MONO-TARGET THERAPY IN SOLID TUMOR, a first step in an actual treatment scenario

Time and again we have seen that targeting the membrane or cytosol individually leads to a 15-30% response.  This is very true in solid tumors. Because of phenotype and genetic heterogeneity, it is hard to break this "ceiling".  Mono-target therapy should serve as a proof of principle.  In actual therapy, the multikinase therapy has shown that hitting multiple targets is always better.  The cancer cell is redundant with loopholes that tend to deviate the negative forces toward survival trends.  The cancer cell produces growth proteins more than inhibitory proteins.  This is also why mutations that protect against protein degradation such as the MDM2 Mutation (12q14 location) are widely found in tough to treat cancers.
In actual treatment, hitting 2 driver Mutations in the same cell, or hitting upstream and downstream targets, would result in better response rates.
In Melanoma, the combination of Ipilimumab, an antibody against the Cytotoxic T-lymphocyte Antigen, and DTIC,or Dacarbazine, an Alkylating agent striking down stream Ipilimumab, has once again confirm this premise.  The experience of adding Everolimus to Tamoxifen in refractory metastatic breast cancer  ascertains this principle.
The key is to pick a combination that makes sense or "go nuclear", meaning attacking nuclear component in combination with the mono-target therapy.
Once again, in every cancer cell there are either Driver Mutation, or Driver pathways.  In some cases, the pathway is upregulated by regulator molecules and amplification of transcription genes.  knocking down these amplifiers (Hedgehog signaling) has proven a legitimate therapeutic target (basal cell cancer).
At CRBCM our focus has been to identify major tangible or non-tangible pathways to cellular destruction.  By non-tangible we mean almost reflex mechanisms.  They appear to be threshold that overwhelm cancer cells.  Threshold beyond which the death or apoptotic processes are immediately begun (we call these uncontrollable cell destruction forces LAW OF NATURE) .  Cancer cell death uses Caspase and non Caspase mechanisms.  This is were the crux of the cure is and anything or pathways leading to this, is our focus.  Time is of the essence, let's keep on progressing!