Carcinogenesis process

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Oncogenesis mutation and deregulation initiation, a phase normally repressed by carcinogen agents (environmental contamination) cause cellular alterations.

However, the altered cell can be preserved from becomming cancerous thanks to other genes knwon as suppressors which fix the mutated DNA or prevent the development of potentially cancerous cells.

But these suppressor genes can also undergo one or several mutations which can alter their function; the cell acquires the first characteristics of a malignant phenotype (development control loss and apoptosis resistance); then they are considered as transformed.

At this stage, food intakes can play a role through antioxidants protecting the DNA from alterations resulting from carcinogenesis, either via various components capable of fixing the DNA or by acting on the body's carcinogenesis process. .
  • Cellular signals and transcriptional factors involve concerned oxidative species in the synthesis of development factors inducing an hyperplasia.
  • Therefore, any pro-oxidant molecule will favour tumorous promotion whereas antioxidants can still offer a protective effect.

The move from hyperplasia to a cosntituted tumour, characterised by infinite cell multiplication (immortality), and the faculty of creating a vascular network (tumour angiogenesis) shall happen under the effect of new genomic alterations related or not to environmental factors including nutritional ones.

Finally, in this progress stage, the tumour having acquired the faculty to invade nearby tissues, as well as a colonising characteristic, will constitute metastasis, once again through the development factors, but also because of several enzymes and eicosanoids. In this very case, particular nutritional factors can change the tumorous progression.