I won't claim to have followed the media nor discussions on this site about HPV, oral sex and oral cancer very closely, but I gather that there have been some media items about a possible relationship?

I refer to this article by Dr. Gabe Mirkin, which expresses his take on the state of what is known about the possible relationships between HPV and cancers with a good description of "cofactors". I think it should be okay to post this link, as Mirkin isn't really selling anything, that I'm aware of:

http://drpinna.com/dr-mirkin-and-skin-cancers-19327
****while dr mirkin is not selling anything, dr pinna certainly is. the link in this post takes you to pinna's website not mirkin's and if you look at products, pinna is going to be selling magic mushrooms****(added by OCF admin)

It is clear that current evidence does point to a causative relationship between sexual promiscuity and the rates of certain cancers (cervical being the most discussed).

However, I will suggest (my opinion) that it will turn out that we as human beings are basically bathing in germs and viruses every day, and perhaps more and more so as the world becomes more crowded, and while it seems likely that certain viruses are a contributing factor to cancer, it will turn out that it requires a combination of cofactors to in fact trigger most cancers.

HPV alone seems to not cause cancer in the vast majority of people who become infected. As Dr. Mirkin states, most HPV goes away on its own within 6 months to two years.

However, chronic HPV infection (perhaps some people can't resolve the infection for whatever reason), repeated exposure to HPV, or HPV in combination with other cofactors such as smoking, being overweight, poor diet, lack of exercise, poor Vitamin D status, or genetic predisposition, may be what it takes to trigger cancer.

Perhaps HPV prevalence in the general population is a new thing, but I will suggest that any notion that you can avoid it may be misguided.

While Mirkin does state that most HPV infection is from sex, he also states that, technically, you could get HPV from a handshake. Also, some of the forms of HPV are what causes warts, and how many of us had warts as kids long before sexual activity began? I did, and I can guarantee I didn't get them from sex!

So what's my point? I feel that any attempt to stigmatize oral cancer as a sexually transmitted condition (or to stigmatize oral sex as particularly risky, for that matter) is misguided and unhelpful, that it will turn out that we're all under attack by thousands of viruses and germs at any given time simply by way of living on the planet among other people (and usually our bodies take care of this), that it takes a combination of cofactors to trigger cancer, and that simply living a healthy lifestyle will turn out to be the best defence against cancer.

Thoughts?

Perhaps you should read at least the articles on the OCF HPV page. The mechanism by which HPV16 causes oral cancer is very well understood. It requires no cofactors. It does require an unknown, and that is an individual with a genetic makeup that includes some genetic sequence (yet unidentified) that prevents their immune system from recognizing it as a threat, allowing the progression of infection, expression of onco proteins E6 and E7, which destroy cellular P53 and RB to immortalize a normal cell and begin the process to malignancy, which will be characteristic in all the daughter cells spun off, to take place.

In 99.1% of those infected with HPV16, either cervically or orally, it is destroyed by a healthy immune system. And yes, you can get HPV from a handshake but it is not one of the oncogenic versions of HPV (there are now cataloged more than 130, only 9 of which are proven oncogenic viruses, the rest cause benign warts or do nothing at all that we can determine at this stage of our knowledge.

All cancers require some genetic predisposition, even when the cancer is caused by a known carcinogen like tobacco use. For instance there are lifetime smokers that never develop cancer. You cannot avoid HPV unless you are non sexual, so that means that the vast majority of the population will be exposed. But to most people HPV infection is a non issue. Plenty of individuals who live healthy lives get cancer, perhaps those that do not, get it more often, but evidence based publications do not exist to support that premise. At the end of the day this is only part nurture and a lot nature (genetic predisposition) from the genes you inherited from your grandparents. If you are predisposed genetically to get cancers you will and no diet or lifestyle regime is going to change that. You can do things that keep you immune system healthy, but if you have a genetically inherited strong or weak one there is little you can do to change that aspect of what it controls in you. All anglo Saxon descendants of the original settlers from Europe in the US are descendants of people who survived the black plague. At the time of the plague there was no real medicine, and 2/3rds of the European population were killed off by it. Only those with a genetic predisposition to not become infected survived it. Their descendants also have that same protection, not that black plague will ever be an issue again. This is evolution of the species at the most basic level.

OCF has never attempted to stigmatize any person for a sexual infection, especially one as common and ubiquitous as HPV, actually quite the opposite. Since we know that it cannot be avoided, and we have no way as individuals to know that we have an infection for the most part, and since most of us will naturally clear it, (and those that do not clear it have no way of knowing till it's too late that they will not) all we ask is that individuals get an oral cancer screening annually for something that does not produce symptoms in its early development that a lay person may not recognize.

More on the impact of genetics and cancer and what it all means for the future here http://blogs.forbes.com/matthewherper/2011/06/05/cancers-new-era-of-promise-and-chaos/

This is the most current thinking presented at the ASCO meeting yesterday.

CHICAGO � Human papillomavirus infection was firmly linked to the recent rise in oropharyngeal cancers in the United States, based on data from the National Cancer Institute�s Surveillance, Epidemiology, and End Results program.

If current trends continue, the incidence of HPV-related oral cancers will soon surpass that of cervical cancers, senior author Dr. Maura Gillison reported at the annual meeting of the American Society of Clinical Oncology.

The incidence of HPV-positive oropharyngeal cancers increased 225% � from 0.8 per 100,000 to 2.8 per 100,000 � between 1988 and 2004, the researchers found. At the same time, the incidence rate for HPV-negative oropharyngeal cancers, which are strongly related to tobacco and alcohol use, declined by 50% � from 2.0 per 100,000 to 1.0 per 100,000.

Consequently, the overall incidence of oropharyngeal cancers increased 28%.

Even by the conservative estimate that 70% of oropharyngeal cancers in 2020 will be HPV positive, the annual number of HPV-positive oral squamous cell carcinomas (8,653 cases) is expected to surpass cervical cancers (7,726 cases). Further, the majority will occur among men (7,426 cases), said Dr. Gillison, a medical oncologist and the Jeg Coughlin Chair in Cancer Research at Ohio State University Comprehensive Cancer Center in Columbus.

Changes in sexual behavior among recent birth cohorts and increased oral HPV exposure probably influenced the increases in incidence and prevalence, Dr. Gillison speculated. Having a high lifetime number of sexual partners is a known risk factor for HPV infection.

Although the rise in oral cancers in the United States has been attributed to HPV infection, the empirical evidence to back the contention was uncovered prior to the SEER study. A previous study by Dr. Gillison and her colleagues helped to establish that HPV infection causes an epidemiologically and clinically different form of oral cancer. Their findings documented a major increase in the incidence of HPV-related oral cancers in the United States, particularly among young, white men, and that survival rates are significantly higher in patients with HPV-related oral cancers than in those with HPV-negative cancers (J. Clin. Oncol. 2008;26:612-9).

