People whose specialty is genetics have not been able to explain this in exact detail. Do not feel bad that you can't find a finite answer.

Well the RO took a long hard look at my BOT last week and said everything looked great - gave me an "A+". I don't even worry about the hep C - I figure the chlordane will kill me first ;-) But at least I won't have termites ha ha

So, the BOT , tonsils and the oral tongue are made up of different cells and viruses thrive in certain types of environments...I was thinking that the whole tongue was one unit and I couldn't understand why HPV attacked the BOT but not the OT. Now I do. Well, they better find a vaccine or a cure before a new strand mutates that likes all areas of the mouth.

How long has HPV been around? And since there are so many forms of HPV does it mutate?

I suppose not knowing bothers me is because now that I'm starting to feel like I'm healing I have time to ponder the "why?" Not "Why me?" just "Why" if that makes sense. I understand that I got cancer because of two things: (1)My immune system was asleep at the wheel and (2)I have a genetic link in my family history, I'm the forth in my family with H & N cancer with Stofko blood. But it would be nice to know the "What the heck set it off in the first place"....I suppose I could have been fighting OC for years and it finally took grasp of my system. ..This could be the case for a lot of us, we'll never know.

Does anyone think it's ironic that a lot of people who don't fit the profile of OC and don't have HPV related OC are getting OC? I have to assume that anyone with OT OC is not HPV related and there seems to be a lot of us...and this makes me curious. I was thinking that maybe my OC was caused by any one of the many chemicals I encounter at work...But, I was talking to a scientist and he told me probably not...That if my cancer was chemical related it wouldn't have been so isolated in my mouth, that the cancer would have been more widespread.

I think something very important is being lost in all of the HPV conversation. Oral Cancer is most frequently Squamous Cell Carcinoma. The virus must "find" Squamous cells to cause the specific cancer. Not all the tissues are made up of squamous cells.

I think it also needs stressing, before we cause a panic, that not every single virus automatically causes a cancer. If this were true this cancer would probably be exceedingly common (and it is not). Several other things have to go wrong at a cellular level before cancer develops. The virus afflicted cell must mutate then the mutation must go un-noticed by all of the systems the body uses to rid itself of cells that are not behaving. (That is probably where our genetic pre-disposition fits in).

In the end, I suggest that the worry about HPV and all that might happen with that virus be left to the Medical Masters. Here on the ground level, we know the virus is around, that it is common and therefore we are exposed to it perhaps daily. Thankfully, on average our bodies are able to deal with it most of the time. Other than urging vaccination to young people we know and living a safe and sane life, there isn't much else we can do. IMHO we should be more cautious of all STD's than worrying about how we "got" our cancer.

By the way Ray, I don't agree that chemical exposure would cause a "wide spread" cancer. Cancers start in individual cells. It is true that some are probably "field" exposure but that does not rule out the small tumor being caused by chemical exposure. Oral cancers ARE considered "exposure" cancers. After all, aren't alcohol and the many carcinogens found in tobacco and smoke chemicals?

There is an element of chance in this. Damage to DNA can occur in many places, some are crucial for the function of the proteins that are encoded and some not. Some location affect production levels of proteins (up or down) and some do not.
If the protein is a tumor suppressor then disabling or lowering it will be bad. If the gene product is an oncogene or grow factor then increasing its amount or changing it (for the worse) it is bad...

Some people are less susceptible to damage and/or can repair or control damage better. That has been well documented and studied.

DNA damage is a fact of life, you cannot escape that no matter what you do. You can however, increase the damage by eternal factors.
In many ways this is like russian roulette, for some, because of genetic predisposition and eternal factors there is a bigger CHANCE that something bad happens, while others get old enough to die from something else.

so why ... is a question you cannot get a full answer for.

M

Geez leave the site for a few minutes and you never hear the end of it!! Man, what if I took a vacation? lol

Again Brian is the expert on HPV and everything else FTM. I have a little knowledge compared to him and you know what they say about people with a little knowledge....I just am very outspoken about getting tested for HPV if there's any doubt as to the "cause" of your OC because 1. It was mentally helpful to me and 2. It may very well prove helpful in answering some or all the unknowns about HPV.

Just a short 2 1/2 years ago I was treated like a step child when I wanted to discuss and raise awareness of HPV and now it is discussed much more openly. Many, many doctors also dismissed the likelihood of HPV causing OC WAY BACK THEN but now it is considered more often (but still not enough).

Lets hope for everyone's sake that research will continue by concerned experts like Maura Gillison and maybe we will know the answers to all these questions one day and maybe those answers will lead to a prevention or cure of HPV+ SCC.

Ray,

I'm glad you brought this up..it sure is a hot topic!!! I spent a lot of time thinking about HPV. "Did I do something wrong?" "Am I the reason this happened to me?" I was driving myself crazy. I did ask my doc to test my last tissue and after month of running around they finally said "Sorry, we can't do that"

So anyway, what I'm trying to say is, I understand where you are coming from. If you know what caused it maybe you can fight it. But I agree with Margaret....I think it's just our genes. I feel like all we can do is try to make ourselves as healthy as possible. In my mix of doctors I see a nutritionist. He also does Kinesiology. It's a great side bar in my treatment.

I'm somewhat of a problem solver myself for a living so it's hard when a problem is out of your control.

