Hi Debjoe,

So sorry to read about your double loss to this terrible disease.

When did you ask the doctors about HPV? I wonder how the doctors were able to tell you that your son's and brother's cancers were not HPV+. I doubt that their tumors were tested back in the late 90's and early 2000's. You didn't mention the location of their tumors, however, if the locations weren't in the oropharyngeal area, base of tongue or tonsils, then they were probably HPV-. What were the locations?

Nancy,

The percentages that I use for the breakdown of OC causes are more like 65% - 70% (on the decline) from tobacco use, 20% - 25% (on the rise) from HPV and about 5% from unknown causes.

Maybe Brian will chime in with more accurate numbers.

Jerry

Judging by what I have seen in the past year or so I think the "unknown" causes are on the rise as we have seen a fair number of non tobacco users, HPV-, young SCC patients with a primary where you typically see tobacco related SCC appear.

National reporting on the numbers is not available right now from any of the big institutions like the NCI or CDC. Since the rate of incidence is growing faster in young HPV positive people, the lecturers and researchers that I talk to are starting to differentiate between them by age groups. In people under 50, and definitely in those under 40, the percentage of HPV+ incidence OSCCC is estimated to be over 50%. This is only being tracked consistently at about 5 institutions, yielding that belief and trend line. So this is not an absolute number, but anecdotal in nature. In people over 50, HPV is much lower as a cause, and what you quoted is about right 20-25%.

Remember that tobacco carcinogenisis is a more protracted process, and decades of tobacco use, and the subsequent cellular disruptive changes and eventual malignant progression, takes decades to occur. So it is not unexpected that because of this, the tobacco group tend to be older.

The mechanism of cellular function disruption caused by the virus is much more rapid, and it requires fewer aberrations in the cell to take place for malignancy to fully develop. The primary instigating keys are the virus's expression of oncoproteins E6 and E7. These two proteins specifically target two genes, that when damaged, move the cell quickly toward full malignancy. E6 targets gene P53 which controls programmed cell death, a normal process in our bodies. With that gene destroyed the cell becomes immortal, one of the simplest definitions/characteristics of a malignant cell. E7 targets gene RB, which is involved in immune system signaling, and effectively hides the aberrant cell from being destroyed by normal immune system processes. This all happens on a very short (compared to tobacco carcinogenisis) time line.

Unknown primaries, I am finding are often just poorly reported and misdiagnosed HPV etiologies. Remember that in much of the medical community the adoption of the knowledge of the role of HPV is still behind the cure I am sorry to say. This does not mean that there are not plenty of REAL unknown primaries. People that I work with have differing opinions about all this. Most would agree that in as many as 5-10% of all cases, we just do not know what causes OSSC. There is some belief that when a positive node is found, that inadequate means are used to find the primary. Here's a real world, but anecdotal example. Hopkins was seeing a fair number of people present with a painless, fixated, indurated node in the neck that tested (through FNB) positive for SCC, but the oral cavity was completely occult when viewed by oncology professionals. They began to do prophylactic bilateral tonsillectomies in these patients, and in that group - 70 % were found to have SCC in the tonsil - that was completely occult in the oral cavity. No longer an unknown primary.

As you can imagine as this tonsillar trend continues to grow, it causes a huge problem for dentists and doctors that do not palpate the neck as part of their oral cancer exam, or do not know how to do this properly. There are obviously tricks (techniques) to doing this correctly that anyone can be taught in 15 minutes, such as the position you put the head in to cause the SCM muscle to protrude so you can run your fingers down each side of it feeling for hard nodes. In these cases there is still an opportunity to find relatively early and survivable disease even with a neck met, as it appears that a stage two or three HPV+ disease may not be a dangerous as the same stage disease from tobacco when it comes to treatment response and survival. When I lecture about all this I am really careful to state that I am talking about what we now consider to be multi-center anecdotal evidence, and published data does not exist.

A genetic/heredity connection has not been proven and published. That does not mean it does not occur, as we have seen in our own family here on the boards. But it is rare in comparison to the other etiologies, and the incidence rate, combined with our poor method of tracking these kind of things, means that it might be decades before we have a definitive answer to how that genetic transfer might take place, and in what population of people, with what genetic make up.

Brian,

I have talked to my Dr Trotti a lot about this possible new subset of OSCC patients presenting themselves as I described above and he didn't offer any possible causes other than perhaps a different strain of HPV or another virus. These patients say their primary's are in regions not typically associated with HPV; they say they don't have a history of tobacco and they say they test negative for HPV. What is your thinking on this seemingly new group?

I wanted to thank everyone for taking the time to respond to my post. I am very happy for the one's that survive this horrible disease and give my condolences to anyone who has lost the battle.
Debbie

I ALSO HAVE A FAMILY CONNECTION TO THIS CANCER. I WAS DIAGNOSED WITH TONGUE CANCER (ORAL TONGUE T1 N0) IN JULY 2007 AT THE AGE OF 37. MY BROTHER CHRISTOPHER WAS ALSO DIAGNOSED WITH TONGUE CANCER (ORAL TONGUE) LAST YEAR AT THE AGE OF 24. OUR CANCERS WERE IDENTICAL IN NATURE AND NEGATIVE FOR HPV. THE ONLY SYMPTOMS WERE A CANKER SORE ON THE TONGUE THAT WOULDN'T GO AWAY. WE BOTH HAVE A HISTORY OF CANKER SORES IN THE MOUTH SINCE WE WERE YOUNG.

I also have a history of cancer sores in my mouth since I can remember...I have to be careful of any citrus in natural or pill(vitamin) form.

Well, canker sores which are actually herpes simplex (HSV1) are caused by a virus that you get for life, and when not active lives on the ganglion of your nerves. HSV1 and 2 has been associated with other viruses that do cause cancers. While this is not definitive proof of an involvement in the development of a malignancy, or even a symbiotic relationship between the viruses, it may speak to a much simpler idea, which would be a genetic predisposition to be susceptible to viral infections of all types. If that was a familial / passed on trait, it could be a genetic vehicle or opportunity for initiation. Just a thought with no evidence to back it up. We are off in an area here where there are no real answers only educated best guesses.

David, since these patients have been tested for HPV and found negative, another strain would show up in the HPV scan - so your idea that it is a different HPV isn't a correct possibility. Sub typing to figure out which HPV is another step after determining HPV itself. And this is done as a matter of routine when a OSCC comes up HPV+ to confirm it is 16. There have been occasional other types found with 16 when sub typing OSCC, but they are so infrequent, and often non oncogenic, that researchers consider them non consequential artifacts.

I want to remind people that in families common risk factors are often shared. Smokers live with smokers, people who eat poor, fatty diets share their bad habits, and pass the habit off to their children through socio-behavioral means. So you have to be careful to distinguish between what is a genetic transfer and what are shared common risk factors engaged in.

We asked the drs about HPV when my son first was diagnosed because my Mom had read a few articles about the link. My brother Jim had a sore on the left side of his tongue that was actually dark green in color and extremely painful. My son Christopher had a sore on the side of his tongue that ended up splitting the tongue open so that it looked like it had been fileted by a knife. It was also extremely painful. Even with my brother being diagnosed with the cancer and passing away, the doctors didn't want to take it serious. We got the run around for a while until they found out he had ear pain also.