Co-carcinogenesis and Liver cancer

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer. (1966 Nobel prize for HPV work)  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2135410/

My co-carcinogenesis takes his further because carcinogens inhibit polymerases.

What I surmise from his hypothesis:

Cancer occurs because a carcinogen inhibits the viral polymerase better than the human polymerase. When a virus infects the same cell as a carcinogen they interact.  Instead of the virus making what it wants in the host the infected cell is transformed into a cancer cell by the carcinogen. 

Alcohol as the carcinogen in liver cancer
http://www.telegraph.co.uk/news/health/news/11492075/Just-three-alcoholic-drinks-a-day-can-cause-liver-cancer-warns-a-new-study..html

Liver cancer

Alcohol abuse has long been linked to increased rates of liver cancer. Alcohol is a known polymerase inhibitor.

Hepatocellular cancer is the most common form of liver cancer.  Hepatitis C and yellow fever both of which are flaviviruses have been linked to Hepatocellular cancer

yellow fever and Hepatocellular cancer
http://onlinelibrary.wiley.com/doi/10.1002/path.1711090202/abstract
hepatitis C and hepatocellular cancer
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840947/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4493352/

Flaviviruses appear to be using melanocortin receptors.  Which seems fitting because the mouse model for hepatocellular cancer involves a mutated melanocortin 4 receptor.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3204024/


Cholangocarcinoma and Hepatitis B virus
https://www.ncbi.nlm.nih.gov/pubmed/27999794
https://www.ncbi.nlm.nih.gov/pubmed/22694354
https://www.ncbi.nlm.nih.gov/pubmed/28030846

As a polyomavirus Hepatitis B is linked to serotonin receptors.  Serotonin metabolism is altered in Cholangocarcinoma.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2593938/

Increased DNA repair enzymes in Cholangocarcinoma which could be linked to the serotonin receptors being triggered by the Hep B.
https://www.ncbi.nlm.nih.gov/pubmed/23480773

Cholangiocarcinoma is a slow growing cancer

I am looking for the embryonic methylation hervs, herv-w and herv-h,  since polyomaviruses and herpes viruses look like they methylate.
http://angelabiggs.blogspot.com/2017/03/hervs-viruses-demethylation-and.html

hepatitis B and cholangiocarcinoma
https://www.ncbi.nlm.nih.gov/pubmed/28030846

(as a polyomavirus Hepatitis B uses serotonin receptors)


Heptocellular is a aggressive and fast growing cancer

Hepatitis C and Heptocellular carcinoma
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840947/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4493352/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3554798/

herv K and Hepatocellular carcinoma
https://www.hindawi.com/journals/bmri/2016/8201642/

HervK is an embryonic gene that appears during demethylation which flaviviruses apparently use. (the demethylation states of embryogenesis have very fast divisions/growth)

As a flavivirus Hepatitis C might use melanocortin receptors. MCR1 is the only one that goes to the nucleus.

MCR5 increased with heptocellular carcinoma...the other receptors are unknown
http://www.proteinatlas.org/ENSG00000176136-MC5R/cancer#top

I can't tell if the MCR1 which is used by the virus to infect has increased.

Yellow fever...a flavivirus infects the liver through MCR4 but ends up in the cytosol

HIV and Hepatic spindle cancer
https://www.ncbi.nlm.nih.gov/pubmed/8008509

HIV as a retrovirus uses albumin/ LH receptors. (hypothesis on this blog). They end up in the nucleus and retroviruses appear to use demethylation causing fast growing cancers.

Are spindle cancers typically retroviruses no matter where in the body?

cannabinoid receptors increased in hepatocellular cancer
https://www.ncbi.nlm.nih.gov/pubmed/17074588