Title: “We are what
we eat” Do our cancer cells wear in high numbers the receptors the viruses used
to infect them? Does Co-carcinogenesis
explain most cancers?
Abstract: Cancer cells appear to express the receptors
that reveal the virus that triggered their cancerous tumor growth. This hypothesis supports Co-carcinogenesis as
the cause of cancer.
This paper will go through several types of cancer looking at the patterns of receptors on tumors, of the cancers that tend to appear together, and looking for the viruses that have been isolated from tumors.
This paper will go through several types of cancer looking at the patterns of receptors on tumors, of the cancers that tend to appear together, and looking for the viruses that have been isolated from tumors.
Introduction:
Francis Peyton Rous challenged
the oncology world first when he suggested that cancers did not spontaneously
occur but could be triggered by something in a contagious way. Unbeknownst to him he was working with the
Rous Sarcoma virus. (when the virus was discovered it was named after him) He could see that he
was transferring some agent from one chicken to another and triggering the tumors. The oncology world seemed to
believe that this was strictly a chicken pattern. Unsuccessfully he alone attempted to isolate
viruses from mammalian tumors for years.
20 years later fellow researcher Richard Shope isolated HPV from mouse tumors. They now had a mammalian virus. Fervently Rous and his coworker Friedewald studied the HPV virus attempting to
prove that it triggered the tumors in mammals.
Their work on HPV got them the Nobel prize in 1966.
One hypothesis of his, Co-carcinogenesis suggests that it is the synergistic actions
of a virus and a carcinogen together on a host cell that causes cancer. Both must be present. However the evidence of viruses can rarely be found in cancer cells. In petridishes viruses and carcinogens have been shown to produce cancer cells. Perhaps because they are merely the triggers at the beginning. Thus the oncology world has
decided that only 20% of cancers are involved with viruses .
Based on what we know of tumors, viruses, and receptors this
paper will attempt to show that Rous and Friedewald’s Co-carcinogenesis could explain
most of the cancers we deal with today. (1-3)
Hypothesis: Cancer
cells express receptors that reveal the virus that triggered
their cancerous tumor process. This hypothesis
supports Co-carcinogenesis as the cause of cancer.
Evaluation of Hypothesis:
Viruses are now known to make proteins that interact with the telemores which are the ends of our chromosomes. The condition of the telomeres, how frayed or pristine, determines how many times the chromosomes can be copied. Viruses are therefor making our DNA, the cookbooks of our cells, immortal and open for use. Carcinogens, such as benzene and phenols, are now known to have multiple actions including inhibiting polymerase which are the DNA readers. Viruses typically make their own polymerases which have a stronger affinity for binding in order to compete with the host's polymerase. Now imagine them coexisting as Co-carcinogenesis suggests. The DNA has been opened up but the viral polymerases are inhibited and a cancer cell has been created. Is this possible? The virus when it enters a cell uses a specific receptor thus stimulates the production of more of those specific receptors to be made. It is my contention that when we look at the cancerous tumors they will be overexpressing the receptor which tells us which virus triggered them. So let's look at a few cancers and see.
Breast cancer has 2 types. An estrogen receptor and non estrogen receptor type. Interestingly enough 2 viruses have been isolated from breast cancer; the HPV virus and the Epstein-barr virus. The Epstein Barr virus is likely using estrogen receptors. In adrenal cells estrogen receptors cycle to the nucleus which would allow herpes viruses to interact with the nucleus but in nerves the estrogen receptors cycle to the mitochondria. Herpes viruses are known to hide in the mitochondria of nerves and to travel down the nerves riding in the mitochondrias like little cars. If the herpes virus, Epstein-barr, triggered the estrogen receptor tumors of breast cancer than the HPV virus must represent the trigger of the other type of tumor. What receptor does HPV use? Non-melanoma skin cancer has also been associated with HPV where increased cannabinoid receptors have been found. The increased expression of cannabinoid receptors on non-estrogen-receptor breast cancer tumors could be easily validated.
Let's look at bone cancers. Each type of bone cancer has already been associated with a specific virus. Ewings has been associated with CMV and Epstein barr. Interestingly Ewings has also been associated with the hormone swings of pregnancy which would elevate estrogen levels. Chondrosarcoma has also been associated with estrogen receptors but as a bone cancer of the facial region the prime suspect should be herpes simplex one.
Osteosarcomas have different receptors over-expressed on the surface, the IGF receptors and somatostatin receptors. Osteosarcoms are the most common type and largest group of bone cancer which might infer that it is caused by more than one virus. Hepatitis B is the polyomavirus which is similar to the JC virus, mouse polyoma virus, the rous sarcoma virus of chickens, sv40, and the murine FBJ virus. When these types of viruses infect cells IFG or somatostatins receptors increase. An overlap exists with these 2 types of receptors.
