Cancers with mutator phenotypes present a genetic diversity that defeat current treatments, all of which are highly specific by design. Resistant cells breed billions more cancer cells and defeat the therapy.
Even the latest treatments suffer from this flaw.
For example, consider this from CytomX’s website:
“CytomX’s Probody™ Platform is broadly enabling to all antibody formats, including traditional monoclonal antibodies, bispecifics, multispecifics and ADCs.
Through precise targeting of the disease microenvironment, Probodies have the potential to address diseases in ways that have not been possible to-date, enabling a new level of tissue targeting, selectivity and activation.
CytomX’s Probodies are fully recombinant, masked antibodies that remain inert in healthy tissue but are activated specifically in the disease microenvironment. Probodies leverage dysregulated protease activity, a hallmark of many disease states, to locally activate in the disease tissue, thereby achieving unprecedented levels of tissue-specific targeting.
CytomX’s proprietary, antibody-masking technology ensures that Probodies only bind to antigens in diseased tissue by blocking their binding ability to healthy tissue. In diseased tissue, certain disease-associated proteases that are dysregulated and active in the microenvironment cleave the substrate and remove the mask.
Probodies have the potential to expand the therapeutic window for diseases by increasing safety and unlocking efficacy. Probodies expand the therapeutic index for targets where therapeutic intervention is expected to have a significant impact on the disease, but also where normal tissue expression patterns are too widespread to allow for adequate safety margins using conventional antibody approaches.”
Clearly, this exquisite specificity is its Achilles heel:
Problem #1. Tumor cells not over-expressing the protease will breed billions more tumor cells.
Problem #2. Normal cells over-expressing the protease will be killed off.
The solution to Problem #1, if there is one: define all of the avenues that cancer cells may take for any particular function they must carry out to survive, and attack them ALL simultaneously. For example, what can cancer cells do if they are NOT over-expressing this protease? Say there are two alternatives. Then one attacks all three ways that cancer cells can accomplish the objective.
Problem #2 will be enhanced because now there will be three separate sets of non-specific interactions. Ouch!
My previous solution:
0. Strengthen and re-balance the body with super-nutrition, stress relief, measured exercise and plenty of rest/sleep.
1. Put all growing cells to rest.
2. Give cancer cells two or more alternative pathways: Apply reagents that can kill growing cells that are resistant to the natural break points (mostly tumor cells) AND
3. Provide for a way in which tumor cells can re-differentiate into normal cells AND/OR yet another alternative. [Steps 2 & 3 amount to a directive: Don’t rely on killing tumor cells alone; otherwise, you’re running uphill, fighting against the powerful, natural survival program of all cells]
4. Remove the break on the growing cells – this does a lot of things; one of the most important is the reactivation of the immune system for killing off of residual tumor cells.