Triple Negative Breast cancer a result of amplification of the JNK and the wnt

Persistent Failure at the receptors leads to a stressful situation that stimulate continuously the JNK/ERK with 2 implications:
1. Through the Caveolin based molecules will affect p66hc, a regulator maintaining ROS phosphorylated and active on the triple molecule Actin-Caherin and Beta-catenin (CBF).   Through the Catenin, PTPRB and ultimately MAGI3 will be affected.  CTNN1 leads to loss of polarity and lumen formation, and will activate Angiopoietin 1 Receptor and VGEF amplification, which in turn further amplification of ROS, the agent of metastasis...
2. JNK/ERK will also have epigenetic increasing TGFBeta and NF-kB  amplification lead to RUNX3 amplification.  Subsequent amplification of PIAS3 and MITF3 will do the rest.

2 main targets!  p66Shc and PIAS3, 2 regulators!

(This information results from speculative interpretation of information readily available on the internet)!

JAK2 at the TGF-Beta receptor, Angiopoitin 1 Receptor Tie2, Receptor, VGEF Receptor 2, IQGAP1, ARF6, ROS and its regulator p66Shc, the cadherin, the RUNX3,   which:

The RUNX3 Tumor Suppressor Upregulates Bim in Gastric Epithelial Cells Undergoing Transforming Growth Factor β-Induced Apoptosis

Takashi Yano,

Are just few of the Targets in the slew of events !