Spindle cell sarcoma has already been documented and accepted to be caused by the RSV. The fact we can see a possible pattern, association of a virus, with each type of bone cancer is suggestive.
Looking at bone marrow cancers, benzene typically settles into the marrow, we find 2 virus families and 2 types of cancers originating there. The flavivirus family which can infect the marrow has strong correlations with leukemia. The herpes family viruses particularly epstein barr has correlations with lymphomas. Note that PAH carcinogens, like that found in tattoos, tend to move not just to bone marrow but the the closest lymph gland.
If we look at prostate cancer we find 2 types. An estrogen receptor form triggered by a herpes virus and melanocortin receptor form. What virus uses the melanocortin receptor? The flavivirus called chikungunya virus has been isolated from prostate tumors. Prostate cancer patients have an increased risk of melanoma, skin cancer. Melanoma cells over express melanocortin receptors too. Interestingly most people who have been bitten by a mosquito carrying west nile or other flaviviruses do not realize they are infected. Flaviviruses could be the cause melanoma.
How about pancreatic cancer? There are 2 types of pancreatic cancer, exocrine and endocrine. Exocrine pancreatic cancers might involve nicotinic acetylcholine receptors since they are involved with digestive juice secretion. Enteroviruses might be using acetylcholine receptors to infect based on their association with acute flaccid paralysis and acetylcholine secretion. Coxsackie, an enterovirus, has already been linked to type one autoimmune diabetes and is the most likely culprit for pancreatic infection triggering exocrine pancreatic cancer.
Looking at the endocrine tumors they appear to be over expressing dopamine receptors on their surfaces. The flu virus which has also been accused of trigger type one diabetes seems to be using the dopamine receptors. Think of parkinson's disease, dopamine receptors and the link of the flu virus triggering that autoimmune disease. If a carcinogen was present during a flu infection one could end up with endocrine pancreatic cancer. If these viral receptor associations are correct.
There is not enough evidence to prove that cancers wear the receptors that the viruses used to infect them but there is enough to investigate the possibility. With luck this will prove Co-carcinogenesis and we can prevent cancer with vaccines. Assuming we figure out how to make vaccines for all of these viruses. One can only hope.
1. Prasanna Kumar, Fredrick A. Murphy. Francis Peyton Rous Emerg Infect Dis 2013 Apr; 19(4): 660-663
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3647430/
2. Haverkos HW. Viruses, chemicals, and co-carcinogenesis. Oncogene. 2004 Aug 23; 23(38);6492-9
http://www.ncbi.nlm.nih.gov/pubmed/15322520
3. Francis Peyton Rous
http://www.encyclopedia.com/topic/Francis_Peyton_Rous.aspx
5. Epstein-Barr virus and telomerase: from cell immortalization to therapy. Infectious Agents and Cancer 2014, 9:8 http://www.infectagentscancer.com/content/9/1/8
6. HSV-1 remodels the host telomeres to facilitate viral Replication. Deng et al., 2014, Cell Reports 9, 2263–2278
http://www.cell.com/cell-reports/pdf/S2211-1247(14)00973-5.pdf
7. The inhibition of mitochondrial DNA replication in vitro by the metabolites of Benzene, hydroquinone and p-benzoquione. Chem Biol Interact 1985 may; 53(3):327-50
http://www.ncbi.nlm.nih.gov/pubmed/4006011
8. Inhibitory effect of benzene metabolites on nuclear DNA synthesis in bone marrow cells. j. Toxicol Environ Health. 1989;26(3);277-91
http://www.ncbi.nlm.nih.gov/pubmed/2926830
9. Viral polymerases Adv Exp Med Biolo 2012; 726: 267-304
http://www.ncbi.nlm.nih.gov/pubmed/22297518
10.Viruses and human breast cancer. Future Microbiol 2006 Jun;1(1):33-51
http://www.ncbi.nlm.nih.gov/pubmed/17661684
Human papilloma virus is associated with breast cancer Br J Cancer 2009 Oct 20; 101(8):1345-1350
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737128/
Cope JU A viral etiology for Ewing's sarcoma. Med hypotheses 200 Nov; 55(5):369-72
http://www.ncbi.nlm.nih.gov/pubmed/11058415
Kebudi R, Bilgic B, Gorgun O, Avan I, Demirvont M. Is the Epstein Barr virus implicated in Ewing sarcoma? Med Pediatr Oncol 2003 Apr; 40(4):256-7
http://www.ncbi.nlm.nih.gov/pubmed/12555258
Palmer JS, Duffy DL, Box NF, Aitken JF, O'Gorman LE, Green AC, Hayward NK, Martin NG, Sturm RA. Melanocortin-1 receptor polymorphisms and risk of melanoma: is the association explained solely by pigmentation phenotype? Am J Hum Genet 2000 Jan; 66(1):176-86
http://www.ncbi.nlm.nih.gov/pubmed/10631149
Aiken WD, Anzinger JJ Case Rep Urol 2015 :120535 Chikungunya virus Infection and Acute Elevation of Serum Prostate-specific Antigen.
