Not exact matches
Within a single tumor exists such an astonishingly varied population of
cells, each with its own combination of normal and
abnormal genes, that at least some
cells nearly always have a way to survive any
particular attack.
A study led by researchers at The Ohio State University Comprehensive Cancer Center — Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James) has identified an
abnormal metabolic pathway that drives cancer -
cell growth in a
particular glioblastoma subtype.
Of
particular interest are the emerging techniques for genomics and proteomics, which allow profiles of gene expression and protein synthesis to be produced and comparisons to be made between normal and
abnormal cells, as well as between
cells before and after exposure to medicines or toxic chemicals.
This
particular liver cancer arises from a mutation that produces an
abnormal form of the enzyme that is the topic of this current work, protein kinase A, and alters the enzyme's role in
cell signaling.
Luckily, different
cell types tend to have different things on their surfaces, which play
particular parts in their specialized roles in the tissue, so it is a matter of identifying and targeting
cell - surface markers that are specific to these
abnormal cell types.
«We need a range of models to learn about the connections among genes, molecules,
cells, synapses and circuits in normal and
abnormal cognition and behavior, and to help us understand the risks of
particular patients,» says the Broad Institute's Steven Hyman.