2000
DOI: 10.1002/(sici)1521-3773(20000515)39:10<1768::aid-anie1768>3.0.co;2-a
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The Tumor Suppressor p53 in the Center of a Strategy Aiming at the Alleviation of Side Effects in Cancer Therapies

Abstract: An inhibitor of the transcriptional functions of p53 was identified as pifitrin α 1 by screening. In cellular stress situations, the tumor suppressor p53 counteracts growth or causes active cell death (apoptosis) to avoid the manifestation of damage within the genome. On the basis of these cytotoxic properties, however, p53 also has detrimantal effects on healthy tissues during cancer therapies. These side effects can possibly be minimized by simultaneous application of 1.

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Cited by 5 publications
(2 citation statements)
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“…17 in human and most mammals; it encodes for a 53 kDa phosphoprotein which has the ability of binding to DNA and acting as a transcription factor. In response to chemical damage, p53 is activated to direct stress-specific transcriptional response programs such as slowing down cell division or induce programmed cell death [6, 7] which makes it a primary target for inactivation in cancer [8]. Therefore, p53 is one of the most frequently mutated genes in human cancers with the most mutations detected are Single-Nucleotide Polymorphisms (SNPs) [9].…”
Section: Introductionmentioning
confidence: 99%
“…17 in human and most mammals; it encodes for a 53 kDa phosphoprotein which has the ability of binding to DNA and acting as a transcription factor. In response to chemical damage, p53 is activated to direct stress-specific transcriptional response programs such as slowing down cell division or induce programmed cell death [6, 7] which makes it a primary target for inactivation in cancer [8]. Therefore, p53 is one of the most frequently mutated genes in human cancers with the most mutations detected are Single-Nucleotide Polymorphisms (SNPs) [9].…”
Section: Introductionmentioning
confidence: 99%
“…Studies on cancer formation of heterozygote over null mive have provided clear evidence of haploinsuffiency at the Trp53 locus [89], and this haploinsuffiency is reflected by a partial loss of HR control functions in mouse embryo fibroblasts from Trp53+/-mice, when using the fluorescence-based test [126]. For the development of p53-based therapeutic strategies scientists have tested the applicability of synthetic peptides and small molecule compounds to enhance or to reconstitute p53-dependent activities in transcription, cell cycle control, and apoptosis induction [127]. Recently, progress has been made in targeting breast cancer by a novel therapeutic approach that selectively kills DSB repair defective cells [128].…”
Section: Conclusion: Dsb Repair Activities As a Potential Marker Of mentioning
confidence: 99%