Viruses are now known to make proteins that interact with the telemores which are the ends of our chromosomes. The condition of the telomeres, how frayed or pristine, determines how many times the chromosomes can be copied. Viruses are therefor making our DNA, the cookbooks of our cells, immortal and open for use. Carcinogens, such as benzene and phenols, are now known to have multiple actions including inhibiting polymerase which are the DNA readers. Viruses typically make their own polymerases which have a stronger affinity for binding in order to compete with the host's polymerase. Now imagine them coexisting as Co-carcinogenesis suggests. The DNA has been opened up but the viral polymerases are inhibited and a cancer cell has been created. Is this possible? The virus when it enters a cell uses a specific receptor thus stimulates the production of more of those specific receptors to be made. It is my contention that when we look at the cancerous tumors they will be overexpressing the receptor which tells us which virus triggered them. So let's look at a few cancers and see.
Breast cancer has 2 types. An estrogen receptor and non estrogen receptor type. Interestingly enough 2 viruses have been isolated from breast cancer; the HPV virus and the Epstein-barr virus. The Epstein Barr virus is likely using estrogen receptors. In adrenal cells estrogen receptors cycle to the nucleus which would allow herpes viruses to interact with the nucleus but in nerves the estrogen receptors cycle to the mitochondria. Herpes viruses are known to hide in the mitochondria of nerves and to travel down the nerves riding in the mitochondrias like little cars. If the herpes virus, Epstein-barr, triggered the estrogen receptor tumors of breast cancer than the HPV virus must represent the trigger of the other type of tumor. What receptor does HPV use? Non-melanoma skin cancer has also been associated with HPV where increased cannabinoid receptors have been found. The increased expression of cannabinoid receptors on non-estrogen-receptor breast cancer tumors could be easily validated.
Let's look at bone cancers. Each type of bone cancer has already been associated with a specific virus. Ewings has been associated with CMV and Epstein barr. Interestingly Ewings has also been associated with the hormone swings of pregnancy which would elevate estrogen levels. Chondrosarcoma has also been associated with estrogen receptors but as a bone cancer of the facial region the prime suspect should be herpes simplex one.
Osteosarcomas have different receptors over-expressed on the surface, the IGF receptors and somatostatin receptors. Osteosarcoms are the most common type and largest group of bone cancer which might infer that it is caused by more than one virus. Hepatitis B is the polyomavirus which is similar to the JC virus, mouse polyoma virus, the rous sarcoma virus of chickens, sv40, and the murine FBJ virus. When these types of viruses infect cells IFG or somatostatins receptors increase. An overlap exists with these 2 types of receptors.
Spindle cell sarcoma has already been documented and accepted to be caused by the RSV. The fact we can see a possible pattern, association of a virus, with each type of bone cancer is suggestive.
Looking at bone marrow cancers, benzene typically settles into the marrow, we find 2 virus families and 2 types of cancers originating there. The flavivirus family which can infect the marrow has strong correlations with leukemia. The herpes family viruses particularly epstein barr has correlations with lymphomas. Note that PAH carcinogens, like that found in tattoos, tend to move not just to bone marrow but the the closest lymph gland.
If we look at prostate cancer we find 2 types. An estrogen receptor form triggered by a herpes virus and melanocortin receptor form. What virus uses the melanocortin receptor? The flavivirus called chikungunya virus has been isolated from prostate tumors. Prostate cancer patients have an increased risk of melanoma, skin cancer. Melanoma cells over express melanocortin receptors too. Interestingly most people who have been bitten by a mosquito carrying west nile or other flaviviruses do not realize they are infected. Flaviviruses could be the cause melanoma.
How about pancreatic cancer? There are 2 types of pancreatic cancer, exocrine and endocrine. Exocrine pancreatic cancers might involve nicotinic acetylcholine receptors since they are involved with digestive juice secretion. Enteroviruses might be using acetylcholine receptors to infect based on their association with acute flaccid paralysis and acetylcholine secretion. Coxsackie, an enterovirus, has already been linked to type one autoimmune diabetes and is the most likely culprit for pancreatic infection triggering exocrine pancreatic cancer.
Looking at the endocrine tumors they appear to be over expressing dopamine receptors on their surfaces. The flu virus which has also been accused of trigger type one diabetes seems to be using the dopamine receptors. Think of parkinson's disease, dopamine receptors and the link of the flu virus triggering that autoimmune disease. If a carcinogen was present during a flu infection one could end up with endocrine pancreatic cancer. If these viral receptor associations are correct.
