If Cellular entropy calculate in different type of cells (stem cell, differentiated cell, cancer cell..) , it provides a valuable information for carcinogenesis.
I am not of expertise in this field. But i found a an interesting article on the entropy measurement in normal and their tumor counter parts such as Cancer stem cells and their parental tumor cells. The article and the corresponding link is mentioned below.
Cellular network entropy as the energy potential in Waddington's differentiation landscape
Interesting. The problem is difficult to measure the amount of distinct cell types. Thus, the problem becomes how to estimate meaningful cell types and the proportion within a given tissue. FACS data could be potentially utilized to resolve this issue yet apparently the entropy appears to be context-dependent.
There are several ways. Some references : from James Watson ,.Quantum worlds" t o Molnar J Thermodynamics and inormation Physics., Current Cancer Therapy Review 2014, 10, and Molnar et al CCTR 5,158, 2009. , "socratus" [email protected],
First, Thanks for yours answers and second, is it possible to calculate genome network "metric entropy," metabolic "metric entropy" via Kolmogrov Sinai entropy
As I remember Prof Klaus Kayser published papers in Diagnostic Pathology,( Charité, Berlin) related to your question. The Kolmogrov entropy was establishe probably on the sililaries ,
My main idea compare the behaviour(chaotic , complex,edge of chaos) of the different cells(stem cell, cancer cell, differentiated cell) in stressed microenvorment . I want use entropy as a indicator of cell behaviour. Please look at my manuscripts entitled": ".Genome’s Chaotic Behavior for Adaptation may explain Carcinogenesis! Suggestion from Surgical Oncologist ,2.Complex system perspective in colorectal carcinogenesis" and I am a clinician then ı need help.
Theoretically your question is related to structural entropy components of various cells at microscopic level based on the "chaos out of order "hypothesis. You need a cytologist' help for the comparison of microscopic structures of cytoskeleton compartments and nucleus of the different cells, I guess. May be you can compare the dielectric structures of the different cells ref. B.S.Thornton publications.
As the cell is a strongly non-equilibrial (non-linear) thermodynamic system, when characterizing a cell one only can say about the changes in entropy, not the actual , particular, momentary value of entropy. The notion of the source of entropy is here more proper, and perhaps calculable or just estimable for particular types of cells. However, I'll find cancer cells closer to the thermodynamic equilibrium (thus - a weaker entropy source) than any normal ones.
I am not of expertise in this field. But i found a an interesting article on the entropy measurement in normal and their tumor counter parts such as Cancer stem cells and their parental tumor cells. The article and the corresponding link is mentioned below.
Cellular network entropy as the energy potential in Waddington's differentiation landscape
Very interesting question and paper (Mr. Paramasivan). Though it seems counter intuitive to me that pluripotent stem cells would have a higher entropy (see figure 1 in the paper) than differentiated cells as a system tends to evolve to states of higher entropy. That would seem to imply that differentiated cells would want to become puripotent. On second thought, I suppose that might be what happens as a cell becomes cancerous.
Dear Mesut, I just answered, if the answer is not useful, just ignore it. Btw. the notion of signalling entropy is based on the Shannon entropy, which again concerns the strongly non-equilibrial systems. But if you ask about just "entropy" without specification, everybody thinks about the thermodynamic function of state which is basic for any other entropies.I personally see no contradiction between the Boltzmann and Shannon notion of entropy, and also between the answers to your question. Thanks for the papers!
You are right adaptability to new conditions by a quorum sensing-like mechanism, and example of metastasis formation by binding to homing receptors of the particulat organs.