I'm very curious...

Why does HPV attack the BOT?

Are we sure that other parts of the tongue are not susceptible to HPV?

The reason for my curiosity is that there seems to be a great number of people on this site that don't fit the typical profile of an OC patient, but yet they don't seem to have OC that is HPV related. Am I missing something?

When I get back to work I might just go ahead and pay out of pocket for my specimen to be tested for HPV...I find this very perplexing...As a child I use to get warts on the bottom of my feet(plantar warts)and on my hands. Once I hit the age of 12 or 13 I stopped getting them altogether. Even though I know that all warts are some form of HPV, and from personal experiences HPV's are very cumbersome--they like to come back. What are the chances of OC related to HPV coming back even after a successful treatment? Or wouldn't the HPV be able to come back to an area that was radiated? My guess is that we don't know yet...

Btw--I'm not sure if this makes a difference in my case or not but when I would drink or eat anything too acidic (citrus or tomatoes) my mouth would get these little white painful sores/ulcers. I was so susceptible to this I couldn't even take vitamin C without getting these sores. So, I know my PH levels must be a little off balance. It bothers me that I don't know what caused my cancer...How can I find out?

I was just told that I had a very unique type of Cancer. Whatever that means. I used to get warts and spots in my mouth from tomatoes but both have gone. I wish i knew what caused mine too.

How I got OC was something that never worried me. I am a former smoker and had my drinking days a long time ago before I had children. My doctor (Andrews) was kind enough to tell me he couldnt say for sure what the cause was, even though I smoked he couldnt blame it on that 100%.

Same goes for my family doctor. He told me some people have heredity factors or are just pre-disposed to have cancer and maybe that was the weakest part of my body for it to show up.
Anyway, I have not been concerned how I got it, just that I somehow did. To me it doesnt matter at all which may sound silly or stupid, Im just happy to have lived thru it twice.

Christine,

That's the problem...What I do for a living is solve problems. I solve these problems in order to fix them. If I cannot find the cause I know the problem will come back--it might take time but it will come back. I'm talking about my job not cancer. But, if I knew what caused my cancer I would feel much more confident in the solution...Maybe I would have more Q's & A's...I would feel better about the situation.

For the most part people don't get sick in my family until they are really old...They can drink all the booze, smoke and eat all the bad foods and they live a long time. I had a great grandfather that died at age 57...but that was before modern medicine. I'm a nonsmoker that touched little alcohol and I get tongue cancer. OC that is on the increase while smoking is decreasing. I just have a hard time accepting, "We don't know what caused your cancer." I don't buy it...You can't sell me on this...If I was a smoker and heavy drinker...I'd say, "Sure, maybe yes..maybe no...but I have a pretty good idea what caused it.." I like answers. I have a feeling I' not going to get them.

I know it doesn't change the treatments...But maybe it would 5, 10 or 20 years from now.

Ray,

I'm only 46 and this is my third cancer - and no, that's not a typo. When asked, the docs just shrug their shoulders 'cause they have no idea why. There's just something about me, my DNA or whatever that grows cancer. I'm trying to eat right, I plan on exercising more but I think that for some things there's just no explanation. And if I spent too much time wondering "Why me?" I'd probably never get out of bed.

Ray,

I can completely understand why you want to understand more about why you might have gotten cancer. My husband wondered the same thing as he was not a smoker and is a light drinker. We requested that his biopsy tissue be tested for HPV and that was the cause for him. It helps him make sense of it (which is important to both of us) but knowing his cancer was caused by HPV raises other questions as we know most people exposed to HPV don't get cancer. But we're glad we at least have this level of understanding.

Sophie H.

margaret gets it. It's in your genes, HPV or not. Some people shed hpv16, some it stays and prospers in. Why? Genetic make up. Thank our grandparents. Everything in this thread has been discussed here ad nauseum. The only new question I will answer, but the answer is on the PDF on the HPV page. People that have hpv16 going into treatments, have it coming out. The treatments do not get rid of the virus. The next logical question would be why. The answer to that is not known. And I can't believe it.... an HPV thread without david.

I'm speechless!

