inducer of p53-dependent apoptosis. Would conversion of relatively well-vascularized solid mouse tumors into freely growing ascitic cell variants favor cells with mutated or deleted p53? PCR and sequence analysis showed

Chat with Paper

AI Agents for this Paper