Sequentially expressed temporal transcription factors in neural stem cells during early development determine which progeny can undergo malignant transformation upon dedifferentiation.

G9a regulates chromatin-bound b-catenin enabling cell-intrinsic control of WNT signaling-mediated cell fate decisions.

The transcription factor RUNX1 marks a distinct lineage of luminal castration-resistant prostate cells established early during development and enriched in the periurethral region of adult mouse prostate.

About twenty temporal patterning genes are identified that drive an irreversible differentiation trajectory governing the heterogeneity and proliferative properties of cells in neural tumors with an early developmental origin.

Different types of epigenetic DNA modifications affect the likelihood of cytosine mutations in cancer.

Ectopic expression of Dnmt3b leads to wide-spread CpG island hypermethylation that is largely defined by chromatin state and has some distinct features when compared to the cancer methylome.

Genes with parent-of-origin specific expression are not as numerous as previously reported and validated parentally-biased expressed genes tend to be peripheral to known imprinted domains indicating shared regional control.

The genetic background of a cancer cell and the chromatin organization of the tissue-of-origin impact the amount, length and position of somatic copy number alterations in cancer.

The unique cell cycle variations of pluripotent stem cells ensures that the first step in DNA replication is particularly fast and this rapid rate, in turn, restrains early differentiation.

The ~20,000 origins of replication in human cell lines that are reproducibly identified by multiple techniques in multiple cell lines are distant from known origin recognition complex and MCM2-7-binding sites.