The Physics of Cancer and Tissue Regeneration

In biology, turgor pressure or turgidity is th...

Inner Tugor Pressure upon Cell Walls

Here I hypothesize a pressure sensitive reaction that is a gateway to cellular mitosis. Were this to be so, then as little as a weakened inter-cellular affinity among neoplastic cells would reveal jostling as a trigger for mitosis in a cohesive tumor. Accordingly more of such cells would undergo necrosis when exposed concurrently to both jostling and cytotoxins specific to mitosis.

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) or both: after all, that inhibition needed to exist well before a cell’s complicated inner cytoskeleton could have evolved. Here I am interested in a remnant, pressure-sensitive inhibition.

There certainly is recognition, as demonstrated by aggregating kindred cells, but collectively this affinity acts much as a golf ball’s elastic layers in tension to induce an internal pressure. That pressure extends to cells on the periphery of their kindred tissue by contact with bounding membranes. It is even local among the flattened cells of such membranes. Furthermore pressure would offer Ockham simplicity to the awareness of contact being transmitted back to the genome and to a ubiquitous, tissue-independent mechanism for such governance.


Image via Wikipedia

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 inter-cellular affinity would expose 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 chance 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: applying various pressures—one at a time—to maturing hydras. Should it rise with the stunting of hydra growth, possibilities may open up in tumor treatment (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 for healthy cell preservation, to near normal (and finally normal).
  • Presume that vibrations, enough to shake a cancer cell pass its gateway reaction but not, to stimulate metastasis, 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 their vulnerability of mitosis. By letting that treatment supply the aforementioned substance; the final step mitosis be the sub-reaction; and a pressure release or penetrating sound wave crash the gate; this hypothesis and its promise could 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 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) Surprisingly I can find no reference of this approach, but leave it in as contrast. It would involve less toxic side-effects, but need sufficient, topical thinning of a cellular wall during mitosis for intrusion of a lethal dose (October 8, 2010). At the last moment 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) An intruding toxin aborts helical separation, the cellular interior turns to soup, defacing (from within) walls whose recognition by leukocytes might have led to a cure (October 8, 2010)

    Or with similar effect that toxin 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 sufficient y initiates the same. 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.
  3. 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 y, awaiting reaction, proves lethal and mitosis is statistically implicated.

After time allotted for the toxin to reach each cell in the abnormal growth, one could introduce cycles of pressure from direct sonic pulses. Alternatively the quivering, low-energy, cadence (gradual acceleration to, sudden halt, gradual acceleration fro, sudden halt) of a contoured resting platform to which the subject had been strapped; or of an oscillating magnetic field applied to magnetically tipped acupuncture needles, embedded into the tumor might prove more effective.

Would there be enough jostling for the hypothesized need? Were this procedure successful, tumors would wane more quickly with less cytotoxin, delaying their adaptation to that toxin. Reduced levels of cytotoxins also promise reduced side-effects; but the resulting intramural stew defaces neoplastic cell walls from within, forfeiting that delicate at death interaction with a leukocyte that promises recognition and immunity.

Death by necrosis fractures the neoplastic wall into ephemeral but potentially recognizable fragments, while leaving unscathed those leukocytes that would recognize them. Such die-offs abound in treatments that either don’t need or at least don’t get FDA approval.

Tissue Regeneration

On March 25th 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.”
  • Scaffolding may be accomplishing this in a better way than any I had thought of.

Witnessing how devastating are cancer and organ failure, each breakthrough is heart warming.

3 responses to “The Physics of Cancer and Tissue Regeneration

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