Cancer metastasis and in vivo dissemination of tissue-dwelling pathogens: extrapolation of mechanisms and exchange of treatment strategies thereof.

Most cancer cells would not result in devastating tumours if it were not for their ability to metastasize. The process of cancer metastasis involves significant cell shape, motility, and adhesive changes of pre-cancerous cells, and the remodelling of the extracellular matrix, as well as cognate properties of neighbouring normal cells. Such changes will be hereafter referred to as "tissue fluidity changes". A number of pathogens are known to disseminate to distant organs from sites of infection within a few days. A compromise on the ability to disseminate rapidly could be deleterious to the pathogen (e.g. the pathogen might be cleared before it reaches immuno-privileged sites within its host). Several ways of dissemination could be envisioned - and some are known to occur - ranging from rather passive such as outgrowth and lysis of tissues, residence in the bloodstream, "hitch-hiking" on migratory cells of the immune and lymphatic systems to an active dissemination process involving tissue fluidity changes similar to those that cancer cells invoke to be able to metastasize. The latter is particularly expected to be an important mechanism for the in vivo dissemination of tissue-dwelling pathogens. The mechanisms behind metastasis can, therefore, be viewed as part of the unifying features between cancer cells and pathogens other than their characteristic high proliferation index (at least in one form in the case of digenetic parasites). The current paper presents a synthesis of the hitherto reported but rather scattered data that broadly reinforce the premise of unifying metastasis processes. The overwhelming research outcome in cancer metastasis might therefore serve as a spring board for facilitating the studies of pathogen metastasis and, importantly, relevant cancer treatment strategies can be adopted to combat infectious diseases.