The evidence surrounding HPV-related oral cancers has been mounting, "but I don�t think there is a lot of awareness in the general medical community," Dr. Gillison said in an interview. Most of her head-and-neck cancer patients who are nonsmokers were referred to her after undergoing months of antibiotic therapy for presumed tonsillitis.

Screening the sexual partners of oropharyngeal cancer patients has been discussed, but there is no evidence to support the practice. The risk for oral cancer is fourfold higher in HPV-positive patients� partners, but the absolute risk is low, Dr. Gillison said. Alternatively, there are now three or four case reports of husband-wife couples with HPV16-positive tonsillar cancer.

"Probably 80% of people have HPV exposures in their life and 99.1% clear the infections without consequence," she said. "So, whatever [stable sexual partners] have swapped in terms of infection, they�ve already swapped. Just because they suddenly found that one of them got cancer from it doesn�t mean the other one will."

The researchers called for more studies to evaluate the efficacy of HPV vaccines in preventing oral HPV infections.

Dr. Gillison worked for 3 years with Merck & Co., the maker of the HPV vaccine Gardasil, and commented that Merck will not likely pursue this indication. Merck was interested in studying the vaccine in prevention of oral cancers but saw the endeavor as too much of an uphill battle in part because oral cancers are not readily accessible visibly or through biopsy. Merck instead successfully opted to seek approval for the prevention of anal cancers, an indication that was approved in December 2010 for male and females 9-26 years old.

It was already approved in the same age groups for the prevention of cervical, vulvar, and vaginal cancer and of genital warts caused by HPV types 6, 11, 16, and 18 in females and for the prevention of genital warts caused by HPV types 6 and 11 in males.

Invited discussant Dr. Lisa Licitra of Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, said that oral cancers are on the rise in Europe in both men and women and that a vaccine should be pursued. Data on oropharyngeal cancer from her institute did not find a greater contribution from men.

"A preventive vaccine is worth considering," she said. "In particular, when we consider the European data, I think that in this direction, action should be taken."

In their study, Dr. Gillison and her colleagues used four different assays to determine the HPV status for 271 oropharyngeal cancer cases collected from 1984 to 2004 by three population-based cancer registries of the National Cancer Institute�s Surveillance, Epidemiology, and End Results program in Hawaii, Iowa, and Los Angeles. Trends in HPV prevalence across four calendar periods were estimated using logistic regression.

The HPV prevalence in oropharyngeal cancer significantly increased across the time period, regardless of the assay used, and remained statistically significant, even after correcting for potential loss in assay sensitivity, Dr. Gillison reported. Genotyping with the Inno-LiPA assay appeared to be the most precise, detecting more than a fourfold increase in HPV prevalence from 16.3% in 1984-1989 to 72.7% in 2000-2004.

Median survival was significantly better for patients with HPV-positive cancer at 131 months vs. 20 months for HPV-negative patients (log rank P value less than .001). HPV-positive cases on all assays had a significant reduction in hazard of death compared with HPV-negative cases after adjustment for age, sex, race, registry, calendar period, stage, surgery, chemotherapy, and radiotherapy.

Survival of HPV-positive cases increased over the study period but remained unchanged for HPV-negative cases. Consequently, survival of all oropharyngeal cancer cases improved over time, according to the results of the study, which was led by Dr. Amil Chaturvedi, an investigator with the division of cancer epidemiology and genetics at the National Cancer Institute, Rockville, Md.

I only have two comments
Firstly, I question the veracity of "dr mirkin" and "dr pinna" as this website just doesn't ring true. To try to put my finger on it, I looked around the website and stopped when I got to Dr Pinna's biography which just sounds ... wrong. A BA in economics??? In Mexico? After which he becomes a purser on a ship?? Then a Masters in Philosophy before his medical degree?? I wonder if these doctors, if in fact they ARE medical doctors are better suited to the "quacksite"

My second comment is around the use of the word promiscuity. If we don't want to stigmatise HPV and oral cancer then we need to watch our language. I remember reading the trial last year that quantified risk against the number of sexual partners we have, (the number 6 springs to mind but don't quote me) and I do not recall thinking that the number was particularly promiscuous.

As a still single 50 year old (although heavily committed to one man), I think I may have hit that number before I was 25. Maybe people DO interpret that as promiscuous but I think some of us were just slow learners:). I wonder how I would have been labelled by my 35th birthday?

We only just DE-stigmatised oral sex during my generation and I know at least half the population would be devastated if we were forced to return to the 50s way of thinking.

Karen

My thoughts are that the link (which I have notified the moderators about) goes not to gabe mirkin's article but rather to dr pinna's website where pinna is indeed selling "products".
Pinna's website is a mismash of health, economics, etc but I agree with Klo that this website link borders on meriting quackwatch listing since dr pinna is touting "magic mushrooms" and not the psychedelic kind I took back in college but instead another "miracle" cure from China that is a combination of a worm and a fungus and of course not available from any recognized medical source but soon to be sold by pinna.

I will say that Trends in Microbiology article on HPV was excellent but of course neither Mirkin nor Pinna discussed it. Brian actually did but in plain english compared to the actual article. Here is a link that I think will go to the pdf version of the article but since it's a redirect, I don't know HPV malignant progression If it does not, here is a link to that issue of the journal Trends in microbiology where you can scroll down for the HPV article

Last but not least, thanks Stily for posting this as I had actinic keratosis three times and had it burned off but the first time was ten years ago and according to my ENT, that was approximately when my cancer tumor started . Of course it wasn't discovered until almost four years ago. So I;ll buy the theory that HPV is involved in actinic keratosis.
Charm

Oops, I certainly did not mean to involve this "Dr. Pinna" person and have no idea who that is. I also certainly did not mean to suggest that OCF has in any way stigmatized anything! If anything I had posted here trying to promote the opposite.

Thank you, Brian, for all the information and certain clarifications.

It certainly is reassuring to read that "The risk for oral cancer is fourfold higher in HPV-positive patients� partners, but the absolute risk is low".

-Seth

not oops Seth, you just scored comments from 3 "tell it how it is" posters. 'Tis the nature of the beast that the written word is often more to the point (and consequently reads as blunt) than our spoken word.

I was mainly agreeing with you but just wanted to add to your important point about ensuring that HPV infection is not stigmatised by reminding people to avoid words such as promiscuous.

Your last paragraph made your point eloquently.

Unfortunate about the link - the problem wasn't the article but where it ended up.

