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Cancer stem cells--perspectives on current status and future directions: AACR Workshop on cancer stem cells.
A workshop was convened by the AACR to discuss the rapidly emerging cancer stem cell model for tumor development and progression. The meeting participants were charged with evaluating data suggesting…
Histone–GFP fusion protein enables sensitive analysis of chromosome dynamics in living mammalian cells
Regulating the p53 pathway: in vitro hypotheses, in vivo veritas
This Review of in vitro studies, human tumour data and recent mouse models shows that p53 post-translational modifications have modulatory roles, and MDM2 andMDM4 have more profound roles for regulating p53.
MDM2, MDMX and p53 in oncogenesis and cancer therapy
This Review highlights the progress made and pitfalls encountered as the field continues to search for MDM-targeted antitumour agents.
A leucine‐rich nuclear export signal in the p53 tetramerization domain: regulation of subcellular localization and p53 activity by NES masking
A model in which regulated p53 tetramerization occludes its NES is proposed, thereby ensuring nuclear retention of the DNA‐binding form and suggesting that attenuation of p53 function involves the conversion of tetramers into monomers or dimers, in which the NES is exposed to the proteins which mediate their export to the cytoplasm.
Efficient transfer of large DNA fragments from agarose gels to diazobenzyloxymethyl-paper and rapid hybridization by using dextran sulfate.
- G. Wahl, M. Stern, G. Stark
- Biology, ChemistryProceedings of the National Academy of Sciences…
- 1 August 1979
Ten percent dextran sulfate accelerates the rate of hybridization of randomly cleaved double-stranded DNA probes to immobilized nucleic acids by as much as 100-fold, without increasing the background significantly.
Hybridization of nucleic acids immobilized on solid supports.
Extrachromosomal oncogene amplification drives tumor evolution and genetic heterogeneity
It is shown that ecDNA was found in nearly half of human cancers; its frequency varied by tumour type, but it was almost never found in normal cells, and the results suggest that ec DNA contributes to accelerated evolution in cancer.
c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function: a mechanism for oncogene-induced genetic instability.