Not a professional—I have enjoyed a long interest in biology. In the early nineties I was struck by the destructiveness of diseases related to an inappropriate immunological response. At that time I chose to read up on the subject and in a chapter on cancer found that I could not continue without resolving a question about what I had just read.

The author had mentioned the normal inhibition of a cell’s division upon contact with other cells, kindred or of bordering tissues. What puzzled me was whether such a healthy inhibition was induced by inter-cellular recognition (biochemistry) or pressure (physics). There certainly is recognition, as demonstrated by the aggregation of kindred cells, but collectively this affinity acts much as a golf ball’s layers of elastic in tension, inducing an internal pressure. That pressure extends to cells on the periphery of their kindred tissue by contact with a bounding membrane. It is even local among the flattened cells of such a membrane. Furthermore pressure would offer Ockham simplicity to the transmission of contact awareness back to the genome as well as a ubiquitous, tissue-independent mechanism for such governance.

These reflections took me to the hydra. During its maturation the bilayered tissue turns inward and, at the very moment of a build up of internal pressure, halts its growth to form the hydrozoan mouth. Although the pressure on an embedded cell would hardly diminish when it became malignant, lack of normal intercellular affinity might submit it to the vagaries of kinetic jostling, to pulses of low pressure . . . to mitosis. So I further wondered about a malignancy's loss of inhibition: “Does such disruption in genetic code desensitize the cell to pressure or merely end its specific affinity for kindred cells?”

Cancer would be practically non-existent, if it depended upon a fortuitous desensitization that left mitosis in tack. By reaching out once more for Ockham simplicity, I concluded that:

·        Normal cell division is ruled by two biochemical cascades, emerging from the helix: one resulting in an affinity between kindred cells; and another, in helical division.

·        Pressure induced by the affinity resulting from the former inhibits some sub-reaction of the latter and with it helical division. I call this the gateway reaction.

·        With cancer, the former is disrupted while the latter is left intact.

Is it possible that such a direction may have lain hidden in a blind spot between an immunological and biophysical approach? This hypothesis should rise or fall on a simple but crucial laboratory experiment: the application of various pressures—one at a time—applied to maturing hydras. Should it rise with the stunting of hydra growth, some direction may open up in the treatment of tumors (May 27, 2010):

·        Reintroducing an affinity among tumor cells seems unlikely. Looking downstream from the pressure-inhibited reaction offers more, exciting possibilities.

·        Presume that enough external pressure can be supplied to slow mitosis and leave many cells ready and waiting for their gateway reaction. Then a substance lethal to the cell beyond that reaction could be introduced along with a gradual return of pressure to normal or (towards preserving healthy cells) near normal. In the latter case, the final return to normal pressure would await reduced toxin levels.

·        Presume that vibrations, sufficient to shake a cancer cell pass its gateway reaction but not to stimulate metastisis, can be introduced. Then preparing for that by introducing a substance lethal to the cell beyond that reaction, might destroy tumors. The hiatus of the pressure sensitive reaction in normal cells would protect them from their own dissolution; while the vibration-induced jostling could only quicken cancerous cells to that now lethal reaction. The diminished rate of attrition for healthy cells would again allow for an easier adjustment by the body.

·        Chemotherapy is all about destroying cells during the vulnerability of mitosis. By letting that treatment supply the aforementioned substance, the final step mitosis be the sub-reaction, and pressure release or penetrating sound wave crash the gate; this hypothesis and the achievement of its promise could both be put to the test.

·       The vibration approach is not effective against freely mobile, malignant cells, nor hardly is plain chemotherapy. In the latter case, chemotherapy’s weakness could be connected to this posited pressure sensitive reaction. In tumors or healthy tissue many chains of sub-reactions would halt awaiting the pressure sensitive one, but in a freely mobile cell, each would continue until a minimal number had triggered mitosis.

·        It seems unlikely that therapeutic toxins could easily traverse cellular walls without generating havoc throughout the body; but currently I do not know, and will consider two explanations for their diminished effect upon metastasized cells: limited but lethal intrusion (a); open intrusion with an impact that may turn lethal (b).

 (a) At the final moments of cellular division, the wall is breached by a lethal dose of toxin. Since freely mobile cells always have an open gate (really no gateway reaction), their mitosis is not held up, and hence more frequent divisions in the toxin's absence make up for its effect.

·       (b) Chemotherapy reduces the level of some substance, x, waiting on the path to mitosis for a product, y, formed by or downstream from the gateway reaction. Consider these descriptions of what may be occurring (May 18, 2010):

1.     The amount of x is crucial to successful mitosis while a sufficient level of y initiates it. In freely mobile cells, the gateway is always open, minimizing the period of vulnerability to an unnaturally low level of x and concomitant catastrophic mitosis.

2.     Alternatively, in freely mobile cells, the gateway is always open allowing x and y to interact, one reaction at a time. Although held up during chemotherapy, afterward and upon replacement of x, the interaction proceeds. For normal or tumor cells, a reduced pressure suddenly opens a multitude of gateways to a plethora of x-y reactions and beyond that to the stimulus of mitosis; but, influenced by chemotherapy, many y molecules find no x and degrade or react otherwise. Somehow, this massive amount of unreacted y proves lethal and mitosis is statistically implicated.

After time allotted for the toxin to reach each cell in the abnormal growth, the introduction of cycles of pressure or spaced, sonic pulses, seems to be the best approaches in testing this hypothesis. If results were positive, heat sensitive examinations concurrent with such pulses may help to discover expansive tumors.

Tissue Regeneration

On March 25^th 2006, I attended a lecture by Dr. Peter Reddien, an associate member of the Whitehead Institute. With the topic, Planarians Can Regenerate a New Head in under a Week (How?); he led us through investigations that may one day light the way towards generating tissue and ultimately organs from human stem cells.

Three thoughts have sprung forth from my attendance:

·        Perhaps a planarian would make a better subject for testing the effects of various pressures upon growth.

·        If pressure does prove influential, then each tissue (or organ) would need its own pressure-regulated, nutrient-feeding “placenta.”

·        The use of scaffolds may be accomplishing this in a better way than I had imagined.

Witnessing the devastation of cancer and organ failure and being ourselves subject to their menace, the compensation that we may one day witness breakthroughs by these or other methods is exciting.