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Showing posts from May, 2017

Musings-Cancers may arise by........

What if the default mode of single cells is replication and differentiation/ maturation is secondary. Depending upon the interaction of replicating cells with the microenvironment, adjacent cells release inhibitory molecules which make a replicating cell differentiate/mature. This is because competition for food resources as a whole will wipe out cells, so for survival cells divide to a certain number and differentiate, so that the tissue survives as a whole.
 In cancer the default replication of cells carrying driver mutations for tumorigenesis  is not inhibited sufficiently by the surrounding cells so uncontrolled cell proliferation occurs. It is possible that driver mutations arise all the time in cells due to replication errors, but then such cells do not survive and proliferate because inhibitory signals by  surrounding cells  impedes their survival to allow tissue/organ/host  formation to occur.
In cancer the tumor survives at the expense of a host, because the cells in the nei…

What If......................

What if one could predict/model tumor size based on driver mutations. If a correlation could be found between size of primary tumor and metastasis-(for e.g cells will tend to leave larger tumors than smaller ones because of nutrient deprivation of cells at periphery,so they migrate to search for nutrients) then metastasis could be predicted based on driver mutation, and preliminary intervention strategies could be designed.