If the concept is right
and with the advent of the importance of vesicular formation and displacement of cellular protein as a major disturbance in this disease, the role of Tankyrase genes (TNKS1,2) is rapidly growing as target in triple negative Breast cancers. How can someone come up empty?
Tankyrases are involved in:
1.Telomere length
2.Insulin resistance
3.Spindle assembly and formation
4.Molecular trafficking (AXIN)
5.Catening degradation (hell the involvement of GSK1 get MUC1,NOTCH, and WNT in this)
6.Cancer cell resistance (Through activity with with MCL1, a BCL-2 family member)
7.Cellular deformation (theses genes through their connection with TERF1 and SALL1 can lead to the famous "Anal-ear syndrome" (so to speak))
8.through the FNBP1 gene, its reach expands exponentially to reach the Grb2 and MITF (through UBE2I)
Just remember our belief that a gene capable of inducing malformation, is a potent oncogene, and that reaching a "wild gene" such as Gerb2 or UBE2I is a dangerous development for all mutation driven processes.
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