The $64 question is can the continuing presence of HPV16 still be a threat?

And we won't know the answer for years and years. The data on HPV recurrence is short. See OCF news story here

http://oralcancernews.org/wp/2008/1...neck-cancers-hold-promise-for-screening/

Oh I forgot. Certain cells attract certain types of viruses and cancers. HPV loves the tissues it is attracted to, tonsils and the base of tongue which is covered with .... lingual tonsils, made from tonsil cells. There not really called that, but for the sake of an easy description. Hepatitis B and C have an affinity for liver cells. Hence they cause liver cancer. Epstein Barr virus loves naso-pharangeal cells and causes cancer there. There are more examples....

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.

Also, I think it goes without saying that cancer is indeed a very complicated disease. It's so complicated that you can have a different set of mutated genes in another person that leads to the same cancer. Different roads leading to the same destination.

On a sad note, my friend's father passed away from mesothelioma of the lungs (a form of lung cancer typically caused by asbestos exposure). They think it's because he did industrial work for a long time. The very sad thing about this case is his wife also developed mesothelioma shortly thereafter. The doctors were highly perplexed, and no one really knows how that could of happened. The only conclusion that makes some amount of sense is she used to wash all of his work clothes. They think she may have been breathing in some asbestos fibers this way. Who knows.

MSG - In spite of the last paragraph you copied from their text, isn't it curious that the Centers for Disease Control this year is recommending that women no longer completely depend on the PAP smear for cervical cancer, (which finds dysplasia, when the cell is on its way to going south) but recommends for the Digene HPV test in addition to PAP during exams for those women that have an ambiguous or positive PAP. So why is this so? More data points.

Routine testing for high grade HPV will show whether a woman has a PERSISTENT infection, one that your immune system is not clearing, and that infection is the mandatory precursor for the development of cervical cancer. Looking at any assay, only traps that one moment in time. Interesting, and in some cases highly important, but trap two sequential moments in time and you see a trend, which is a line pointing to an event. Add additional data points like person has a histology result that is suspect and also has HPV... This is a person that is in a different group than everyone else, and needs one of three possible resolutions that they have recommended. While very useful, the PAP test isn't known for its high sensitivity nor specificity.

Least anyone take MSG's opinion about recurrence to the point of worry, it would seem that at least at the 5 year mark there is actually a survival advantage and not a propensity for recurrence in individuals with HPV16+ primaries. I am at the 10 year timeline, and an recurrence free. There is no data to support a recurrence tendency for people with HPV16 as the original primary cause. But until large numbers of people reach 10, 15, 20 years we will not know for sure. As to carcinogenesis from other sources like tobacco, we already have the dismal recurrence data.

No, I don't think that's so. The argument against that is HPV DNA testing picks up any HPV-residential, episomal, integrated. It's only the integrated forms that lead to high grade cervical dysplasia, and eventually cervical cancer. Infact, ALTS does not recommend using the HPV DNA digene test in LSIL cases, because the vast majority will test positive. Why cause needless worry and expenses? There is another test that is able to pick up integrated HPV in the form of E6 and E7 proteins. That is a much better indicator of potential cancer than the digene test.

Routine testing is another way, true, but that may go on for several years to determine persistence and integration. It would be better just to test for the oncogenic proteins.

When that becomes an affordable alternative test, maybe they will, it is not today.... perhaps you should write to the CDC. Bottom line, is we still test for may things which are vague precursor events and they have helped greatly, if not an absolute test for something. Like the PSA test for Prostate specific antigen. Remember that detection of early stage disease is the goal, not finite determination of every individual that will definitively get it. We have to sift out of a population of 300 million people those most at risk, so that they can end up in accelerated monitoring programs for the earliest detection of actual disease events, when survival is the greatest. Trying to test that many people with a finite, expensive test is never going to be in the game.

Since we have diverged significantly in to areas outside of oral cancer thisis the ALTS programs definition for those that wish to know.
ALTS was a clinical trial to find the best way to help women and their doctors decide what to do about the mildly abnormal and very common Pap test results known as ASCUS and LSIL. About three million women in the United States are diagnosed with ASCUS and LSIL each year. Organized and funded by the National Cancer Institute, ALTS included more than 5,000 women. It began in November 1996 and concluded at the end of 2000. Data analysis of the trial's findings is ongoing.

