The Mutagenic Effects of HPV that Lead to Head and Neck Squamous Cell Carcinoma

Sounds like a pretty good title for a comprehensive article on the process.

However for a free article written under a pseudonym, I hope that the reader’s expectations are not too high.

If a person avoids all “risk factors” for mutagenesis, perhaps cancer can be completely avoided. However, the relative-weight or the “factor” part of “risk factor” is politicized rather than using statistical analysis. While “factor” is a mathematical term, in terms of the “risk factor” jargon, it is meaningless. Moreover, I’ve read elsewhere that pretty much everyone, if they live long enough, will eventually get cancer, regardless of whether their eventual cause of death is cancer or some other cause.

Therefore, obsessive “avoidance behavior” might not necessarily make one live longer. It would only feel longer.

For those who would like to see some scholarly links on the process of the cancer that is killing Axel, I recommend these:

The first article, however, is not without politically-motivated jargon. It starts out promisingly however:

Over the past 20 years, high-risk human papillomavirus (HPV) infection has been established as a risk factor for developing head and neck squamous cell carcinoma, independent of tobacco and alcohol use.

I point out to the reader that the phrase, “independent of” could be a substitution for “without taking into consideration the presence or lack of”. In other words, a nonsmoker and nondrinker with HPV exposure may still possibly get oral cancer, with the level of risk for the combined effect, if any, not specified herewith.

An active participant in The Sexual Revolution to include group sex, swinging, anonymous hook-ups, etc., is very likely to be exposed to HPV, as well as tobacco and alcohol. However, according to some, pretty much everyone who has had sex during the period which encompasses the 1970’s, 1980’s, and 1990’s has been exposed to HPV. Most people, however, fight it off successfully, meaning that there is no active infection at some point after exposure. However, even fighting off such an infection does not rule out the latter possibility of HPV-induced mutagenesis leading to SCC, or some other cancer, even without having an active HPV infection. It is a risk of multiple-intimate partners for sure but by no means a foregone conclusion. There may indeed be additional co-factors not yet discovered such as say, mercury fillings.

Axel has been a two-pack-a-day smoker from the age of about 11 until he met me four years ago. After meeting me, I switched him to a stronger, purer, higher-quality cigarette which I roll myself. This effectively brought his habit down to about a pack a day, albeit each puff was a hair stronger, albeit free of those nasty “additives” that everyone is so terrified of that they eschew new carpet, new cars, paints, and walking around in the city, where the concentration of those “additives” exceed that found in ambient or directly inhaled tobacco smoke. But, I digress. Back to the article:

In particular, HPV is strongly associated with the development of oropharyngeal cancer and a small minority of oral cavity cancers. In this review, we summarize what is currently known about the biology of HPV, the mechanisms by which it effects malignant transformation, and the potential impact of HPV status on the clinical management of persons with head and neck cancer.

Axel started experiencing his first symptoms of SCC on his wrists and neck, one year after his experience as a first-responder at Katrina, whereby, coincidentally, he decided to temporarily quit smoking. He was treated in an unusual manner with regards to an unusual condition, whereby a mass was removed from his neck in a horrific, inexplicable, or largely unbelievable treatment plan. Katrina occurred in October 2005. I could relay his tale here of what happened in 2006 but it would be heresay and thereby a distraction from my argument. If someone else has a story to tell of a similar incidence, I recommend that you relay it to me privately and we can decide how to approach it.

Back to the article:

In 2008, an estimated 47,500 people were diagnosed with head and neck cancer in the United States, representing approximately 3% of new cancer diagnoses, and an estimated 11,260 people died from this disease (Jemal et al., 2008). The vast majority of these head and neck cancers were squamous cell carcinomas. Over the past 20 years, the overall incidence of head and neck squamous cell carcinoma (HNSCC) has been declining in the United States, a decline which has been attributed to a decrease in the prevalence of smoking (Sturgis and Cinciripini, 2007). Although there has been a reduction in the overall incidence of HNSCC, an analysis of the National Cancer Institute’s Surveillance, Epidemiology and End Results (SEER) data from 1975-1998 found that the incidence of tonsillar cancer increased by 2-3% annually in males under 60 yrs of age from 1975-1998 (Canto and Devesa, 2002). A more recent analysis of SEER data from 1973-2001 showed an annual increase in the incidence of oral tongue, palatine tonsil, and base-of-tongue cancers, by 2.1%, 3.9%, and 1.7%, respectively, in 20- to 44-year-old white patients, while the incidence of HNSCC at other sites declined (Shiboski et al., 2005).

