There’s lots of attention, not to mention several therapeutics, focused on chromatin’s part in cancer. Take a look at some of the research featured in EpiGenie that makes chromatin such a hot topic with cancer researchers.
The Role of Chromatin in Cancer
Epigenetic Changes in a Hard-to-Treat Childhood Cancer
A very difficult-to-treat childhood leukemia may benefit from the discovery of a small but potent epigenetic change that launches the cancer⎯but could potentially be reversed relatively easily, preventing cancer-promoting genes from being turned on.
Non-Hodgkin Lymphoma’s Trouble with Histone-Modifiers
They say it’s the quiet ones that you have to watch out for. Canadian researchers may have had that in mind when they pondered the genetic causes of non-Hodgkin lymphoma (NHL). Through some extra digging (and sequencing), they uncovered several mutant genes that had remained hidden until now, including some that have roles in histone methylation and acetylation.
EZH2: Cancer Villain or MDS Hero?
EZH2 takes a lot of abuse, and is often labeled as a dreaded oncogene , but like a movie villain who redeems themselves in the end, the histone methyltransferase isn’t all evil. According to two new papers published simultaneously in Nature Genetics, EZH2 may in fact function as a tumor suppressor in some blood cancers.
Methylation and HDAC Inhibitors Rouse Cancer-Fighting miRNAs into Action
Recent advances in epigenetic therapy are promising, but their mechanisms of action and impact elsewhere in the epigenome remain a bit of a mystery. Armed with microarrays and ChIP assays, a talented team of Japanese researchers took a closer look at these approaches and found DNA methylation inhibitors and histone deacetylase (HDAC) inhibitors kill gastric cancer cells by waking up silenced miRNAs nestled near Alu repeats. Once activated, these miRNAs are ready to do battle, silencing oncogenes and driving cancer cells into apoptosis.
What is Suppressing The Suppressors?: Modified CTCFs linked to silenced tumor suppressors
Looking for exotic enzymes to silence tumor suppressor genes? You might be searching in vain. Maybe try looking for heterochromatin instead.
Salk Institute postdoc Michael Witcher was baffled by what made p16INK4a not tick in breast cancer cells. He fed the genetic sequence into some prediction software, but it wasn’t much help. So he did what any technophobe might do – he eyeballed it, upstream and down and eventually found long repeat elements and AT-rich regions, which are classically associated with nuclear matrix and condensed chromatin structure, along with a curious CCCTC motif, about 2 kb upstream of the proximal promoter.