Gastric (stomach) cancer
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.
Cancer cells can make unlimited copies because of the telomere modifications. Co-carcinogenesis requires a virus and a carcinogen to start the cancer. The cancer tumor wears the entry receptor on the surface.
The types of gastric cancer are:
Adenocarcinomas, lymphomas, gastrointestinal stromal tumors, carcinoid tumors
This post will focus on Adenocarcinomas
Epstein-barr and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/25633561
http://www.ncbi.nlm.nih.gov/pubmed/26337667
http://www.ncbi.nlm.nih.gov/pubmed/11091849
estrogen receptors and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/2845639
http://www.ncbi.nlm.nih.gov/pubmed/7898114
Herpes viruses might be using the estrogen receptors. (which does explain how they end up in the mitochondria of nerves since the estrogen receptor cycles there, update...virus families use receptor families. There are 3 types of herpes viruses and 3 types of estrogen receptors: alpha beta and estrogen-like. Epstein barr would end up in the nucleus using the alpha estrogen receptor while zoster the mitochondria using the beta estrogen receptor)
Carcinogens of the digestive track?
H.pylori and sulfur
http://www.ncbi.nlm.nih.gov/pubmed/16721224
Sulfur as a carcinogen
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566939/
H.pylori increases the rate of stomach cancer
http://scienceblog.cancerresearchuk.org/2014/03/07/a-bugs-life-h-pylori-and-stomach-cancer/
H.pylori lowers the pH of the stomach (more acidic)
viruses infect better in lower pH
http://www.meridianinstitute.com/newslet/Vol7-3/7-3.html
Adenoviruses infect the stomach the most probably trigger the common stomach tumors
10% Gastric cancer and epstein-barr
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528272/
epstein-barr and pernicious anemia
http://www.jle.com/en/revues/hma/e-docs/maladie_de_biermer_revelee_par_une_hepatite_a_epstein_barr_virus_271904/article.phtml
pernicious anemia and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/506804
http://www.ncbi.nlm.nih.gov/pubmed/3383791
estrogen receptors and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/2845639
http://www.ncbi.nlm.nih.gov/pubmed/7898114
Herpes viruses might be using the estrogen receptors. (which does explain how they end up in the mitochondria of nerves since the estrogen receptor cycles there)
Gastric carcinoid tumour associated with enteroviruses
http://www.ncbi.nlm.nih.gov/pubmed/21278394
Gastrointestinal stroma tumors and somatostatin receptors (hepatitis?)
http://www.ncbi.nlm.nih.gov/pubmed/23116418
Hepatitis B and gastric cancer????
http://www.ncbi.nlm.nih.gov/pubmed/26010504
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.
Cancer cells can make unlimited copies because of the telomere modifications. Co-carcinogenesis requires a virus and a carcinogen to start the cancer. The cancer tumor wears the entry receptor on the surface.
Adenocarcinomas, lymphomas, gastrointestinal stromal tumors, carcinoid tumors
This post will focus on Adenocarcinomas
Epstein-barr and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/25633561
http://www.ncbi.nlm.nih.gov/pubmed/26337667
http://www.ncbi.nlm.nih.gov/pubmed/11091849
estrogen receptors and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/2845639
http://www.ncbi.nlm.nih.gov/pubmed/7898114
Herpes viruses might be using the estrogen receptors. (which does explain how they end up in the mitochondria of nerves since the estrogen receptor cycles there, update...virus families use receptor families. There are 3 types of herpes viruses and 3 types of estrogen receptors: alpha beta and estrogen-like. Epstein barr would end up in the nucleus using the alpha estrogen receptor while zoster the mitochondria using the beta estrogen receptor)
H.pylori and sulfur
http://www.ncbi.nlm.nih.gov/pubmed/16721224
Sulfur as a carcinogen
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566939/
H.pylori increases the rate of stomach cancer
http://scienceblog.cancerresearchuk.org/2014/03/07/a-bugs-life-h-pylori-and-stomach-cancer/
H.pylori lowers the pH of the stomach (more acidic)
viruses infect better in lower pH
http://www.meridianinstitute.com/newslet/Vol7-3/7-3.html
Adenoviruses infect the stomach the most probably trigger the common stomach tumors
10% Gastric cancer and epstein-barr
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528272/
epstein-barr and pernicious anemia
http://www.jle.com/en/revues/hma/e-docs/maladie_de_biermer_revelee_par_une_hepatite_a_epstein_barr_virus_271904/article.phtml
pernicious anemia and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/506804
http://www.ncbi.nlm.nih.gov/pubmed/3383791
estrogen receptors and gastric cancer
http://www.ncbi.nlm.nih.gov/pubmed/2845639
http://www.ncbi.nlm.nih.gov/pubmed/7898114
Herpes viruses might be using the estrogen receptors. (which does explain how they end up in the mitochondria of nerves since the estrogen receptor cycles there)
Gastric carcinoid tumour associated with enteroviruses
http://www.ncbi.nlm.nih.gov/pubmed/21278394
Gastrointestinal stroma tumors and somatostatin receptors (hepatitis?)
http://www.ncbi.nlm.nih.gov/pubmed/23116418
Hepatitis B and gastric cancer????
http://www.ncbi.nlm.nih.gov/pubmed/26010504
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