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Fig. 3 | BMC Cancer

Fig. 3

From: Tracing the path of cancer initiation: the AA protein-based model for cancer genesis

Fig. 3

The hallmarks of cancer as viewed in the AA protein-based model for cancer genesis: evasion from senescence is coupled with the breakup of AA protein into A1 and A2 entities leading to the formation of a cancerous cell. Inflammation is at the head of cancer hallmarks fueled by the breakup of AA protein (dark brown). Immortality of cancer cells is linked to the acquisition of a highly adaptive capacity, leading therefore to first control death processes i.e. apoptosis and immune destruction, in addition to a control over autophagy, added here as a cancer hallmark (green). This three-dimensional control continues throughout the life of cancer cells and may involve different mechanisms. Loss of sensitivity to anti-growth signals and self-sufficiency in growth signals follow as early traits earned at the birth of cancer (purple). The latter facilitate the reprogramming of normal cellular metabolism to create malignancy through accumulation of epigenetic-genetic changes and chromosome instability in parallel to deregulation of cellular energetics (blue). Multiple rounds of cell division need telomere maintenance (blue light). Once the tumor becomes large enough it creates new blood vessels to gain access to oxygen/nutrients (pink), and prepares for invasion and metastases formation (black)

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