Tumor – see the opportunity

TUMORS DEVELOP IN CHRONIC
inflammatory ENVIRONMENTS
Virchow saw a correlation between inflammation and tumor
back in 1863. Ever since, research has been changing
in such a way that can barely be compared to those times.
And yet, this postulate gained more relevance than ever.
In the meantime we know from some chronic viral infections
that they can make the way for tumors to develop.
And the same applies to chronic inflammations like rheumatism
or chronic inflammatory gastro-intestinal diseases.
Inflammations are usually self-limiting processes. With a
fine-tuned immune response, the immune system makes
sure that inflammatory and anti-inflammatory processes
ultimately lead to healing. Characteristic of the immune
situation of tumor patients is the fact that the immunity
is weakened (suppressed). When a tumor start to grow or
metastasize, then it has usually already infiltrated the immune
system with its monitoring strategies. An intact immune
system patrols the body and removes the cells that
are no longer behaving properly.
Dvorak recognized the similarities between wound healing
and tumors back in 1986. In contrast to a tumor, a wound
heals itself. In a tumor, the process continues by factors
being released unremittingly, which maintain the inflammation.
As is the case with wound healing, the formation
of vessels in the scope of a tumor emerging plays an important
role for a tumor that measures more than one to
two millimeters, blood vessels are vital.
TO PUT IT A NUTSHELL:
In order for a malignant tumor to start growing, an external
or internal trigger, an inflamed environment and damage to
the DNA must concur. An improbable event for an individual?
Many malignant tumors are triggered off by infections. A
history of infection can be assigned to more than 15% of all
tumors worldwide; that is more than 1.2 million cases a year.
Thus, tumors develop as the result of a multi-leveled process,
which leads from an initial benign change to the cells to an
invasive and then metastasizing disease. This process takes
many years until it has fully developed. The long period this
process requires strongly implies that it has to assert itself
against a background of strict and diversified control mechanisms
that are supposed to prevent anarchical cell behavior.
It is thus probable that a certain environment tied to a genetic
disposition changes the cells to such an extent that they
become more receptive for endogenous and exogenous carcinogen
influences. It may depend on whether the carcinogens
can actually trigger off tumor growth and how long it
takes until the process is clinically proven.
IF YOU WANT TO KNOW MORE THEN
YOU MAY BE interested IN WHAT HYPOTHESES
SCIENTISTS ARE CURRENTLY WORKING WITH.
One hypothesis reads as follows: The cell reveals a gene
defect that can no longer be repaired. For this reason, the
external appearance of the cell deviates from that of the
normal cell. Such a cell no longer divides itself up asymmetrically
into a cell with a function (effector cell), which
depends upon which organ or apparatus it is allocated to
and into a stem cell but symmetrically into two cells with
functions. Yet, it is not a tumor cell. As long as the environment
surrounding the cell suppresses cell proliferation, a
tumor does not yet develop.
If, however, a carcinogen or a chronically inflammatory
changed environment affects the cell to the extent that
the brake preventing cell proliferation is released, then the
cell begins to proliferate in an uncontrolled manner. The
result is a mass of cells such as polyps in the colon or papilloma
in the skin. For a so-called malignant tumor to develop,
a number of additional genetic or cellular changes
must occur. It‘s not until now that the step towards the
tumor becoming malignant follows.
Another hypothesis - worded by Potter back in 1978 - explains
the emergence of a tumor as being a blockage of
cell development on their way from the stem cell, where it
still carries a large number of possibilities, to the cell that
is equipped with the function determined for that cell. An
interruption to this development can happen at any stage
of this process. Influences from the cell‘s environment can
speed up cell division and prevent the normal death of the
cell. You have probably often come across the term oncogene.
More than 100 oncogenes have already been identified.
Oncogenes are DNA parts that serve as the template
for the synthesis of protein substances with differing tasks
like growth factors, receptors, signal-transferring molecules.
The tumor suppressor genes have a quasi contrary
task to the oncogenes. They form the template for the
growth of inhibitive factors such as bridging molecules.
These are structural proteins in cell membranes that form
channels for the direct transfer of small molecules and ions
between the cells. The bridging molecules between the
cells are central structures of monitoring growth and differentiating
normal cells. If a gene-defect cell still has bridging
connections, it is still able to develop in its target cell
to a certain extent. Its direct contact to the other cells in
the network inhibits uncontrolled proliferation.
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BIESTMILCH
Tumor – see the opportunity