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


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.

Additional reading:
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
Back to New Medicine