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Restoration of the tumor suppressor function to mutant p53 by a low-molecular-weight compound
This work found one compound capable of inducing apoptosis in human tumor cells through restoration of the transcriptional transactivation function to mutant p53, named PRIMA-1, which rescued both DNA contact and structural p53 mutants in vitro and in living cells. Expand
PRIMA-1 reactivates mutant p53 by covalent binding to the core domain.
It is shown that PRIMA-1 is converted to compounds that form adducts with thiols in mutant p53, which is sufficient to induce apoptosis in tumor cells and facilitate the design of more potent and specific mutant p 53-targeting anticancer drugs. Expand
Contrasting patterns of retinoblastoma protein expression in mouse embryonic stem cells and embryonic fibroblasts.
Absence of hypophosphorylated RB and cell cycle-dependent change in total RB protein level may be relevant to the high proliferation rate and to the tumorigenic nature of mouse embryonic stem cells. Expand
Wrap53, a Natural p53 Antisense Transcript Required for p53 Induction upon DNA Damage.
This data indicates that cell signaling in the immune system is regulated by a number of mechanisms, including “cell reprograming” and “self-consistency”, and the use of these mechanisms alone is likely to improve the prognosis for cancer patients. Expand
Targeting mutant p53 for efficient cancer therapy
Recent progress in pharmacological reactivation of mutant p53 is discussed and problems and promises with these strategies are highlighted. Expand
Myc and E2F1 induce p53 through p14ARF-independent mechanisms in human fibroblasts
The results indicate that p53 phosphorylation, but not p14ARF, plays a major role for the induction of p53 in response to Myc and E2F1 activation in normal human fibroblasts. Expand
Downregulation of telomerase reverse transcriptase mRNA expression by wild type p53 in human tumor cells
It is demonstrated that p53 is also a powerful inhibitor of human telomerase reverse transcriptase (hTERT), a key component for telomersase, and wt p53-triggered inhibition of hTERT/telomerase expression may reflect yet another mechanism of p 53-mediated tumor suppression. Expand
p14ARF Deletion and Methylation in Genetic Pathways to Glioblastomas
It is suggested that aberrant p14ARF expression due to homozygous deletion or promoter hypermethylation is associated with the evolution of both primary and secondary glioblastomas, and that p14 ARF promoter methylation is an early event in subset of astrocytomas that undergo malignant progression to secondary gl ioblastoma. Expand
Restoration of the growth suppression function of mutant p53 by a synthetic peptide derived from the p53 C-terminal domain
We demonstrate here that synthetic 22-mer peptide 46, corresponding to the car boxy-terminal amino acid residues 361–382 of p53, can activate specific DNA binding of wild-type p53 in vitro and canExpand
Targeting p53 in vivo: a first-in-human study with p53-targeting compound APR-246 in refractory hematologic malignancies and prostate cancer.
It is concluded that APR-246 is safe at predicted therapeutic plasma levels, shows a favorable pharmacokinetic profile, and can induce p53-dependent biologic effects in tumor cells in vivo. Expand