Cancer: A state where the immune system recognize non-self as self.
Tuesday, 22 August 2017
Thursday, 4 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 neighbouring microenvironment of the cell carrying the driver mutation are not able to give out sufficient inhibitory signals to inhibit proliferation of cells carrying the driver mutation. One reason could be that a sufficient number of neighbouring cells lacking the driver mutation is needed to give out sufficient signal to inhibit proliferation of cells lacking the driver mutation. If cells lacking the driver mutation divide at a slower rate than cells with the driver mutation, then they will not be able to provide sufficient inhibitory signal against the cell carrying the driver mutation.
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 neighbouring microenvironment of the cell carrying the driver mutation are not able to give out sufficient inhibitory signals to inhibit proliferation of cells carrying the driver mutation. One reason could be that a sufficient number of neighbouring cells lacking the driver mutation is needed to give out sufficient signal to inhibit proliferation of cells lacking the driver mutation. If cells lacking the driver mutation divide at a slower rate than cells with the driver mutation, then they will not be able to provide sufficient inhibitory signal against the cell carrying the driver mutation.
Wednesday, 3 May 2017
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.
Friday, 28 April 2017
Incompleteness
Godels incompleteness theorem-undecided statements-statements that cannot be proved to be true or false. What about under certain conditions-depending on the assumption. Contextual truth or falsehood. Is this problem similar to the manyworlds problem in quantum physics-manyworlds exist but as humans we experience one world.
What is a mathematical object ? Are two objects really identical to be counted ?
What is a mathematical object ? Are two objects really identical to be counted ?
Thursday, 27 April 2017
Wednesday, 26 April 2017
tumor heterogeneity-chaos
Does tumor heterogeneity parallel chaos,such as a bifurcation diagram for a logistic map.
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