Seth

Considering Dr. Pinna's lack of credibility (BTW, if you look at the link you posted you will see that the very first words are drpinna), I began to wondering if this is even a Gabe Mirkin article at all. I could not find it on the real Dr. Mirkin's website and a google search didn't turn it up either. Finally blogspot did the trick. There was never any such article.
Well, it turns out Dr. Pinna simply cut and pasted excerpts from three different different Dr. Mirkin blog posts and gave the impression that it was one article. Pinna took parts of Mirin's April 5, 2011 blog on HPV/cancer, Mirkin's blog entry a full year ago on June 19,2010 which was the one on HPV/ skin cancer and a Mirkin blog on March 10, 2010 about Cofactors for cancer.

That's why I objected to your linking directly to Pinna's page; he's just not credible plus hawks fraudlent products.
Like most quacks, he puts in just enough real stuff to trick readers. Technically his composite of three blog entries spanning a full year is "Dr. Mirkin on skin cancer", but it's hardly a Dr. Mirkin article. Pinna also left out some of Mirkin's cautions and common sense.

I know I'm a bit of nag on this, but I have always like Dr. Mirkin and this "article" seemed too loose with the facts to be truly his. At least Pinna left in Dr. Mirkin's cites to a real medical article.

Charm

Related to changing sexual behaviors as a solution. I have read several articles in the last week that do however, from a very conservative viewpoint, wish to alter American's and teenagers sexual behaviors. My observations are two things about this that have a history of not working. The first is prohibition of ANYTHING. I don't care what you pick, alcohol, prostitution, illegal drugs etc. it has never worked. You can make it illegal, you can stigmatize those that engage in it, but at the end of the day you can't eliminate it.

So using OCF tobacco policy as an example, we are proponents of "harm reduction" vs. prohibition. Essentially this means acceptance of the behavior, but offering alternatives that in some way reduce the harm. Clearly in tobacco use this would be replacement of the addictive portion of the product, nicotine with a strong enough supplement to have an equal effect to what was currently being used. The gums and patches do not, and OCF is an advocate for a controlled availability of nicotine inhalers and nasal sprays as higher dose delivery systems that do little harm, but reduce the incidence of inhaled combustion products from burning tobacco. It's not a perfect solution, people are still addicted and some will have higher blood pressure (not more than tobacco use but more than a non smoker), but cancer incidence particularly lung and oral will go down.

Since there is some argument about what constitutes "good" harm reduction, here are a couple of examples. In heroin use, we have FREE methadone to anyone that wants it without too many questions associated with getting it. They are still addicts, but the element of crime to generate capital to buy their habit is eliminated. Some harm reduction (particularly to others, some less revenues going into organized crime) but not a perfect solution. The key is there is no introduction of any new harm in the process. Another good harm reduction strategy are needle exchange programs. They do not stop people from being addicts, but they do stop the spread of HIV, hepatitis and other deadly diseases through their use.

Right now the idea of harm reduction in sex is limited to condom use (partially helpful in HPV, certainly helpful in the AIDS paradigm) and education (whatever is left after our current politics eliminate most of it from our schools for reasons I won't go into here). After that there are no real behavior changes that we can really count on - anyone that remembers their early years when hormones were raging and the opposite sex took a disproportionate amount of your thought process, understands why. Really what we have now is a chance to help the next generation through vaccination, and early discovery of disease stages in HPV+ oral cancers to reduce treatment related morbidity and death.

In an effort to be responsible but realistic parents, some of us parents of teens think about condom use this way: Abstinence is what we want and expect. But, we know it isn't always that simple nor is it safe and/or healthy not to advocate the use of condoms. So, we find we're saying, "we don't want you to have sex but if you do, use a condom."

Personally, I keep the lines of communication open with my sons all the time, seize upon "teachable moments", and have made it a part of family life to talk about things we see or hear about in the media or even in our community. It surprises me how many people are still very shy and won't talk to their children about sex. I handle talking about illegal drug use and alcohol abuse in the same way.

When we had the Gardisil vaccination series started for our sons, we talked very openly with them about the reasons for them to have the vaccine. Also, I sat with my 17 year old son and his pediatrician and discussed it. Although he's a shy kid, he didn't get embarassed, and didn't complain about what we were talking about.

As parents, it's not that were advocating a particular behavior...we're just aware we can't prevent it from happening. So, it's best to protect them and educate them.

My daughter recently took her two boys for their check-ups. She and the two boys were together in the same exam room as the doctor who examined both boys (the oldest just entering puberty) at the same time, which I thought really helped to eliminate any possibly embarrassing moments. Everything was discussed including the Gardasil shots due to be given next year to the oldest. Then the doctor gave each boy the opportunity to talk with him privately w/o their Mom there . I'm all for "teachable moments" starting very young which provides for later situations to be that much easier. Sandy, I agree, it's best to protect and educate. There are unforeseen circumstances that arise where even the best intentions or personal beliefs go awry.

A friend of mine had his 13 year old suspended from school recently because he accepted oral sex from 2 of his classmates (who were also suspended). When questioned about it, he was genuinely perplexed for 2 reasons:
He didn't think it was sex
He didn't see a problem because "everybody does it"

My own discussion with doctors in this area suggest this child's thinking is not uncommon and oral sex is seen as a commodity to be traded. Somehow it has become disassociated with intimacy, and is not sex in their eyes. Therefore, they are doing nothing wrong.

Sounds very much like a very high profile politician a few years ago...

Seems like Middle School is really getting very informative and exciting these days. All the more reason for parents to make sure and have a frank discussion very early with their children about their "commodities" and what to do with them (or not do) - And hopefully before they get it from their peers whose info (and demos) may be slightly distorted.

We've heard about some shocking middle school moments where my son goes to school. A few years back, there was a group of boys and girls who habitually went to a house at lunchtime when no parent was home during the day. They were having orgies!!!...And, a few times, adult campus supervisors would turn a corner on a building and find a girl on her knees giving oral sex!!! You are right, Karen, the mindset with these kids is that it isn't sex. Hummmm...well then, what do they think it is?!? What part of the phrase "oral sex" doesn't mean it is sex?!?

Educate and prepare and keep educating and preparing...then educate and prepare them some more!!!!

I am going with Brian on "harm reduction". If we can vaccinate all the boys and girls against the cancer causing HPV virus, then we can have a discussion on sexual mores. I'm old and to me, oral sex is most definitely sex but I wish the Guardisil vaccine was mandatory. Colleges all require menigitis vaccination, realisically the chances of a college student having oral sex are much higher than getting menigitis, yet the HPV vaccine is not mandatory. Give the usual religious exemptions and move on, please. Sorry, I know I am preaching to the choir here at OCF.
Keep the Faith
charm

I suppose the good news with the kids described above is that the likelihood of stigmatisation is lessened if they don't even equate oral sex with sex. If it is no big deal, it should be easier to convince them (and their parents) to have the HPV vaccine.

