Friday, October 30, 2015

Insulin resistance and mycobacterias?

Insulin resistance doesn't appear to be an autoimmune issue but could be caused by the mycobacteria infections.

mycobacteria (TB) and insulin resistance
http://www.ncbi.nlm.nih.gov/pubmed/21459520
http://www.ncbi.nlm.nih.gov/pubmed/10546470
http://drbroxmeyer.netfirms.com/diabetes.pdf

psoriasis and type 2 diabetes
http://www.ncbi.nlm.nih.gov/pubmed/16494655

psoriasis and mycobacteria
http://www.ncbi.nlm.nih.gov/pubmed/26236445
http://www.ncbi.nlm.nih.gov/pubmed/26500993
http://www.ncbi.nlm.nih.gov/pubmed/24050284

type 2 diabetes and parkinson's
http://www.ncbi.nlm.nih.gov/pubmed/17251276
http://www.ncbi.nlm.nih.gov/pubmed/24059307

Parkinson's and mycobacteria
http://www.ncbi.nlm.nih.gov/pubmed/12208174
http://www.ncbi.nlm.nih.gov/pubmed/25459140

insulin like growth factor and mycobacterias

http://www.leprosy-ila.org/congress/presentations/Oral%20Presentations/Immunology%203/O-249%20-INSULIN-LIKE%20GROWTH%20FACTOR-I%20IN%20LEPROSY%20POSSIBLE%20ROLE%20ON%20MACROPHAGE%20DEACTIVATION%20AND%20INTRACELLULAR%20MYCOBACTERIUM%20LEPRAE%20PERSISTENCE.pdf

IGF and insulin sensitivity
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC300772/

IGF-1 deficient mice and insulin resistant
http://www.ncbi.nlm.nih.gov/pubmed/14514630
http://www.ncbi.nlm.nih.gov/pubmed/11334415

mycobacteria and gout
http://www.ncbi.nlm.nih.gov/pubmed/12136887
http://www.medscape.com/viewarticle/524766_6


Cholesterol and mycobacteria
http://www.ncbi.nlm.nih.gov/pubmed/19634704
http://www.ncbi.nlm.nih.gov/pubmed/18334639
 http://www.ncbi.nlm.nih.gov/pubmed/18505807

gout and high cholesterol
http://www.livestrong.com/article/490117-what-is-the-relation-between-high-levels-of-cholesterol-uric-acid/

crohn's and insulin resistance
http://www.ncbi.nlm.nih.gov/pubmed/16374259
http://www.ncbi.nlm.nih.gov/pubmed/10102952

crohn's and mycobacteria
http://www.ncbi.nlm.nih.gov/pubmed/17913536
http://www.ncbi.nlm.nih.gov/pubmed/8867176

type 2 diabetes, crohn's, and gout ( CPPD?)
http://www.ncbi.nlm.nih.gov/pubmed/24854413






Thursday, October 29, 2015

The progression of herpes shingles to stroke to glioma or alzheimer's (just links right now)

Shingles to hemorrohagic stroke and heart attack

Does the herpes virus infect the heart tissue and the astrocytes of the blood brain barrier causing this?

http://thechart.blogs.cnn.com/2014/01/02/shingles-may-increase-stroke-heart-attack-risk/

 2014 Jun;58(11):1497-503. doi: 10.1093/cid/ciu098. Epub 2014 Apr 2.

Risk of stroke following herpes zoster: a self-controlled case-series study.

 2015 Apr;15(4):16. doi: 10.1007/s11910-015-0534-4.

The relationship between herpes zoster and stroke.


Herpes and stroke

 2015 Oct 6. [Epub ahead of print]

Multiple strokes associated with herpes simplex virus type-2 infection: case report.


Hemorrohagic stroke and herpes virus

http://www.neurology.org/content/78/3/e12.short
http://www.ncbi.nlm.nih.gov/pubmed/25840954


 2014 Aug;20(4):419-22. doi: 10.1007/s13365-014-0253-7. Epub 2014 May 8.

Hemorrhagic and ischemic stroke secondary to herpes simplex virus type 2 meningitis and vasculopathy.


