How does co- Carcinogenesis explain anti-depressants, blood thinners, and glioblastomas consuming themselves?

 Recently in the news cancer cells, specifically glioblastomas, were found to be self-destructive with anti-depressants and blood thinners.
http://www.sciencedaily.com/releases/2015/09/150924142514.htm

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer. (1966 nobel prize)

What I surmise from his hypothesis:

A virus enters a cell through a receptor, opens up and alters host DNA telomeres. The carcinogen with a benzene ring inhibits the virus' polymerase because viral polymerases have stronger binding affinities than the host's.


Glioblastomas have several virus culprits: hhv6, cmv, sv40, and jcv

HHV6 and CMV seem to use estrogen receptors to infect cells. (these might not be sensitive to the blood thinner treatment)

SV40 and JCV (simian virus and human polyoavirus) seem to use serotonin receptors.
These viruses are in the same family.

JCV and serotonin
http://www.ncbi.nlm.nih.gov/pubmed/19703243
serotonin inhibitors and block JCV infections

SV40 and serotonin
http://www.ncbi.nlm.nih.gov/pubmed/3022874
transgenic mice infected with sv40 have increased serotonin receptors

JCV, SV40 and BK virus are highly homologous viruses (related and similar)

Are these glioblastomas in the experiment sensitive to anti-depressants because started by JCV or SV40 use serotonin receptors?

serotonin receptors and anti-depressants (do they act like inhibitors ?)
http://www.ncbi.nlm.nih.gov/pubmed/21256009

What about the anti-depressants? The affect was a synergy between anti-depressants and blood thinners.

If telomeres have a central role in cancer is it possible blood thinners act on them?

Cycloastragenol was shown to stimulate telomere growth in 2009 (nobel prize)
http://www.luxivi.com/inform/7.html

Cycloastragenol was a chinese herb known to increase blood flow.

So the anti-depressants interfere with the virus at the receptor while the blood thinners are interfering with the viral telomere binding proteins?

When this came out I had mentally lumped ginko and cinnamon with it. Cinnamon and ginko both had life extentending properties and some suggested they had cancer protective abilities.  Why know one could pin point.  Both cinnamon and gingko seemed to be blood thinners too.

Gingko and rat's lifespan
http://www.ergo-log.com/ginkgolifespan.html

Cinnamon and worm's lifespan
http://www.life-enhancement.com/magazine/article/2285-cinnamon-extends-lifespan

Gingko is currently being examined for telomere lengthening
http://www.ncbi.nlm.nih.gov/pubmed/17312453

This might even be visable in the Gingko tree itself
http://www.ncbi.nlm.nih.gov/pubmed/20842436

Can medical blood thinners be acting on telomeres too?
Can simple cinnamon be lengthening telomeres?

What needs to be tested out:

Do other types of cancers with different virus triggers and different receptors fit this pattern? Can you put blood thinners with estrogen receptors inhibitors with  breast cancer cells and see the same self destruction of cancer? Is it a matter of selecting the right receptor?  At the same time? why do the drugs act together?

 Does cinnamon have an effect on telomeres? Can cinnamon replace the blood thinners in these experiments?