CANCER CURE IN PHASES /CANCER MODE
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Now it is clear to those that are deep in the fight against cancer that cancer cell can be attacked at different cellular phases or layers:
1. The membrane Phase: where receptors, stimuli, integrins and Actinic based pathways are in actions.
*talking about  Receptors on should include notably the Death Receptors which could trigger Caspase cascade at membrane stimulation.  It goes without saying that the cell hide these Death receptors well throwing all kind of barriers, inhibitors and decoy receptors.   If you find these Death receptors, cure is yours.  Cancer cells makes these death Receptor few and far apart by clearly methylating or suppressing the genes involved in their expression.  In therapeutic Targeting, Receptors of  growth factors have been the most looked at. It is now known that growth factors have both the role of causing cancers by causing secondary amplification of pathways, but also by driving cancer growth by playing an autocrine growth and giving cancer an advantage of growth over surrounding cells.  This role is critical in cancer seeding during metastasis.  One of the Growth factor that has been insufficiently looked at is the Tumor Necrosis Factor (TNF).
TNF has been poorly looked at because It can induce Necrosis that we can't control.  Necrosis is an alternative Apoptosis that is independent of Caspase induced cell death.  It is said that when a sepsis is uncontrolled it is because there is too much TNF released and we have no effective way of controlling TNF
to date.   Anti TNF product have been introduced cautiously introduced (ENBREL use in psoriasis) but warnings about overall global immune suppression tell you of danger using this modality.  And this is mostly aplha receptor suppression.  Work is in progress in this area. 

Some tumor growth factor actually control or impact the expression of ICAMS, the adhesion molecules including the Cadherins which are decreased prior to cancer Metastasis or readiness  to be on the move!
 
*Stimuli are chemical, traumatic, pressure like but also growth driven.  In cancer biology, they involve the pathogenesis of cancers as they leading to causing it (ie. Esophageal and lung cancers), but they also involve cancer growth and cell survival.  It is the stimulus interpretated as stress that will reach the c-JUN instead of the regular MAPK pathway.  The MTOR will insure cancer or cell survival through their multiple effect which include thier impact of Telomeres!
Through c-JUN, proliferation or overproduction of Cyclins and growth factors will secondarily occur or expand to amplify the actions.   Cyclins and growth factors belongs to the Integrins mentioned above.  Every molecule belonging to the Integrins is attached a specific family of Metalloproteases.   We believe that this is doe through a Flippase and floppase modality (don't forget the scramblase modality).   In essence, when cyclin molecule is thrown in the cytoplasm, a Metalloprotease in thrown in the Extracellular space. Metalloproteases act as collagenase and open the road for cell migration.   The cell has collagen also in its membrane.  It is clear that knowing its metalloprotease, it will make an inhibitor that covers and protect its own Collagen structure.  It is believed that the insufficiency of these inhibitors lead to autodistruction of the cell in TTP.  But that is another topic.

*Actinic based pathways lead to a quick notification by the nucleus of what is going on the cell surface. Microtubules act as nerve for the cell and through the Reticulum Endothelium, take the message to the cell faster for initiation of the Nuclear Phase, by-passing the Cytoplasmic phase.  The Wnt pathway seems globally to take this approach and is important in Breast and Ovarian Cancer.  We will revist this topic at length!

2. Cytoplasmic Phase

Receptors and stimuli are the critical determinants of this phase.  And Growth factors, pyrogenes, and various stimuli act on receptors which are transmenbrane  (Decoy receptors lack a post membrane section) and therefore can trigger an intramembrane stimulation of the GTPase and other molecule complexes attached to the membrane at the inside surface,  the SRC and RAS families are located in this area  (to be continued.)