A new method has been found for identifying therapeutic targets in cancers lacking specific
key tumor suppressor genes.
However, the impact of the two methylation - regulating enzymes was still seen at 10 to 15 months, when scientists found decreased expression of hundreds of genes — many of which are
key tumor suppressor genes such as BMP3, SFRP2 and GATA4 — in the smoke - exposed cells and a five - or - more-fold increase in the signaling of the KRAS oncogene that is known to be mutated in smoking - related lung cancers.
Not exact matches
A study in this week's Neuron provides
key evidence that DNA methylation — also known to occur as cancerous cells divide, when
tumor suppressor genes are silenced — occurs in adult brains and can be triggered by environmental cues.
Another
key finding was observing the inhibitor effect on
tumor models with a
gene PTEN deficiency as a biomarker — of huge interest because PTEN, a
tumor suppressor, is known to be defective in as many as half of all advanced solid
tumor cancers.
Inactivation of the
tumor suppressor gene RASSF1A by promoter hypermethylation represents a
key event underlying the initiation and progression of lung cancer.
These two histones thus have a
key role of epigenetic silencing of
tumor suppressor genes in breast cancer (and likely other cancers), suggesting that they may represent new therapeutic targets.
«The genotoxicity of mainstream smoke carcinogens manifests as mutations occurring in
key cancer - related
genes, i.e., proto - oncogenes or
tumor suppressor genes that control crucial cellular functions, e.g., growth and survival, in lung
tumors of active smokers.»