Xin Lu

TL;DR: Understanding the complex mechanisms that regulate whether or not a cell dies in response to p53 will ultimately contribute to the development of therapeutic strategies to repair the apoptotic p53 response in cancers.

TL;DR: A functional classification of cell death subroutines is proposed that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic programmed cell death, regulated necrosis, autophagic cell death and mitotic catastrophe.

TL;DR: The authors find no substantive defect in the p53 response of cells from ataxia telangiectasia or xeroderma pigmentosum complementation group A patients, and 2 out of 11 primary cultures from Bloom's patients showed a complete absence of p53 accumulation following UV irradiation or SV40 infection and a grossly delayed and aberrant response following X-ray.

TL;DR: The expression of ASPP is frequently downregulated in human breast carcinomas expressing wild-type p53 but not mutant p53, therefore, ASPP regulate the tumor suppression function of p53 in vivo.

TL;DR: Polymorphism in p53 may influence individual responsiveness to cancer therapy, and clinical response following cisplatin-based chemo-radiotherapy for advanced head and neck cancer is influenced by this polymorphism, cancers expressing 72R mutants having lower response rates than those expressing 72P mutants.