In IBC, the clinical response has been correlated with survival [ 48, 52, 57, 58].
EXPERIMENTAL DESIGN: Here we focus on characterizing and targeting PDGFRA in IBC.
RESULTS: In IBC patients, we show more frequent PDGFRA activation signature than non-IBC samples.
CONCLUSIONS: Our data suggest that PDGFRA may be a promising target for therapy in IBC.
These relative biases are consistent with a number of structural differences of the reporting in IBC and SIGACT.
The analysis revealed that only 23.8% of the events in their SIGACT sample had corresponding entries in IBC.
There are two signal coupling types in IBC, which are capacitive coupling and galvanic coupling, respectively [4 8].
VEGF expression accounts for high levels of angiogenesis in IBC and resistance to hypoxia.
For all CpG loci, methylation values were increased in IBC in comparison to non-IBC.
As such, they represent new candidates for further clinical and functional validation in IBC.
The deletion of the RB1 tumor suppressor gene likely contributes to the genomic instability in IBC.