There is not enough evidence to prove that cancers wear the receptors that the viruses used to infect them but there is enough to investigate the possibility. With luck this will prove Co-carcinogenesis and we can prevent cancer with vaccines. Assuming we figure out how to make vaccines for all of these viruses. One can only hope.
1. Prasanna Kumar, Fredrick A. Murphy. Francis Peyton Rous Emerg Infect Dis 2013 Apr; 19(4): 660-663
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3647430/
2. Haverkos HW. Viruses, chemicals, and co-carcinogenesis. Oncogene. 2004 Aug 23; 23(38);6492-9
http://www.ncbi.nlm.nih.gov/pubmed/15322520
3. Francis Peyton Rous
http://www.encyclopedia.com/topic/Francis_Peyton_Rous.aspx
4.Chemical interactions with herpes simplex 2 virus: enhancement of transformation by selected chemical carcinogens and pro-carcinogens. Carcinogenesis 1982;3(10):1235-40
http://www.ncbi.nlm.nih.gov/pubmed/62937375. Epstein-Barr virus and telomerase: from cell immortalization to therapy. Infectious Agents and Cancer 2014, 9:8 http://www.infectagentscancer.com/content/9/1/8
6. HSV-1 remodels the host telomeres to facilitate viral Replication. Deng et al., 2014, Cell Reports 9, 2263–2278
http://www.cell.com/cell-reports/pdf/S2211-1247(14)00973-5.pdf
http://www.ncbi.nlm.nih.gov/pubmed/4006011
8. Inhibitory effect of benzene metabolites on nuclear DNA synthesis in bone marrow cells. j. Toxicol Environ Health. 1989;26(3);277-91
http://www.ncbi.nlm.nih.gov/pubmed/2926830
9. Viral polymerases Adv Exp Med Biolo 2012; 726: 267-304
http://www.ncbi.nlm.nih.gov/pubmed/22297518
10.Viruses and human breast cancer. Future Microbiol 2006 Jun;1(1):33-51
http://www.ncbi.nlm.nih.gov/pubmed/17661684
Human papilloma virus is associated with breast cancer Br J Cancer 2009 Oct 20; 101(8):1345-1350
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737128/
Treatment of estrogen receptor positive breast cancer. Curr Med Chen 2013; 20(5):596-604
http://www.ncbi.nlm.nih.gov/pubmed/23278394
Cannabinoids, endocannabinoids, and cancer
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366283/
Cannnabinoid receptors as a novel target for the treatment of prostate cancer
http://cancerres.aacrjournals.org/content/65/5/1635.full
Cannabinoids, endocannabinoids, and cancer
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366283/
Cannnabinoid receptors as a novel target for the treatment of prostate cancer
http://cancerres.aacrjournals.org/content/65/5/1635.full
Cope JU A viral etiology for Ewing's sarcoma. Med hypotheses 200 Nov; 55(5):369-72
http://www.ncbi.nlm.nih.gov/pubmed/11058415
Kebudi R, Bilgic B, Gorgun O, Avan I, Demirvont M. Is the Epstein Barr virus implicated in Ewing sarcoma? Med Pediatr Oncol 2003 Apr; 40(4):256-7
http://www.ncbi.nlm.nih.gov/pubmed/12555258
Dubois SG, Perez-Atayde AR, McLean TW, Grier HE. J Pediatr Hematol Onco. 2008 Sep; 30(9)' 716-8 Late recurrence of ewing sarcoma during pregnancy: a report of 2 cases.
Chondrosarcoma and estrogen receptors
Chordoma and herpes
Chordoma and estrogen receptors
Rous P. J Exp Med 1911 Apr 1;13(4):397-411 A sarcoma of the fowl transmissible by an agent separable from the tumor cells.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2213042/#bib2Palmer JS, Duffy DL, Box NF, Aitken JF, O'Gorman LE, Green AC, Hayward NK, Martin NG, Sturm RA. Melanocortin-1 receptor polymorphisms and risk of melanoma: is the association explained solely by pigmentation phenotype? Am J Hum Genet 2000 Jan; 66(1):176-86
http://www.ncbi.nlm.nih.gov/pubmed/10631149
Aiken WD, Anzinger JJ Case Rep Urol 2015 :120535 Chikungunya virus Infection and Acute Elevation of Serum Prostate-specific Antigen.
Hafiz S, Dennis JC, Schwartz D, Judd R, Tao YX, Khazal K, Akingbemi B, Mo XL, Abdel-Mageed AB, Morrison E, Mansour M. Int J Oncol 2012 Oct; 41(4):1373-80 Expression of melanocrotin receptors in human prostate cancer cell lines: MC2R activations increases prostate cancer cell proliferation.
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