The discovery of
how the epidermal growth factor receptor (EGFR) is activated offers insight into how current EGFR - blocking drugs interact with the receptor and an important avenue for the...
The authors of the study say their new understanding of
how epidermal cells form a barrier may explain the paradox of how we can shed them without compromising our skin's integrity.
Not exact matches
«It makes considerable headway in resolving a brewing controversy in the
epidermal stem cell field» over exactly
how the skin regenerates, she says.
The study, called «Molecular Determinants of Drug - Specific Sensitivity for
Epidermal Growth Factor Receptor (EGFR) Exon 19 and 20 Mutants in Non-Small Cell Lung Cancer,» and published online in the journal Oncotarget, demonstrates
how computer modeling of EGFR mutations found in lung cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat patients.
The Alabama scientists have now shown
how it works against head and neck cancers: It blocks a protein called
epidermal growth factor receptor, or EGFR.
Now, a team from Keio University in Japan, working with a researcher at Imperial College London, have discovered that the shape of the
epidermal cells combined with their ability to temporarily glue together, may explain
how they form this strong barrier.
The discovery of the shape and binding capability of
epidermal cells could explain
how skin maintains a barrier even when it is shedding.