Don't know if you having the same problem in the US but according to the manufacturers in Australia approximately 1/3 of the people who get the first needle complete the course. We need education around THAT as well.

I can see why kids may not consider oral sex as sex. They probably feel that it is more like mutual masturbation (hope I can say that!) And everybody says that's ok, unless you find yourself in "polite" company, of course.
Re the "first needle", my daughter's doctor told her that even if the second shot is way past the due date, the 2nd and 3rd needles can resume without having to start the series over from beginning.

The online magazine Slate has a column by Kent Sepkowitz, a physician at Memorial Sloan-Kettering in New York City, about the HPV vaccine issue as it relates to vaccinating boys. (He's for it.)

Does anyone have ideas on how information about the link between "risky behavior" and oral cancer can be presented in a school setting. The program I am working with here is interested in presenting information in an acceptable way - legally and socially.
If so you can reply here or send me a message
Thanks,
Malka

If the students read Slate, then they may challenge the predicate of your presentation. My thoughts on this are very similar to that in the article posted above in this thread from Slate and set forth below in an excerpt of Dr. Kent Sepkowitz of Memorial Sloan-Ketterings Cancer Center:
[quote]If the past is any indication, though, I suspect a more eyebrow-raising angle will overshadow this important public health story. Since the link between HPV and oral cancer was first floated 10 years ago, the media has tended to focus on just one aspect�the possible connection between oral sex and the rise in oropharyngeal cancers. However, there's no definitive evidence yet of a causal relationship between the activity and the disease. That's not to say that people shouldn't exercise a reasonable amount of caution when having oral sex. But when popular opinion (particularly in matters sexual), wags science, no one benefits.

It's easy to see why the notion that oral sex can give you cancer is so attractive. It makes for an irresistibly lurid headline, of course, and it appeals to the secret Victorian hidden less or more deeply in all of us. (Everything fun has a price�everything!) And to be fair, the circumstantial evidence is compelling. It's well understood that HPV is transmitted through other kinds of intimate contact, such as vaginal sex. HPV seems to grow quite well on mucous membranes, those nonskin tissues that line the mouth, nose, vagina, anus, and a few other anatomic areas, and which may touch quite a bit during oral sex.

As an explanation for the uptick in oropharyngeal cancers, though, oral sex has one glaring problem: HPV-positive head and neck cancer is, inexplicably, a guy's disease. If oral sex were driving the issue, wouldn't we see a commensurate rise in HPV-positive tumors among women? Unless the announcement was screened out by my workplace email filter, I don't think anyone has demonstrated that cunnilingus is being practiced more often than fellatio.

Furthermore, many people with HPV-positive head and neck tumors deny having had much oral sex. According to a 2010 review of several studies on the topic, more than half of such patients reported five or fewer lifetime oral sex partners, and 8 to 40 percent said they had never had oral sex.

Finally, the argument that oral sex is driving the rise in these cancers carries the implicit suggestion that oral sex patterns of recent years vary considerably from previous generations. Among the many things we don't know about our forebears, what they did and didn't do in the bedroom surely ranks near the top. And it always is a bad wager to bet against the likelihood that everyone, in every decade, was having all types of sex, and as often as possible. [/quote]
As I posted before on this thread, the time and energy spent on trying to convince young people not to have oral sex would be much better spent on getting them all vaccinated. IMO The real "risky behavior" is not to get the vaccine.
Charm

Leslie

Thanks for the link to such a relevant article for this thread. As you can see, I couldn't resist a little cut and paste on his oral sex remarks.
Charm

Malka

Let me make clear that what you are doing is great. Educating the kids that smoking, drinking, and HPV can cause oral cancer is very much needed. My comments above deal with some of the other issues raised on this thread.
I wish I did know a way to get a message effectively across to teenagers but I don't. As long as you stick to the facts, throw in a few cites to some of the studies on the OCF main page, I'm sure your presentations will be both legally and socially acceptable. Don't forget these kids watch South Park. My wife and I were amazed at the graphic stuff just last night - it was funny and we laughed but it would never have been on TV when I was these kids ages.
Keep up the good work
Charm

I read this article, but I didn't get that he was a doctors because a couple of his facts were way wrong in spite of it being overall good. As to the oral sex connection - that has been throughly explored and peer reviewed published in the journal of cancer. It is the mechanism of transfer.

If he understood that HPV16 is attracted to two types of cells one of them predominantly, he would get that the wet cells of the body are its first choice. (Squamous cells) They line every opening to the human body. When a woman goes down on a man, how much of his anatomy is composed of squamous cells, and therefore harboring potential HPV virus? Only the opening to the penis, a pretty small piece of geography. When a guy goes down on a woman, how much of her anatomy is covered in squamous cells? LIkely more than 90% of where his attention is going. The leap from these simple anatomical facts to men getting oral cancers from oral sex more than women is a putt, not a drive....

And there was a sexual revolution in the developed world in the 60's and 70's, sexual behaviors changed dramatically - in spite of his opinion - that it is something that remains constant. Anyone who was a teenager in the sixties, wasn't routinely getting lucking in the back seat of dad's Chevy being orally satisfied by his girlfriend. The recent 60 minutes show interviewing high school kids of all ages, that ALL said they were doing it, would never have been a truism in 40-50 years ago.

Lastly, he completely ignores mathematical progression as a cause in the uptick of the HPV disease. In a model that uses tobacco as the prime mover, it requires that people engage in a new lifestyle choice to get the cancer. That model is accurate and as smoking has declined from 44% of the American population in the 50's to about 19% today, there was a matching decline in oral cancer of a tobacco etiology. We didn't know that 10 years ago, but we know that today looking retrospectively at the data by anatomical site. This has recently been reviewed and published by Gillison and partners inside the statistics and information branch of NCI, with a view towards what will be going on in 2020. When you speak about the spread of a virus however, it is not a choice, it is a mathematically increasing progression, as the population of infected people do what they were already doing to new uninfected people. This is the very basis of the most common of information we have on viral outbreaks that are spread through human contacts, and has been well understood for decades. If he is a doctor... epidemiology cannot be his area of expertise.

OK so now I have Googled the guy, and he is an infectious disease doc at one of the best cancer centers which is close, but not an epidemiologist. So he's got the letters after his name.

But for sure he has not read the most current stuff, and the logic which I have heard HPV experts speak to about its transfer at so many conferences, is too obvious. I can't believe that someone with his credentials missed the idea. (Or disagrees with it) We'll see what he says when he returns (I hope) my email I just sent him. He may have knowledge that I haven't heard or read, and certainly he has clinical experience that is leading his thought process.

