Lynch syndrome, Hypermethylation, DNA repair proteins, and the herpes viruses

MSH2, MSH3, MLH2, and PMS2

Methylation of  these genes, or mutations, favors cancer during co-carcinogenesis. The cell division would be triggered by a viral infection. Co-carcinogenesis is what awakens the state of embryonic cell division not these mutations.

As "repair" genes they do not cause cell division but they would accelerate chaos once it had started if they were turned off.  Risking the lost off genes that are critical to control of cell cycle.

Colon rectal cancer and Herpes viruses
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075144/

herpes viruses use estrogen receptors

estrogen receptors which when magnified would methylate (shown in breast cancer)
https://www.ncbi.nlm.nih.gov/pubmed/24434785

hypermethylation of MSH2 in lynch syndrome
https://www.ncbi.nlm.nih.gov/pubmed/20388775

MSH2 combines with MSH3 to repair DNA

hypermethylation of MLH2 in lynch syndrome
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376264/

MLH1 combines with PMS2 to repair DNA

Co-carcinogeness
http://angelabiggs.blogspot.com/2017/04/co-carcinogenesis-emphasis-of-5-nuclear.html

Lynch syndrome involves the inheritance of mutations in these repair genes. Which means that HPV with it's demethylation would have these types of mutations...not methylation.

Lynch and DNA repair genes and TNBC
https://www.ncbi.nlm.nih.gov/pubmed/22992699
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548324/

Lynch is therefore the inheritance of a few mutations but not mutations in all of them.