Is this glioma the cancer of the astrocytes that are infected with herpes virus?

stroke and glioma

 2015 Oct;125(1):143-8. doi: 10.1007/s11060-015-1880-4. Epub 2015 Aug 14.

Ischemic stroke in patients with gliomas at The University of Texas-M.D. Anderson Cancer Center.


 When the virus spreads from the astrocytes to neurons in the brain.

Alzheimer's and herpes

 2015 Jul 24;47(2):351-64. doi: 10.3233/JAD-140822.

Herpes Viruses Increase the Risk of Alzheimer's Disease: A Meta-Analysis.

Tuesday, October 27, 2015

Co-carcinogenesis: the synergistic actions of carcinogens and viruses to cause cancer (references done)

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. Co-carcinogenesis is the synergistic actions of a virus and a carcinogen together on a host cell.

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. The most likely carcinogen for each cancer will be examined for viral polymerase inhibiting ability.

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.

In 1933 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 when combined with carcinogens.  In 1944 they published a co-carcinogenesis paper entitled “ The effect of chemical carcinogens on virus induced rabbit papillomas.”  Rous got the Nobel prize in 1966 for his work on HPV. (1-6)

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 of cancer acting only at the beginning.  The oncology world has decided that only 20% of cancers are involved with viruses because they could not find viruses in the tumors but what if they had been there at the start and the receptors expressed reflect that.

Based on what we know of tumors, viruses, and receptors this paper will attempt to show that Rous’s Co-carcinogenesis could explain most of the cancers we deal with today. 

Hypothesis:  Cancer cells express receptors that reveal the virus that triggered their cancerous tumor process.  Carcinogens are present that can inhibit the viral polymerases. 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 therefore 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 polymerases 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 by the carcinogen 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 over expressing the receptor which tells us which virus triggered them. So let's look at a few cancers and see. (7-11)

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.  (12)

The Epstein Barr virus is likely using estrogen receptors.  Herpes viruses bind heptad motifs. Estrogen receptors have heptad motifs.  The pattern of herpes viral infection appears to match that of the estrogen receptor.
Estrogen alpha receptors cycle to the nucleus which would allow herpes viruses to interact with the nucleus but in nerves the estrogen beta 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 thus explaining how shingles spreads down nerves. Using the estrogen receptor would explain how the herpes virus ends up in different locations.  In Breast cancer the herpes virus would be carried to the nucleus by the estrogen receptor. (11-16)

If the herpes virus Epstein-barr triggers the estrogen receptor type of breast cancer then the HPV virus could be the trigger of the estrogen-negative type of breast cancer tumor.  Estrogen negative receptor breast cancers have been found to contain HPV.  Inhibition of cannabinoid receptors has shown to inhibit tumor growth of some breast cancer cells. Are there  cannabinoid receptors on these tumors specifically? Does HPV use cannabinoid receptors? (17, 18)

Cannabinoids inhibited cervical cancer cells migration, a known HPV cancer.  Interestingly enough cannabinus oil has also been a suggested remedy for non-melanoma cancers.  Non-melanoma skin cancer has associations with HPV.  Non-melanoma skin cancer has increased cannabinoid receptors.  Negative- estrogen-receptor-breast cancers and cervical cancers should be examined for increased cannabinoid receptors. (19-22)

For the two types of breast cancer we can associate two types of viruses but an increase in receptors is only known for the herpes- estrogen type.  Can we now connect a specific carcinogen to breast cancer?

The carcinogen has to collect at the target tissue which in this case is the breast.  Heptachlor which was an insecticide of the 1980s and is still currently used on fire ants has been found to collect in the breast.  Since heptochlor is not metabolized and is fat soluble it merely collects increasing in concentration at the breast until the virus is caught. Organochlorides have  been suspected of triggering breast cancer but studies seem to indicate the mere collection of the compounds do not cause cancer. However Co-carcinogenesis could explain the data. (23-24) Does heptoclor inhibit polymerases?