@ Malka-Maybe the best way to get the kids and their parents educated about HPV would be at a yearly check-up starting at age 11 or so. I think a pediatrician would be the best source to address the subject legally and informatively. If not at a yearly check-up, it could be incorporated into a consultation when the child receives any of the mandated vaccines required for older children.

Parents are given the opportunity to attend information sessions regarding sex education at school. But, many parents don't attend them and don't review the materials that come home from school with their child. There is a huge lack of awareness of HPV. I don't think the public schools can reach enough of the target audience to make much of a difference.

@ Brian-You're probably familiar with a study done in Hawaii that looked at transmission methods and rates between partners. It seemed quite thorough. It didn't stop at the oral/genital contact but also genital/hand/oral, genital/genital/oral, and genital/genital/anal as well. A woman can infect herself orally or can infect herself orally through her male partner. None of this stuff should have been a mystery to the good doctor.

Thanks Brian - I won't be forwarding that article to anyone now.
The anatomical differences between male and female oral sex re mucous membranes would account for the disparity in male/female patients and undercut the doctor's rebuttal.
I always find better and more accurate information here at OCF than any article or story. Keep up the great work
Charm

Not sure I agree with the obvious conclusion the doctors have jumped to. The anatomical differences makes sense at first glance but then if HPV is transferred to the oral cavity, then why doesn't it transfer between couples just as easily once it is sitting in the oral cavity? Maybe there is a genetic difference that protects more women than men? Or maybe it is just a matter of time before the women catch up with the men?

Klo - these are good questions. Regarding a delay in women catching up to men at some point in the future, my question would be; when compared to other viral infections which have no gender bias in incidence or latency of occurrence, why would this virus be any different? Remember what we know about this virus has been explored heavily in the cervical arena and there is no guarantee that that experience will transfer exactly to oral. For instance, we know that it can take upwards of a year for the immune system to clear an HPV16 infection from the cervix, but it certainly does it. Normal defenders of the mutation cascade in a cell that exist, (there are many but the most common would be p53 regulated apoptosis) are likely different in different cell types. One possibility that has be postulated is that HPV infections in the mouth will be cleared more quickly by the immune system than on the cervix because of the significantly shorter normal life span of cells in the oral mucosa and lymphoid tissues than of the cervix. Programed normal cell death time lines, could potentially influence the impact of a necessarily cellular cascade of events to malignancy, and that is a core component of our natural immunity to things.

Time line bias is certainly an issue in some cancers. The most published example is in men's prostate cancer. There is no evidence that in the diagnosed HPV+ OC patent population going back more than a decade that there is any gender based time line bias in oral HPV carcinogenesis. If there is a genetic protection based on gender, it hasn't been identified, and to my knowledge no one is looking at that in the research world as an area of exploration. (given that the cell types in both sexes are identical)

The couples issue is a different thing. First, the virus is only a freely circulating entity for a very short period of time, and it must enter a cell (become episomal) to survive. Even if and when that happens, that does not mean that the invasion will not trigger the immune response that destroys the cell and the contained virus. As stated earlier this happens in 99.1% of those that encounter the virus. Couples are still each unique biological entities, and just because one immune system defends against it or does not defend against it, is no guarantee that the partner will have exactly the same response to the virus. And since in 99.1% of the people that are exposed to the virus naturally clear it without incident, they will not be impacted by it, so how would they know that they have even been infected by it, unless they were also a person with no immune protection against it? There are only a couple of published cases of husband/wife oral HPV+ oral cancers ever documented�. So the mathematical probabilities of it occurring are not zero, but very very small. So in essence it likely does transfer between couples orally, both routinely and commonly, it just does not progress into a negative event.

The FDA cut off vaccinations for HPV at age 26. Why? Because they determined by that time/age everyone has been exposed to the versions of the virus that it protects against. The vaccine does not work in previously exposed individuals.

One factor that may account for more men having HPV+ oral cancer is that, in the past, men tended to have more sexual partners than women and engage in more dangerous sexual behaviors. I'll wager that there are now more HPV+ young women than HPV+ older women.

I am 49 and, if the divorce ever happens, I want to have the HPV vaccine since I am HPV-. Women over 30 are routinely screened for HPV when they have a Pap. I really want to avoid HPV. I'll see if I can talk my GP into giving me the vaccine series.

Sandy - just because you are HPV- today, does not mean that you have not been exposed to it. If you have every fought it off, the vaccine does not work on you. The only way to know would be a test you just can't get easily, and that would be looking for an HPV16 antibody in you, and even that test is not 100% conclusive if you could find some research lab to do it, and also be wiling to pay an expensive price to get it done. For some unknown reasons not everyone that successfully fights off HPV retains an lifelong antibody for it. Like I said in the previous post, the FDA's data made them believe that after age 26 doing the vaccine would be a waste of $ in most American women.

Thanks, Brian. I can completely understand the FDA's age parameters given the percentage of women identified by their gynecologist as being infected. The only way a vaccine would not work on me is if I had been exposed to HPV-16 because I would already have antibodies for it. According to my doctor, I have never been exposed to HPV-16. I do not have antibodies for it.

I also spoke with a gynecologic oncologist about HPV and about general immunology as well. This is the information I received: Once someone contracts any virus, the body either dies from it or recovers from it. But, the virus antibody remains identifiable in the host. Rarely, a virus is active in a host without symptoms causing a carrier situation. It is never really "cleared" by the body. This is why vaccination is unnecessary when immunity has been conferred by a virus such as chicken pox, etc. With vaccination or illness, there are antibodies present--the proteins from the dead virus present, either way. However, regarding the more insidious viruses such as HPV and HIV, exposure causes changes to take place within the cells that eventually cause immune system damage in the case of HIV and, often times, cancer in the case of HPV-16. Regarding HPV, there are no symptoms of the active virus. It is only when tissue cells begin to show signs of abnormal structure does it usually become detected and an HPV-16 or other cancer causing strain is identified. At this point, the host is more than likely no longer contagious but the permanent damage has already been inflicted. The cells are acting on the programming caused by the initial virus not actually the virus itself.

With the chicken pox virus, it can cause shingles long after the host has recovered from the virus. However, a host can only get chicken pox once and immunity is conferred. In the herpes virus, it can flare up because of some trigger experienced by the host or the host can be outbreak-free. However, in both cases, antibodies are still present. Transmission and systemic exposure depends on the virus and to what body system(s) it prefers to attack and what type of contagion is present when it manifests. It is presumed that HPV is not contagious after the host has recovered from the initial exposure. However, with other viruses, such as herpes, the host is contagious whenever there is an outbreak present.

