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Before reading this chapter please start with:
First concepts
WOB is optimal
As their name implies, carcinogens cause cancer. However long before its appearance they induce the following structural changes:
1. DNA level: Gene mutations.
2. Cell level: Change in nuclear (chromatin) structure.
3. Tissue level: Inflammation.
4. Organism level: Weight loss..
During prolonged carcinogen treatment the experimental animal proceeds through
the following phases:
1. Reversible changes. .Animal recovers when treatment stops.
2. Irreversible changes. Accumulation
of structural changes without tumor formation.
3. Full compensation: Structural changes with a microscopic tumor.
4. Decompensation: Structural changes with a macroscopic tumor and metastasis.
Additional reading:
WOB in experimental cancer
Solution
During carcinogenesis WOB controls
all processes and adjusts them so as to meet the requirements of the organism.
The adjustment of processes at any instant is called WOB solution.
It is always the most optimal solution
in circumstances. Structural changes are a manifestation of WOB solutions.
Gene mutations
Medicine regards gene mutations as the essence of cancer. In the colon they
are the 'Molecular Basis of Colon Cancer'.
According to Bert Vogelstein, two classes of genes
drive the process of colon neoplasia. 'Gatekeepers' are
genes that directly control cell birth and cell death, and 'Caretaker' control the rate of mutations. This theory highlights the great influence
of Platonism
and Cartesian reductionism on medicine.
Cancer is driven by genetic errors which overpower a corrupt organism.
Actually genes are controlled by WOB which controls also
cell division, and gene mutation. Carcinogen treatment
poisons the animal and in order to keep it alive
WOB restructures processes, like in the 'Polyp cancer sequence'. It restructures also genes, which is manifested by gene mutations. Gene
mutations are WOB response to the poison.
The polyp cancer sequence is an evolution of optimal WOB solutions.
Gene
mutations are disease indicators (DI),
and do not cause cancer. However molecular biologists regard them as the essence of cancer, in the same way as hyperglycemia
is viewed as the essence of diabetes mellitus.
Controlled mutations in cancer
Carcinogens induce necrosis
Carcinogens are poisons that kill cells (necrosis). There are two kinds
of cells: Long-lived stem
cells, and their short-lived progeny, the transitional
cells. Tissues are made of units, each nourished
by a stem cell which breeds transitional
cells. When carcinogens kills transitional cells they
are swiftly regenerated by their parent stem cells. However death
of stem cells results in the loss of tissue units (atrophy) which
regenerate extremely slowly.
In other words, when a tissue unit is hit, if the poison kills only
transitional cells, the unit regenerates (per primam). When stem cells die,
the entire unit is lost (atrophy).
Since being undifferentiated, stem cells resist poison better than transitional cells.
Carcinogens induce inflammation
Short carcinogen treatment induces an acute inflammation which hits transitional cells and spares stem cells.
In order to initiate cancer the carcinogen has to induce a chronic inflammation. Asbestosis
is a chronic inflammation which ends in lung cancer. Apparently most
chronic carcinogens are infections.
Hodgkin's disease
Hodgkin's
disease, is the only cancer that is called a disease, indicating
that it behaves in a different way than genuine cancers. Some authors
suspect that it starts as a granulomatous inflammation ending as
lymphoma. Granulomatous disease hits mainly
young adults while patients over 50 years get lymphoma
Hodgkin's age specific mortality curve exhibits a distinct shoulder
which accounts for a population of young adults with a 'benign'
Hodgkin. From the age of 50 years the curve ascends nearly exponentially
and represents patients with genuine lymphoma.
Childhood cancers
Hodgkin's disease is a prototype
of cancer evolution which starts as
a chronic inflammation and ends as cancer. Childhood cancers evolve in two
ways:1. Congenital malformations like neuroblastoma, 2. Appear following
a chronic inflammations, e.g., childhood leukemia, osteosarcoma, and chondrosarcoma. According to McCredie
(1), chronic neuritis, may induce congenital
malformations, which suggests that chronic inflammation may precede also
intrauterine cancers.
Adult cancers
The most prominent is hepatoma which
generally evolves as follows:
acute hepatitis -> sub acute unresolved hepatitis -> cirrhosis ->
hepatoma. Cancer of the
lung: (smoking) -> chronic bronchitis -> Carcinoma. Breast
cancer: chronic fibrocystic breast disease -> carcinoma. Uterine
cervix: chronic cervicitis -> epithelial dysplasia -> carcinoma
in situ -> cervix carcinoma. Ulcerative colitis -> colon carcinoma A de novo formation of cancer without
a preceding inflammation is
rare.
When does an inflammation
become a cancer?
As long as infections spare stem cells, WOB regenerates damaged units. When
infection kills stem cells
and tissue units are lost WOB grows a tumor. Stem cells regenerate extremely slowly. Cancer is driven by
an ongoing stem cell death and tissue unit loss manifested by atrophy. Like in gastric cancer which
starts as chronic atrophic gastritis
(aplasia of parietal cells). Or, solar keratosis, where cancer arises
from an atrophic skin.
Two repair mechanisms
Inflammation and neoplasia are
two repair mechanisms. Inflammation repairs necrosis, and neoplasia, stem
cell aplasia.
Additional reading:
Injury
and repair
Inflammatory cancers
1.
McCredie J Embryonic neuropathy. A
hypothesis of neural crest injury as the pathogenesis of congenital malformations.
Med J. Aust. 1:159-163,1974
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