 Chlorine has been shown to inhibit adenovirus DNA synthesis.  If chlorine inhibits the polymerase of the viruses found in the breast which are HPV and Herpes Zoster then it is highly likely that heptachlor and the other organochlorides do too. Note that the chlorine in tap waster is at extremely low levels.  Tap water consumption has been associated with bladder cancers, so the amount of chlorine added needs to be regulated.  The key here is dose and viruses. Too much at one time could result in the compounds absorbed in the fatty tissue.  (25,26)

The virus culprits for bladder cancer are the polyomaviruses like BK or hepatitis B. Interesting serotonin receptors are found on bladder cancers which could be the receptor they are using.  (27-29)

Another cancer associated with heptachlor is prostate cancer. If we look at prostate cancer we find 2 types there too.  An estrogen receptor form triggered by a herpes virus and a 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. It is not clear if these melanocortin receptors have been increased in the tumors of prostate cancers but they have been associated with an increased proliferation of the prostate cancer cells. (30-33)

 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. As herpes viruses they would be using estrogen receptors and the tumors would have increased estrogen receptors.   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.  (34-39)

 Osteosarcomas are the most common type and largest group of bone cancers with a higher rate in African males.   Polyomaviruses which includes hepatitis B, the JC virus, mouse polyomavirus, the rous sarcoma virus of chickens, sv40, and the murine FBJ virus have been associated with bone cancers. The JC virus being of African origin is found in slightly higher rates in african americans.  Can JC be found in osteosarcomas? Simian virus 40 specifically has been found in dozens of osterosarcomas. SV40 infected cells have increased serotonin receptors too.  JC virus was proven to use serotonin receptors which begs the question, do the serotonin receptors increase with all polyomaviruses? Canine osteosarcomas have increased expression of serotonin receptors.  Serotonin receptors have also been described as immortalized on osteosarcomas.   Note that gangliosides were originally considered serotonin receptors and that SV40 uses them. Although gangliosides might be used to gain access to cells they do not appear to increase in cancers.  Polyomaviruses could be using a serotonin like ligand to gain access to cells but only the serotonin receptor is apparently increased. (40- )

Spindle cell sarcoma has already been documented and accepted to be caused by the Rous sarcoma virus. Rous sarcoma viruses are a type of retrovirus.  Retroviruses have also been associated with gangliosides as receptors.  The fact we can see a possible pattern, association of a virus, with each type of bone cancer is suggestive. It would be interesting to see if spindle cell sarcomas have increased serotonin receptors.(  -53)

 Cadmium is the possible carcinogen for bones it collects at the growth tip of the bones and has strong associations with the cancer. Further because teen boys tend to grow rapidly and taller than girls they would have more cadmium added which could explain why they have higher rates of bone cancers. Occupations dealing with cadmium have higher rates of osteosarcoma and heavy metal implants have been found associated with sarcomas. Cadmium is found in cigarettes, and cigarette smoke. Cadmium can be found with fertilizers and in Africa the cadmium has been found to contaminate the hot chocolate of Africa because of this.  Cadmium has also been found in shellfish and oysters in high levels which could explain the clusters of cases in the northeast coast. Toxic levels of cadmium were also dumped into Tampa Bay in 2011 and there are clusters there too.  Osterosarcoma case clusters should appear near high cadmium areas. Cadmium can inhibit DNA polymerases directly.  This inhibition fits with our theme of a carcinogen present at the site which can inhibit the viral polymerases. (55,56)

How about pancreatic cancer? There are 2 types of pancreatic cancer, exocrine and endocrine. Endocrine cells secrete enzymes into the bloodstream whereas exocrine cells secrete into the intestine. The exocrine form is the most common so this must be a common virus. There seem to be multiple types of endocrine cancers which might match up with the different viral infections.

