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.