ASCUS stands for atypical squamous cells of undetermined significance and LSIL for low-grade squamous intraepithelial lesions. Most of these mild abnormalities will go away without treatment, but some may signal a precancerous condition or, rarely, cancer, ALTS looked at three ways to manage these abnormalities:
immediate colposcopy (magnified viewing and testing of the cervix)
repeat Pap tests
testing for human papillomavirus (HPV), an infection linked to cervical cancer

OCF is sponsoring salivary diagnostic work with Wong at UCLA. That test is a sieving process. It looks for proteins and RNA factors that we know to be associated with the development of oral cancer. (and many other diseases as well.) The value of the saliva test is that it is a cheap mass screening process to sieve out of a huge population a smaller group to watch. The issue has always been about identifying those at risk, not those with the actual disease already. Now we know who to be paying attention to, and we are not spending money and time (neither of which we have in our broken medical system) to do expensive, labor intensive, tests on large numbers of people. In salivary diagnostics anyone can collect your spit (non doctor) and it can be read by a computer chip programed to look for the markers) no pathologist, and quickly and cheaply say you are in a risk group. This is what is needed today. Affordable, quick, and sorting out those most at risk so that the more expensive processes and interventions may be applied to them.

The real world argument against the DNA testing that you are referring to, is that it disregards the realities of pubic health. It is expensive, it is time consuming, and it requires very highly trained, knowledgeable professionals to conduct it and interpret the findings. We can't even do much simpler and less expensive things in public health that would save lives.

Salivary diagnostics will be a commercial reality for oral cancer in less than 24 months, for other diseases like diabetes, Alzheimer's, and pancreatic cancer in years quickly following. Imagine, a test that would allow pancreatic cancer to no longer be a less than one year death sentence, from the saliva in your mouth, and early detection.

Wow, 24 months away? That's really cool.

Brian & MSG,

All I have to say is WOW and thank you for explaining "Cancer".

So, in really simple language, cancer acts like a parasite creating it's own little atmosphere where it can prosper until it kills it's host. I never understood cancer and how we're basically in trouble the minute our body decides to accept the cancer and feed it with new blood vessels.

If blood flow to cancer cells was blocked would the cancer die? Is that what chemo and radiation does?

I apologize for starting a thread breaking away from OC...But, this is really helping me understand my cancer for the first time since I was dx'ed.

I got my answer reading another post in another thread...thank you though.

It is amazing what we know about how the HPV virus does it's thing yet we really can't stop it without a lot of collateral damage. When I first read how HPV attacked my mouth I was shocked to find out the level of known detail and how smart the virus is at surviving. As Brain said our cells have like 2 guards. Guard #1 makes sure the cell has accumulated enough "good stuff" to reproduce another good cell and Guard #2 must get the OK from Guard #1 before he determines that he can give the final OK to reproduce. Now HPV comes along and goes to Guard #1 and says forget your rules and listen to me...I say it's Ok to tell Guard #2 that you are ready to go and then the virus goes to Guard #2 and says regardless of what you think, it's OK to signal reproduction so the cell reproduces without being ready or good enough to do so.

Now that's the children's version.

Ray,

There was some pioneering work done along those lines: starving the tumor by cutting off the blood flow. The scientific name for this process is called anti-angiogenesis, or, the blocking of new blood vessel creation. The doctor who pioneered this theory work won a Nobel Prize, I believe. The sad thing is, the idea never really worked well in clinical practice.

There is a new idea that is taking root in the scientific community regarding the treatment of cancer. Instead of finding a "cure", which most believe will not happen in our lifetimes, they should focus on finding cancer in the early stages where it's most treatable. There is some interesting work, as Brian mentioned earlier, that is going on with that.

Some of the most interesting and productive new ideas are in targeted therapies. The OCF page on this is here http://www.oralcancerfoundation.org/treatment/targeted_therapies.htm