First the endocrine pancreatic cancers such as Insulinoma, Glucogonoma, and gastrinoma duct tumors.

Coxsackie, an enterovirus, has been found in Insulinomas.  Enteroviruses might be using acetylcholine receptors to infect based on their association with acute flaccid paralysis and acetylcholine secretion.  Mouse insulinomas were found expressing in high number nicotinic acetylcholine receptors. (57-58)

Serotonin producing endocrine cancers appear to be triggered by a polyomavirus. Pancreatic duct blocking endocrine tumors have been associated with serotonin secretion and these same tumors have had Hepatitis B viruses isolated from them. Hepatitis B as a polyomavirus could be using the serotonin receptors.  Called gastrinomas, these endocrine tumors should be analyzed for serotonin receptors. Gastrinomas over lap with other parathyroid cancers. Hepatitis B can infect the parathyroid as well as the liver. (56-60)

Glucagonomas have been associated with necrolytic migratory erythema.
Glucagonomas have somatostatin receptors expressed.  Merkel cells have been connected with a new polyomavirus and also have somatostatin receptors expressed.  Necrolytic migratory erythema has also been connected to hepatitis B, another polyomavirus.  Are glucagonomas triggered by merkel polyomaviruses or a similar polyomavirus? (63-68)

The most common pancreatic cancer, adenocarcinomas are the exocrine pancreatic cancers.  Looking at the rest of the exocrine pancreatic tumors they appear to be over expressing dopamine receptors on their surfaces. Can the flu virus be found in adenocarcinomas?   This is not known. The flu virus which has also been accused of triggering type one diabetes seems to be using the dopamine receptors. Diabetes increases the risk for developing pancreatic cancer and why has been unclear. If viruses trigger diabetes they could also be there to trigger cancer.  Patient history of both diabetes and alcoholism increases the likelihood of pancreatic cancer even more. (69-71)

2/3 of pancreatic cancers occur in alcoholics.  Alcohol does inhibit polymerases and could easily inhibit a viral polymerase. The other pancreatic carcinogen could be N-nitros also known as nitrates or nitrites in foods. Highly processed foods like meat, cheese, and beer have high quantities and it's impact has been questioned. Viral polymerases can be inhibited by nitrogen oxides which nitrates and nitrites are and this feature fits with the co-carcinogen hypothesis. The influenza replication has been halted by nitric oxide in mouse models. So does this mean people with the flu should not have processed meats because of the pancreatic cancer risk? (72-74)

When we look for carcinogens of the brain nitrates, alcohol,  and benzodiazepine are the most likely candidates.   Again, alcohol and nitrates can and do inhibit polymerases contributing to the stunting of growth and likely inhibits viral polymerases if they are there.  Astrocytes, the nurturing and protecting cells of the brain’s neurons make up the blood brain barrier.  Alcohol is first absorbed by these cells. Astrocytes are one of the 3 types of glial cells. (75)

 Benzodiazepine which is an anxiety medication can be absorbed into the fats in the brain when in high concentrations.  Benzodiazepine has be proven to inhibit the polymerases of Hepatits C specifically. The benzene ring of  these medications could be what inhibits the viral polymerases when alcohol is not involved. This is a side effect of an anxiety drug. (76)

 Acyclovir is a medicine prescribed  for it's ability to inhibit the polymerase of herpes viruses and is currently used as a treatment to stop viral infections. There are cases where herpes encephalitis was diagnosed, acyclovir was prescribed and then the patient was discovered to have gliomas tumors. The question is were they misdiagnosed or did the viral infections become high grade glioma tumors.  Acyclovir is not considered carcinogenic because when fed to rats and mice log term no tumors developed. What if the rats had herpes infections at the same time? The reason that acyclovir does not cause cancer in shingles patients has to do with where the virus is.  Herpes viruses use estrogen receptors. The estrogen receptors of nerves cycle to the mitochondria and use the mitochondria's little DNA.  Cancer only occurs when the virus is at the nuclear DNA which is the huge cookbook. In the breast or in the glial cells of the brain acyclovir would be a carcinogen and should never be used in those cases. (77,78)