In other words, one form of cancer has gone down, another form of cancer has gone up, and supposedly tobacco is the changing factor? How about the virulence of HPV itself? Could it be possible that HPV has become less virulent and mutagenic? Could it be possible that HPV is no longer the danger that it was? That would not be politically expedient to the mandatory HPV vaccine crowd, now would it? As for the anti-tobacco crowd, they have some pretty deep pockets too.

What if the increase of tonsillar cancer can be attributed to a reduction in tobacco use? Or what if HPV is itself mutating to be more mutagenic in tonsils and tongues? Viruses mutate. For the record, Axel is free of tumors in his gums, tongue, and tonsils. His cancer is largely in the lymph nodes, lip, and chin, and impeding on the vocal chords, and carotid artery, along with general oral irritation that may be a function of the cancer’s necrosis.

Here is the radiologist’s report on Axel’s chest X-ray after about 47 years of “heavy smoking”:


Back to the article:

Tobacco and alcohol use are the primary risk factors for HNSCC and are associated with the majority of these tumors worldwide. In addition to these traditional risk factors, high-risk human papillomaviruses (HPV), and in particular HPV-16, are recognized as independent risk factors for a subset of HNSCC and are most strongly associated with oropharyngeal squamous cell carcinomas (OPSCC) (Schwartz et al., 1998; Gillison et al., 2000; Morket al., 2001; Wiest et al., 2002; Herrero et al., 2003; Hobbs et al., 2006; Ernster et al., 2007; Andrews et al., 2008). HPV has also been associated with the pathogenesis of oral cancer; however, the association of HPV with HNSCC is strongest for oropharyngeal cancer (Gillison et al., 2000; Furniss et al., 2007; Sturgis and Cinciripini, 2007; Chaturvedi et al., 2008; Liang et al., 2008). In this review, we briefly summarize the current, generally accepted knowledge regarding the biology of HPV, and the mechanisms by which it effects malignant transformation, and subsequently focus on presenting recent research relating to the association of HPV with HNSCC, as well as on the future implications this research may have for the clinical management of persons with head and neck cancer.

That first sentence sounds like a contradiction of the very first sentence quoted above. How much money and from whom determined whether tobacco and alcohol use are the “primary” risk factors for HNSCC when HNSCC has already been found to be independent of tobacco and alcohol use when there is HPV?

Frank Davis, as usual, weighs in on the subject in a manner more articulate than mine:

Davis even entertains the possibility that tobacco might possibly increase susceptibility to HPV. Could be, however, perhaps tobacco does not increase susceptibility to HPV but rather is part of a pattern of oral exploration risk-taking which would increase the likelihood of exposure. For all we know, use of a fluoride-containing toothpaste soon after exposure might increase the likelihood of immune compromise. There are too many agendas and deep pockets to back them up to ever know for certain. As society becomes more polarized, all researchers are forced to choose alliances, and therefore no one is truly objective.

While I would certainly not be one to discourage someone from quitting smoking, if that’s the individual’s reasoned choice or if one feels better as a nonsmoker than a smoker, personally I prefer to focus on discouraging men from cunnilingus, in that engaging in the practice has not resulted in a quid pro quo from feminists in terms of permission to reopen men-only smoking lounges.

4 thoughts on “The Mutagenic Effects of HPV that Lead to Head and Neck Squamous Cell Carcinoma

  1. Pingback: The Mutagenic Effects of HPV that Lead to Head and Neck Squamous Cell Carcinoma |

  2. Pingback: Who Is Our Hospice Nurse? | caprizchka

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