Whether someone has been infected once or multiple times with HPV or any combination of it's strains, it will have produced antibodies. Does multiple exposures cause more of a risk for cellular damage? Probably. But, once someone has gotten it, they have it for the rest of their life. Like the old saying goes, "love may come and love may go...but HPV (like herpes) is forever."

One thing that is happening with HPV is a mutation process that is producing new strains of HPV. There are over 100 strains of HPV and more to come. Some are benign and some are not. If you think about the influenza virus, that is why no one becomes immune from the flu and why there isn't an effective vaccine. It mutates from year to year. When a virus mutates, there is no built in immunity to the new virus strain. If someone does not retain a life-long immunity to HPV, the mutation process may be to blame. However, antibodies would still be present. Therefore, if no antibody to a particular strain exists in an individual, then a vaccine would be effective at preventing that individual from becoming infected with that particular strain. Medicine will be forever playing catch-up with HPV. The HPV vaccination program is a step in the right direction, without a doubt.

So, that's the information I have received from a general gyn and an oncologic gyn who deals with cervical cancer detection and treatment on an every day basis.

Immunology and and HPV are both tricky subjects. There is still so much to be learned about HPV. Considering I have had one partner in 27 years and am testing negative, I don't think it is unreasonable to assume I have not been exposed to an active HPV-16 virus. Certainly, I can contract it at some point forward. But, who's to say I'm not one of the 20% who won't have it by the time I'm 60?

I will be more than happy to pay the $150-$180 per dose x 3 if my doctor would be allowed to administer it. After all, there are many other therapies, Erbitux for one, that don't work on everyone. And, there is no way of knowing on whom it will work. Erbitux costs tens of thousands of dollars by the time someone has received 8 infusions at $4,600 a dose. Considering what oral cancer does to a person and the havoc treatment wreaks on him or her, I think I'd rather take my chances with the vaccine.

As for the few married couples who have developed HPV+ oral cancer, perhaps one of them had the active virus and exposed the other. They just both happened to be unlucky or their lifestyle contributed to developing oral cancer. Since the odds allow for that to happen...it had to happen to someone.

I am new here and study for doctor specializing in venereal diseases, now I read all about HPV and cancer.
I am convinced that only HPV in the throat does not cause cancer, it requires additional impact as many tests indicate there is an investigation which can be bought here;
http://www.amjoto.com/article/PIIS0196070911000287/abstract
I copy a snippet below.

In the case of transfer between a man and woman and woman who is performing oral sex;

I disagree that the risk is greater when a man performs oral sex on a woman than vice versa, there are also other things that makes this not true, among gay men is oral cancer increases most and why there is no increase of lesbians, HPV is almost as common among them.
That transmission is easier for a man? HPV requires friction to get into the skin, usually through small wounds, friction occurs during intercourse and when a woman gives you oral sex, when a man gives, it is usually only lightly touched, the virus is present in all skin, someone wrote
"(Squamous cell) They line every opening To The Human Body" this is not true squamous cell exist on all skin and to the entire penis.
Men infecting women very easily through sexual intercourse when the penis enters a hot and humid area, compared to the mouth.

One reason may be that women's infection in the vagina persists longer than a man's penis and that therefore the man who gives oral sex to the same woman several times subjected to virus for several years, which seems to be a prerequisite for cancer, repeated exposures.

In the U.S., approximately 7000 cases of oral cancer caused by HPV, 2 / 3 is a smoker and 2 / 3 is men, there is absolutely a connection, the other a few thousand people who do not smoke and get cancer ... amazingly few people and we know nothing about their status, HIV, oral health, etc.

They are very quick to link oral sex to increase with HIV sweep under the rug, we must not forget that oral cancer is most common in HIV infected and this infection following the development of oral cancer late 70's and 80's

4. Discussion
Overall, the putative evidence from the above review
points to smoking posing an additional risk of development
of HNSCC in the presence of HPV infection. Where
counterexamples of such an association exist, the studies
are limited by small sample sizes [16,24], weak statistical
evidence [16,17,24-26], and inconsistent definitions of
smoking status [25]. Criteria of light and heavy smoking, as
well as the definition of current, never, and former smokers,
are not uniform. The dose and duration of tobacco exposure
in most of the studies are self-reported. The strength of the
reported conclusions would have been greater if the exposure
had been confirmed with cotinine or other bioassays. On the
other hand, the studies showing an additive or synergistic
interaction between smoking and HPV have larger sample
sizes and adequate controls [20�23], which support greater
generalizability of these results to other populations.
4.1. Is it biologically plausible that smoking can promote
development of HPV-related HNSCC?
A positive association between smoking and HPV toward
causation of HNSCC appears to be biologically plausible
based on our review of clinical studies and supporting
evidence of pathologic interactions between the 2 risk
factors. Human papillomavirus may have evolved mechanisms
to escape immunosurveillance, but the transient nature
of infection lends little credence to its ability to cause
neoplastic changes in the absence of any contributory factors
[11,14,22,34]. In HPV infection of head and neck particularly,
the viral copy number has not been found to be
substantially increased, suggesting that alternate pathways
mediated by cocarcinogens such as tobacco may be involved
in HNSCC related to HPV [35].
Tobacco has been potentially linked with all major phases of
HPV-related carcinogenesis: initiation, promotion, and progression.
Histopathologically, smoking causes cellular and
structural alterations in tonsils, leading to an increased oral
acquisition of HPV [36]. This has been corroborated clinically,
as researchers have observed a high prevalence of HPV
infection in smokers, particularly current smokers [37].
Smoking is also known to suppress the mediators of immune
function, thus facilitating persistence of HPV infection�a step
crucial to development of HPV-related cancer [8,11]. Inactivation
of the tumor-suppressor gene p53 by the HPV E6
oncoprotein is an important step in causation of HPV-related
malignancy at the molecular level [19,20,26,38]. The DNA
damage caused by smoking may further impair the cell's ability
to recuperate from the mutagenic insults along with an increase
in frequency of p53 mutations [39,40]. It has also been
suggested that the carcinogenetic potential of HPV increases
with viral integration with host DNA, an effect resulting in
overexpression of HPV oncogenes. The process of integration
occurs at fragile sites or �hot spots� ofDNA breakage, and there
is evidence that tobacco smoking induces DNA breaks in
human cells [41-43]. Thus, an increased frequency of HPV
integration in smokers may increase the risk of carcinogenesis in
the presence of HPV infection. Moreover, laboratory research
has found current smokers to have statistically significantly
greater viral loads than never smokers, thus implying that
cessation may result in attenuation of the viral load [44].
Tobacco-associated genetic or epigenetic alterations have
also been postulated to result in acceleration of the disease
progression in HPV-infected individuals [31,32,45]. This is
supported by clinical and pathologic evidence of a poorer
survival of HPV-positive HNSCC patients who are smokers
as compared with HPV-positive patients who are nonsmokers
[31-33,45,46].
4.2. Can individual susceptibilities influence measures of
association between HPV and tobacco exposure
for development of HNSCC in different studies?
As the current paradigm is shifting toward understanding
the molecular progression of HPV-related head and neck
tumors, it is becoming recognized that individual susceptibilities
may explain the variation in relationship between
smoking and HPV. Variants of highly polymorphic but
critical tumor-suppressor genes such as p53 and p73 interact
with the HPV oncoproteins E6 and E7 and result in a much
higher risk of HPV-16�associated oral cancer in nonsmokers
than never smokers [47-49]. The frequency of the high-risk
polymorphisms among cases in one of the studies was 40%
to 44% [48]. Although a detailed discussion of these
individual variations is beyond the scope of our review, it
would be a relevant factor for future studies on the
interaction between HPV and smoking.
5. Conclusion
Our review of the existing literature on the association
between smoking and HPV in causation of HNSCC identifies
smoking to have the potential to promote infection,
persistence, and the carcinogenetic effect of HPV. Although
prospective studies on the natural history would better
unravel the possible interactions, on the basis of the current
laboratory and clinical studies, we conclude that the HPVrelated
tumors should not be considered as an occurrence
exclusive to nonsmokers. Thus, along with close surveillance
for early detection of HNSCC, early cessation of smoking
should be considered imperative in smokers, particularly
heavy smokers with HPV infection. Current evidence
indicates that stop-smoking efforts can lead to a reduction
in the viral loads and slow the progression to HPV-related
malignancy. Cessation is also important in view of evidence
of a poorer survival status in smokers with HPV-positive
HNSCC as compared with nonsmokers.