 Gliomas, brain cancers of glial cells, are also associated with Alzheimer's disease. If some forms of Alzheimer's are due to a herpes virus infecting and destroying a neuron's mitochondria then could gliomas be the herpes virus infecting the nucleus of the glial cells when the carcinogen such as nitrates or alcohol are there?  The overlap of the gliomas and Alzheimer's is the herpes virus. Herpes simplex virus encephalitis has been found in glioma patients. Cmv, another type of herpes virus, has also been connected to gliomas especially in children. Herpes zoster has been connect to gliomas too. With all the connections to herpes viruses it is not surprising that some gliomas express estrogen receptors. (79-85)

Shingles, which is the emerging of herpes zoster, has already been shown to be a risk factor for stroke. Could this be the herpes zoster starting to infect the astrocyte glial cells of the blood brain barrier? Is stroke a risk factor for glioma? Should people refrain from drinking after strokes to prevent glioma? (86-88)

Meningiomas are the brain cancers of the meninge cells which are the connective tissue cells between the brain and the skull. Meningiomas are associated with polyomaviruses like sv40. Meningiomas have somatostatin receptors not estrogen receptors expressed.  Again the virus and the receptors expressed are matching up. (89,90)

As for my original carcinogen example of simple benzene, it has been associated with Leukemia when consumed, which means it goes to the bone marrow.  Viruses that infect the bone marrow like respiratory syncytial virus have been associated with the disease too.  Children with acute lymphoblastic leukemia have often been exposed to RSV in the first nine to 12 months of life. Was it a combination of RSV and benzene exposure? Benzene appears in the waste water of fracking and could be contaminating the well waters of people living near them. (91-93)

Respiratory syncytial virus, measles and mumps as paramyxoviruses could be using Nectin 4 as a receptor to enter cells.  Ovarian cancer has over expressed Nectin 4 receptors. Interestingly enough measles was once considered to be protective against ovarian cancer. Is this because a paramyxovirus actually infects the ovary triggering the ovarian cancer? Inflammation of the ovary is a symptom of the measles, which makes sense because it has Nectin 4. Could measles vaccines as a paramyxovirus protect against the RSV? (94-97)

The carcinogen of ovarian cancer is asbestos or talc powder. The asbestos fibers have been found in the ovaries and fallopian tube of asbestos workers correlating with the increased rates of ovarian cancer but what about the use of talc? The association of talc has not been proven but is suspected. (98-101)

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.

Intro

1.   Prasanna Kumar, Fredrick A. Murphy. Francis Peyton Rous Emerg Infect Dis 2013 Apr; 19(4): 660-663

2.   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. 

3.   Rous P, Friedewald WF. The effect of chemical carcinogens on virus-induced rabbit papillomas. J Exp Med 1944 May 1;79(5):511-538

4.   Haverkos HW. Viruses, chemicals, and co-carcinogenesis. Oncogene. 2004 Aug 23; 23(38);6492-9

5.   Francis Peyton Rous

6.   Johnson FB. Chemical interactions with herpes simplex 2 virus: enhancement of transformation by selected chemical carcinogens and pro-carcinogens. Carcinogenesis 1982;3(10):1235-40

Evaluation of hypothesis

7.   Dolcetti R.,  Guinco S., Dal Col J., Celeghin A, Mastorci K, De Rossi A.   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

8.   Deng Z.,  Kim E., Weitzman MD, Lieberman PM. HSV-1 remodels the host telomeres to facilitate viral Replication. Deng et al., 2014, Cell Reports 9, 2263–2278


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11.                Choi KH. Viral polymerases Adv Exp Med Biolo 2012; 726: 267-304

