Tuesday, November 18, 2014

Progression even in cancer detection

The study of cancer particularly as it comes to genes, gene alterations and their quality and quantity  modifications is one of the most exciting field of scientific research.  The cell, even the neoplastic cell, continue to be alive meaning undergoing constant changes and molecular transformations.  Often times, these transformations seem purposeful and clearly directed.  And often times the direction intends to reach "survival".  Less often though, the ultimate purpose is clear death ie when the Telomeres are shortened or the Caspases are engaged.
It is obvious that cancer detection should follow these transitions because some genes may not be over-expressed all the time, and some are even depressed during the neoplastic transformation.  The shear number of cells may affect secreted membrane proteins (such as the Prostate specific membrane Antigens (PSMA) to influence detection (by antibody) but often the predominant ongoing cellular phenomena can only be detected by studies of gene amplifications.
There seem to be 3-4 phases of cancer progression that require adapted detection:

1. The initial phase
where an amplified gene is inducing changes that will initiate the Neoplastic process,
ie effect of smoking on the MDM-2 gene and resultant effect on the P53.
ie. Viral effect on the Src or CSK genes,  this of course before the FUS gets into the frey! YES1! Rho gene...

2.The period of proliferation, that is when the MYC gene is involved to amplify all the genes
but not only the MYC but NPM1, Cyclin B1, and of course the many genes of proliferation

3.Metastatic phase (initial or during disease recurrence) here comes the Ros gene

4. Cellular death where Telomere and Mitochondrial phenomena come into play

we still have to wonder about the NCOA, the EZH2, ATRX, and MED1, TIMP3, where do these fit?
Post a Comment