I forgot to write ... there is research to suggest that when infection of the membrane of the mouth occurs, and it is not "massaged" through friction when the virus can infect only the upper layer of the membrane, also induces an immune response and virsuet fought normal, but the reaction is not as strong as if the virus infects through wounds, etc., because the body does not get immune to the infected HPV variant without infection can occur again and again with the same virus.

That would explain a lot of differences between man o woman, the woman create a lasting immunrespins by the virus penetrates further down, perhaps in the mouth but mostly in the vagina and then the woman is immune.

Conclusion better to get a big infection than many small ... just as in the case of the common cold

I think we should award college credit for anyone keeping up with this thread.

Good stuff.

Overall, our review points to smoking tobacco posing an additional risk for development of head and neck cancer in the presence of HPV infection. This is consistent with available laboratory data that show evidence of biological plausibility for interaction between smoking and progression of HPV infection to carcinogenesis. It is therefore important that cessation of smoking is promoted in smokers with HPV infection. In the end this is kind of a no shit statement� when you have two strong risk factors instead of one, the world is going to be worse for you. Please note they use of the word plausibility, In spite of many articles not in their bibliography which clearly show that HPV is a unique pathway, they say that it is plausible that there is some synergy between the two.

Rightfully the article piece you have posted states that they have poorer outcomes. That is not the same as saying that it requires the two things to have happened (smoking and HPV infection) simultaneously to develop a malignancy. This is just observations on a subset of patients that smoke and have HPV, which is not the largest group of HPV+ oral cancer patents. Most oral cancer patients in the US that are HPV etiology are non smokers.

This paper is part of a meta analysis of many other papers. It is just indicating that there is indeed a sub set of individuals that are both smokers and HPV+, but it is very clear at the end where they say that we do not know the life history of the virus, and that would give definite answers to things which they are only speculating on. This is not a study, it is a review of many studies.

Meta analysis is highly useful. But there is always the potential for bias in them as they select the articles that they wish to look at, and that introduces bias of its own. The most recent example was one done by the ADA that was listed over 100 articles in its bibliography, but when I questioned a friend that had been part of the process he acknowledged that they omitted 60 of them as not worthy of being included in their analysis. Those 60 were peer reviewed published articles!! The ADA's conclusion was that screening in oral cancer does not work�. The Cochran Group is notorious for doing this kind of thing as well.

The penis is covered with normal epithelium, not squamous cells. There is more but I don't agree with most of your conclusions.

I can understand that we all can not have the same opinions, and HPV is a difficult virus to understand, there are so many different research findings, I am not suggesting that there is no cancer in which only the HPV is involved, I know that this does happend , but oral cancer is on the whole a multifactorial disease and the number who get cancer of the only HPV is incredibly small number, so small that it is difficult to statement as statistics or draw conclusions, there are many adoption from all sides




http://www.merckmanuals.com/home/sec18/ch216/ch216c.html

http://www.springerlink.com/content/870485v71w88nw67


Tobacco, alcohol, and human papillomavirus (HPV) are major risk factors for head and neck cancer (HNC), but it is unclear whether there are two distinct HNC risk groups, one associated with HPV and the other with tobacco/alcohol. Because HPV-positive HNC are clinically distinct from HPV-negative cases in treatment response and with more favorable prognoses, determining whether these differences result from infection alone or in association with other HNC risk factors is important for developing future therapeutic strategies. Incident cases of HNC (n = 201) and age-gender frequency-matched controls (n = 324) were recruited to assess anti-HPV VLP (virus like particles) antibodies 16, 18, 31, and 33. Multivariate logistic regression and stratified analyses were used to calculate adjusted odds ratios (OR). HPV-seronegative and seropositive/heavy tobacco users had similar increased adjusted risks of HNC (HPV-seronegative OR = 2.6, 1.4�5.0; HPV-seropositive OR = 2.3, 1.1�4.8), as did HPV-seronegative (OR = 4.3, 2.1�9.1) versus HPV-seropositive/heavy alcohol users (OR = 3.9, 1.6�9.4). Similar HPV/tobacco/alcohol risk profiles also were seen in oropharyngeal and oral cavity tumor sites. Our finding that tobacco/alcohol use increased the risk of HNC in both HPV-seropositive and HPV-seronegative individuals is consistent with the observation that HPV infection is not a sufficient cause of HNC but requires the accumulation of additional cellular changes.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917346/

CONCLUSIONS:
HPV16 E6 and E7 alone are not sufficient for invasive growth. However, the synergistic activity of H-Ras and E6 was sufficient to result in invasive growth.
Our findings also suggest that HPV related carcinogenesis is a multi-step process. We have found that expression of HPV viral oncogenes alone is not sufficient to permit metastatic growth. This result supports the clinical finding that not all patients with persistent HPV infection develop cancer. It is likely that at least one additional cellular mutation in the presence of HPV oncogenes is required for metastatic growth. E6 transgenic mouse data also support these findings. In one study, only 14% of mice that overexpressed E6 developed malignant tumors, suggesting that E6 is not sufficient to induce tumor growth by itself. Chromosomal analysis of the tumors that developed in these mice indicated that they exhibited other genetic alterations compared to the surrounding tissue10. The fact that H-Ras synergizes with E6 to result in invasive growth may shed light into what other cellular pathways need to be altered to result in invasive tumorigenic growth. H-Ras activation is a downstream event of growth factor signaling34. Growth factor receptor overexpression is common in HNSCCA35. Although H-Ras mutations have not been reported in HPV related HSCCA, it is possible that alterations like growth factor overexpression or other components of the growth factor signaling cascade could synergize with HPV oncogenes to allow invasive growth.

