Dear Researcher:
Not a professional--I have enjoyed a long, intense interest in
microscopic
life. Abhorred by so many immunilogical pathologies, I read up on the
subject
and in a chapter on cancer began a train of thought. It is your interest
in
this area that encourages me to write and solicit comment upon or
redirection
of what follows.
First I pondered how cell division is normally inhibited by a cell's
multifaced contact with either kindred or membrane cells and wondered if
such
a healthy inhibition were induced by intercellular recognition
(biochemistry)
or pressure (physics). There certainly is recognition, as demonstrated by
the
aggregation of kindred cells, but said aggregation's collective affinity
also
induces an internal pressure that extends to peripheral cells upon their
growing up to a bounding membrane. Furthermore pressure would offer an
Ockham simplicity to the mechanism by which boundary conditions might be
transmitted to the genome back from both kindred and membrane cells. So I
further wondered about a malignancy's loss of inhibition; does the
disruption
in genetic code also desensitize the cell to pressure or merely end its
idiospecific affinity with kindred cells?
My reflections took me to the hydra. During 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. Again there was a simplicity
in
Ockham's razor and in the physics for which I am qualified. I concluded
that
normal cell division is ruled by two biochemical cascades emerging from
the
helix: one ending in an affinity and hence pressure between kindred cells
and
another--inhibited by that pressure--ending in helical division. I further
believe that with cancer the former is disrupted while the latter is left
in
tact.
Is it possible that such a direction may have lain hidden in a blind
spot
between an immunological and biophysical approach. Pressure clearly builds
up
from increases within a circle of adhering membrane cells or within a
sphere
of adhering organ cells. Although the pressure on an embedded tumor hardly
diminishes, lack of adhesion could submit those cells to the vagaries of
kinetic jostling, to brief pulses of low pressure . . . to mitosis.
My hypothesis should rise or fall on a simple but crucial laboratory
experiment--the application of pressure to an immature hydra. If it rose,
that is if the hydra's growth were stunted or, better yet, completely
halted,
where would we be vis a vis cancer? Metastasized cancer would probably
remain
an immunological problem but tumors might--under this scenario--be made
benign by
a. Inducing adhesion among their clonal elements.
b. Applying topical pressure to those elements.
c. Neutralizing one or more of the precursors of the pressure inhibited
reaction.
This last possibility seems to me the most promising. The lab work
necessary to determine the precise nature of that reaction would be
wonderously more complicated than the crucial test determining its
existence.
Yet poised beyond that laboratory is the removal of tumors by appropriate
implant, by attrition. Local to the implant both healthy and tumorous
cells
would undergo a gradual replacement by more distant healthy cells. Because
the claimed reaction is often surpressed anyways its interdiction has a
decent chance of being biochemically inobtrusive.
I have a GIF or Word document with drawings to help the physics along.
Contact me if you're interested.
Sincerely,
David Weitzler