Breast Cancer

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13.                Gianni T, Piccoli A, Bertucci C, Campadelli-Fuime G. Heptad Repeat 2 in herpes simplex virus 1 gH interacts with heptad repeat 1 and is critical of virus entry and fusion. J virol 2006 Mar 80(5):2216-24

14.                Fawell SE, Lees JA, White R, Parker MG. Characterization and colocalization of steroid binding and dimerization activities in the mouse estrogen receptor.  Cell 1990 Mar 23;60(6):953-62

15.                Liao TL, Tzeng CR, Yu CL, Wang YP, Kao SH. Estrogen receptor-B in mitochondria: implications for mitochondrial bioenergetics and tumorigenesis. Ann N Y Acad Sci 2015 Sep;1350(1):52-60


16.                Kramer T, Enquist LW. Alphaherpesvirus infection disrupts mitochondrial transport in neurons. Cell Host Microbe 2012 May 17;11(5):504-14


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19.                Eichele K, Ramer R, Hinz B. R(+)-methanandiamide-induced apoptosis of human cervical carcinoma cells involves a cyclooxygenase-2-dependent pathway. Pharm Res 2009 Feb;26(2):346-55

20.                De Villiers EM. Human papillomavirus infections in skin cancers. Biomed Pharmacother 1998;52(1):26-33

21.                 Casanova, M. Llanos et al. “Inhibition of Skin Tumor Growth and Angiogenesis in Vivo by Activation of Cannabinoid Receptors.” Journal of Clinical Investigation 111.1 (2003): 43–50. PMC. Web. 26 Oct. 2015.

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25.                  Gall AM, Shisler JL, Marinas BJ. Analysis of the viral replication cycle of adenovirus serotype 2 after inactivation by free chlorine. Environ Sci Technol 2015 Apr 7; 49(7):4584-90

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27.                Alexiev BA, Randhawa P, Vazquez Martul E. Zeng G, Luo C, Ramos E, Drachenberg CB, Papadimitriou JC.  BK virus-associated urinary bladder carcinoma in transplant recipients: report of 2 cases, review of the literature, and proposed pahtogenetic mode. Hum Pathol 2013 May;44(5):908-17

28.                Alexiev BA, Papadimitriou JC, Chai TC, Ramos E, Staats PN, Drachenberg CB. Polyomavirus (BK)-associated pleomorphic giant cell carcinoma of the urinary bladder: a case report. Pathol Res Pract 2013 April;209(4):255-9

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Prostate Cancer and Melanoma

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31.                Aiken WD, Anzinger JJ Case Rep Urol 2015 :120535 Chikungunya virus Infection and Acute Elevation of Serum Prostate-specific Antigen.

32.                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

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Bone Cancers: Ewing, chondrosarcoma, osteosarcoma, spindle

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35.                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

36.                Dubois Sg, Perez-Atayde AR, McLean TW, Grier HE.  Late recurrence of ewing sarcoma durning pregnancy: a report of 2 cases. J Pediatr Hematol Onco 2008 Sep; 30(9):716-8

37.                Grifone TJ, Haupt HM, Podolski V, Brooks JJ. Immunohitochemical expression of estrogen receptors in chondrosarcomas and enchondromas Int J Surg Pathol 2008Jan:16(1):31-7

38.                Najioullah F, Avari S, Thouvenot D, Dubreuil C, Aymard M, Lina B.  Herpes simplex menintitis after surgical removal of a clivus chordoma.  Eur J. clin Microbiol Infect Dis 1997 Apr 16(4):327-8

39.                Fasif JH, Dupont WD, Olson SJ, Lafleur BJ, Cates JM. Steroid Hormone receptor and cox-2 expression in chordoma. Am J Clin Pathol, 2007 Sep, 128(3):375-81

40.                Berebbi M, Dandolo L, Hassoun J, Bernard AM, Blangy D. Specific tissue targeting of polyomavirus ocogenicity in athymic nude mice. Oncogene 1988 Feb;2(2):149-56

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