With all due respect to Brian and as the founder of the association,but what is your goal?
Is it that it should be in the headlines "Oral sex cause cancer, everyone should immediately stop oral sex"? in my country we have about 100 cases per year of tonsilcancer are caused by HPV, and no overestimation was probably 3 million people is in oral sex, maybe 40-50 times a year, there are 150 million exposures, the number of cases HPV exist, we can only speculate
Blaming the oral sex is enough to make it all too easy

The rules of the forum is that you do not "sell something" or representing economic interests, I do not think DR. Gillison would clear the entrance exam:)

Dr. Gillison worked for 3 years with Merck & Co., the maker of the HPV vaccine Gardasil

Forum monitors comment: This post is staying on the boards only to demonstrate this individuals prejudice and lack of information, particularly about someone that is clearly recognized as an authority on the subject matter by her peers. This is the kind of attack and nonsense that unregulated boards allow everyday.

forgetting, of these 100 cases, nearly 70 people smoking and haveinfection with HPV.
10% have HIV, 80% are over 65 years, 20% are immigrants from countries with a history of chewing tobacco

How many cancer cases do you have in us? is there a national register of the number of cases and Whether the man had another cofactor to HPV infection, you say that there are more non smokers, would be interesting to see statistics on paper

Sorry it was not my intention, but I understand that you may have a different culture in the U.S. than I am used to, that one must be careful to question.

I am convinced that he is right in substance, but that one must be careful to exploit people's fears in this case the link oral cancer, some cup was placed there by the weak with regard to the selection and the result, no other activity would be linked to cancer if so few results of the activity was cancer, but to do it with oral sex just because so many are frightened. I lead a group of students in the subject and it has gone so far that it begins to look each other in the throat, I try to calm reflection and understanding.

Certainly one must be cautious in their sexual relationships, but fear not to take unreasonable proportions, to be aware of any. changes in the neck is as important and natural as to draw attention to other bodily changes that may indicate cancer, I hope that's the direction you have and not so scared to give oral sex cancer, that's where I think it's that simple not.

http://www.medhelp.org/doctor_profiles/show/30098

I think Edward is a knowledgeable person in the field, I'm not saying he is right in everything and I do not think Brian is right in everything, but we should not see everything in black and white, but look vulnerable to a diskusition.




http://www.medhelp.org/posts/STDs/Oral-HPV-Transmission-Question/show/1137937

http://www.medhelp.org/posts/STDs/HPV-transmission/show/1239679

http://www.medhelp.org/posts/STDs/Oral-Sex-Performed-on-High-Risk-HPV-Girl/show/1423318

Forum Monitors comment: These last three links state the very things that we have stated on these forums so often that they are only being put here, because you clearly haven't read them. HPV is the most common sexually transferred infection in the US. The good news is that 99.1% of the people that are exposed to it have an immune system that defends them against it, so it is not of major concern and should not dictate sexual behavior.

In the United States, it is widely known there is a link between passive tobacco exposure (second hand smoke) and the development of disease. My mother-in-law has emphysema most likely as result of living with my father-in-law who smoked for many years. I hate to throw gasoline on the fire here, but, who knows how much or in what ways years of concentrated passive tobacco smoke exposure compromises a person's long term health. Maybe, it is the culprit or an accessory to the crime in more diseases than we are aware.

I am thankful to Brian Hill for founding the Oral Cancer Foundation. His position is not merely an occupation but a vocation and a passion. While no one wants their calling to a vocation to be born of cancer, Brian's came in that way. He took one of the biggest negatives anyone could have been given, and not only survived but turned it into perhaps the biggest positive anyone could hope to achieve. To be that strong, that altruistic, and that dedicated to a cause is a priceless gift to countless people who have turned to the OCF for support. It is a life-defining work. It is an example to which many other people and organizations would do well to aspire.

Malin, I have read your profile. Your life has been touched by oral cancer. I am so sorry. I am thinking it is the basis of your passion and the driving force behind your educational pursuits? Welcome to this community. Sending positive thoughts to you and the one who you care about regarding tongue cancer.

Sandy

Malin. I cannot fathom your intentions. But enough already. You are suggesting that the world's most published authority on HPV and oral cancer is a fraud or incorrect, or biased towards vaccines perhaps, because she took research dollars from Merck early in her career? Then you must condemn every researcher there is, as they all at some point in time get funding from commercial entities, even if not directly, through grants to their universities. Really, do you also believe that the experience in the US is the same as the experience in your country, or perhaps India? They are all different, and the data collection mechanisms are equally so.

You have clearly misunderstood the reason for the message boards, and these kinds of discussions about something your clearly have opinions on, but have not properly explored, are a waste of time. Of course we have a cancer registry, we have the SEER database, and we know the numbers. Do you think the researchers who publish from this country do not have their work reviewed by their peers and are not held to the strictest standards of scientific inquiry? So you don't even know these basic things about the issue, and you are posting all these opinions?

Everyone is entitled to their own opinions, but they are not entitled to their own facts. Until you learn some more, and quit posting one particular study as the answer to everything, (when hundreds contribute to the final conclusions), perhaps you should not engage so passionately in the world of opinions. If you had read the foundation's web site, and my other postings you would clearly know that neither are anti-sex, neither are about prohibition of any behavior, nor about creating fear in anyone�they are about giving them the best information to make good decisions from.

This "debate" is not productive as the facts that we know today are drawn from hundreds of articles, and to post a clipping from one out of hundreds of them that happens to disagree with the rest, only confuses the patients here, and is not productive.

I do not wish to be rude, but I am at a conference this weekend lecturing, and I cannot continue this dialog with you, nor let you confuse the issues (and new patients that are just getting their minds around some of this information and their situations) with half truths and speculations on the forum.