Oxygen Model of Cancer-Inflammation Co-Morbidity Dynamics

 

Oxygen Model of Cancer-Inflammation Co-Morbidity Dynamics

Majid Ali, M.D.

 

The subjects of cancer and inflammation are inherently intertwined. Inflammation sets the stage for the beginning of cancer. Cancer, by its nature, triggers and perpetuate inflammation. So “nflammation-cancer comorbidity” is a crucial aspect of the cause, diagnosis, progression, and treatment of cancer. The clonal growth of cancer cells is supported by the degrees of inflammation in the microenvironments of cancer, in which genetic factors of inflammation participate in the cooperative cellular interaction of cancer.

Consider the following text from Nature (508, 52–53, April 3, 2014)

Sequencing of human cancer genomes has revealed a high degree of genetic heterogeneity among cells of a given tumour. In most cases, tumour growth is thought to be driven by the most ‘advanced’ cancer-cell subpopulation — that carrying the highest number of cancer-driving mutations. However, the presence of many mutations that occur at only low frequency implies that tumours contain multiple subclones, and the relevance of these is not fully understood. On page 113 of this issue, Cleary et al.2 provide a potential explanation for some forms of intratumoral heterogeneity, by describing a cooperative cellular interaction in mouse mammary tumours in which the presence of two types of clone is required for tumour formation.

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