OCF is funding (with the NCI) Gillison's next look at HPV beginning in January. She will by then have moved to Ohio, and no longer be part of Hopkins. Someone offered her some significant research money to come and do her work at their place instead. To give you an idea of how brilliant she is (IMHO) after joining OCF's board in 2001 she has constantly had epiphanies about the disease, and as a good researcher, followed the bread-crumbs to each subsequent elucidation/revelation about it. Most of her work is in PDF form on our HPV page. Her sequence of peer reviewed and published papers in the best journals has been; HPV is a distinct cause of OC, then what anatomical sites it goes for, then what is the demographic of the people getting it, then the mechanism of transfer 1, then the mechanism of transfer 2. 09 will see more papers from her, and we will begin to understand this better. In the meantime we have no tools to fight it. We are still trying to understand the life cycle of the virus, so we can interrupt it perhaps at some stage. We already know that we can prevent a persistent infection from it (necessary to cause malignancy), as long as you have never been exposed to it. But that does not help sexually active adults.

I've read that BOT and tonsils are lymph tissue and, because of that, traps bacteria and viruses. Most tonsillitis is due to some bacterial or viral infection that causes the inflammation.

I think that there needs to be some clarification of the saying that most HPV infections are transient. High risk HPV infections generally fall into three camps: residential, episomal, and integrated. Only a few percentage of these infections become integrated, and once they do, they are part of the host DNA. It becomes a part of the host like HIV or herpes would--although, it is now known that it is possible to get rid of HIV using bone marrow transplation, and radiation. When HPV16 becomes integrated, that's when the real damage begins as it begins to produce E6 and E7 proteins. I believe, based on the biology, recurrence is likely.

Here is an excerpt from The HPV Handbook "Human Papillomavirus and Cervical Cancer", edited by Professor Walter Prendiville and Dr Philip Davies, which supports detection of oncogenic activity vs. DNA or PCR detection (page 75 and 76):

"Testing for HPV oncogenic activity, rather than for the presence of HPV DNA, may therefore be a more relevant clinical indicator of the development of cervical cancer. The detection of HPV E6/E7 mRNA indicates HPV oncogenic activity and may be used as a clinically predicitive marker to identify women at risk of developing high-grade cervical dysplastic lesions and cervical carcinoma."


The HPV Handbook further elaborates on the subject HPV protein and DNA testing:

"Several methods exist for the detection, typing and quantitation of HPV. Commercially available HPV antibodies can be employed for the detection of HPV proteins using techniques such as immunohistochemistry, western blotting and immunoprecipitation. However, it is difficult to detect the HPV oncoproteins themselves, firstly because of insufficiently sensitive and specific monoclonal antibodies and, secondly, because of the very short half-life and turnover rate of E6 and E7 gene products. Consequently, the standard practical methods for the diagnosis of HPV infection are based on the detection of HPV DNA.

The incorporation of HPV DNA testing into primary screening remains controversial, however. The great majority of HPV infections are transient and clinically non-significant, although they frequently produce temporary cytologic changes. Only 10-20% of HPV infections become persistent and contribute to the development of high-grade precancerous lesions or cervical cancer. This is particularly relevant to women in their teens and 20s. It is possible that widespread use of HPV DNA testing will result in the identification of large numbers of women at risk, even though their infections are likely to be transient. Such misclassification would result in over-treatment of lesions, unnecessary expenditure and considerable anxiety for patients."

When our bodies evolved to how they are today, the process of apoptosis was part of that evolutionary change. Cells have specific life cycles, they live and they die on a schedule. Some areas of our body have a very rapid turnover of cells through this natural programed cell death and replacement. In the oral environment squamous cells live about 14 days... not very long. Why? Because the suffer constant insults and bombardment with toxins. Nice design that they get shed and replaced with nice new ones so frequently.

I posted this at length someone else awhile back but just to BRIEFLY say it again, this is a very complex process of conversion to malignant from normal. HPV16 enters a living normal cell, it can't live on it's own for very long. It sends out a couple of onco-proteins E6 and E7. E6 heads for a gene called P53, that controls the apoptosis process. It destroys it. Now the cell is immortal. A characteristic of cancers cells of all types. E7 heads for gene RB which is the tumor suppressor gene. with that one destroyed, the immune system does not recognze the cell as aborrent and in need of destruction. With that all done, the cell duplicates, and the daughter cells are created without RB and P53, a bunch of these gther together and you have a party... a little tumor is born. Now that it is an entity and not a single cell, it needs nutrition and the process of angiogenisis begins to take place. The body actually creates new blood vessels to feed it.

This is an over simplification of the whole thing, but what you should get out of it is that there are a variety of times and places in which our immune system, if in tune, can find these defective cells and destroy them. But everyone's immune system -while of the same overall design- is unique, based on your hereditary genome and proteome, and not everyone has an immune system that recognizes everything. So we have inherited susceptibility to certain diseases. We also have inherited protection from certain diseases.

Those of us that came from Europe ancestrally, have some commonalities that people from South America or Asia do not have. We are all descendants of people who were naturally protected (there were no treatments for it) from the black plague that ravaged a major portion of that population. We have that natural genetic make up passed down to us. Other genetic lines in humanoids died off during the plague. This is essentially evolution on the genetic level that we are seeing. The problem is, that the make up that allowed your ancestors to survive the plague, may today make you susceptible to something that wasn't around then. And what once was a genetic asset is now a genetic deficit. As a species we are not static, but constantly evolving and biologically changing.