HPV Cancer Resources

WARNING: the answer below contains info about sex and sexual practices. If this makes you uncomfortable, please stop reading now.

The short answer to the question above is: very likely from oral sex.

HPV is a sexually transmitted infection (STI) and the most common one by far. It’s estimated that about 14 million people in the US get infected every year, and about 90% of adults will be infected with the virus during their lifetimes.

Besides sex, the information available on catching these infections is murky, to say the least. Can it be passed sharing a bottle of soda with an infected friend? Most researchers would say probably not. How about by casual kissing (e.g. a quick peck on the lips)? Most researchers again would say that’s unlikely. How about deep (“French”) kissing? Again, that may be more likely, but most researchers wouldn’t say that causes many cases either.

Why is it so hard to answer this question clearly? The answer is human behavior. In order to get an answer to this question, you’d have to compare people who limited their “interactions” with others to “just kissing”, and compare their infection rate with people who either did “no kissing at all”, or “kissing with additional more intimate activities.” It would be very difficult to identify a group of people who limited their intimacies to kissing. With most people, things usually move along from kissing to other activities. Without being able to do this comparison study, it’s difficult to say with any assurance that HPV can be transmitted by other methods (i.e. kissing or the shared soda bottle).

Many of you have heard that the incidence of HPV+ oral cancer is much higher in men than women, and this is true. Between four and five men will develop an HPV+ oral cancer for every woman that does. Why is this tilted so much in this direction? It’s thought to be because it’s much easier for women to transmit the virus from their genitals than men. Why would that be? It’s likely due to the fact that wet, moist tissues (e.g. vaginas) provide a more “easy to transmit the virus environment” than drier tissues (e.g. penises). Condoms provide some protection against HPV infections, but they are not fully protective because secretions may get around the barrier the condom provides. It’s possible that fingers or sex toys can also transmit HPV infections to others.

The only other tissue type that HPV causes cancer in that is shared by men and women (besides oral cancer) is anal cancer. In this case, HPV+ anal cancers are much more prevalent in women than men (by about 2 to 1). Is this because more women have anal sex? Not necessarily. The distance from the vagina to the anus is pretty close, and it’s thought that “fluids” may transfer the infection from one place to the other. One of the best explanations I’ve read about this compared vaginal secretions to glitter. You know how someone can mail you a holiday card with glitter on it, and later you find that glitter all over your house? It’s sort of like that.

There should be no shame in getting an HPV infection as they are incredibly widespread. In general they’re only problematic if they cause either genital warts or cancer. Early detection for cancer is very important, especially for cervical cancer. One hundred years ago, the Pap exam had not yet been invented yet. That happened in 1928, although the exam didn’t become widespread in the US until the 1950s. By the way, Pap does not refer to papillomas; it’s actually a shortened version of the name of the Greek doctor who developed the test, George Papanicolaou. In 1923, the number one cause of cancer deaths in women in the US was cervical cancer. The Pap test revolutionized the discovery of early pre-cancers of the cervix while they were readily treatable. As a result, cervical cancer now ranks 14th on the list of cancer deaths for women in the US. Sadly, in places around the world where the Pap test is not widely available, the cervical cancer incidence is still very high. Worldwide, HPV infections cause about 1% of all cancers in men, whereas for women it’s closer to 9%. The vast majority of those cases are cervical cancer.

Since the HPV vaccine can prevent cervical cancer (we have solid data on this), as it gets used more, the incidence of cervical cancer is expected to drop steadily. Australia was the first country to adopt the HPV vaccine, and the incidence of cervical infections and cervical cancer there is plunging. It may be essentially eliminated in the next decade. HPV-caused oral cancer rates are also expected to decline eventually, but that will take much longer for two reasons. One is that many parents think that boys don’t benefit from the vaccine, which of course they do. The other one is that cervical cancers develop much faster than oral HPV cancers (I don’t know why that is). The median age for men and women to be diagnosed with an oral HPV cancer is about 61 to 63; the median age for cervical cancer diagnosis is 49 (and there are many cases that occur while women are in their 20s or 30s).

The answer is: maybe. Possibly. It's a complicated issue. There are really three situations here:

1) If you're an adult and you don't know if you already have an HPV infection.
2) If you're an adult, already know you have an HPV infection, and want to prevent being infected with another strain of the virus.
3) You're an HPV cancer (or in the case of cervical cancer, have had a precancerous lesion), and want to lessen the chances of it turning into a new cancer or getting a recurrence.

Let's look at each of these situations:

1) If you're an adult and you don't know if you already have an HPV infection.

No vaccine is perfect, but the Gardasil 9 vaccine has a very strong safety and effectiveness record. The strains chosen for the vaccine are the ones most commonly circulating, so the vaccine will protect you from the majority of strains that are out there. Keep in mind that there are still other “non cancerous” and cancer-causing strains of HPV that the vaccine will not protect you from .How likely are you to run into one of these other cancer-causing strains? Not too likely, but it also depends on where you live (or more properly, where your partner lives now or lived before). The distribution of cancer-causing strains varies between areas e.g. different continents. Some of the ones common in Africa or Europe you might not run into here, and vice versa. There’s no way to predict which strains you might come across because you may not know where your partner has been, or who their previous partners have been.

Considerations: are you in, or planning on getting back in, to the dating pool? TThe vaccine is now approved in the US up to age 45. This means the cost of it will be covered by most people that have insurance and are that age or younger. If you don’t have health insurance and you’re over 45, you may need to pay for it yourself if you can get your doctor to prescribe it.

How many individuals need to be vaccinated to prevent a single case of any HPV cancer? A study in 2024 attempted to answer this question by comparing different groups age 27-45 and compared that with the previous standard vaccination group of 9-26 year olds in the United States. The estimated number of individuals that model projected that needed to be vaccinated to prevent a single case of HPV-cancer was 7,670 for those considered "mid-adults;" 3,190 for those who were highly sexually active; and 5,150 for those who recently separated, respectively. Compare this to the ages 9-26 year old group, where only 223 patients need to be vaccinated to prevent a single case of HP-caused cancer.
Laprise JF, Chesson HW, Markowitz LE, Drolet M, Brisson M. Cost-Effectiveness of Extending Human Papillomavirus Vaccination to Population Subgroups Older Than 26 Years Who Are at Higher Risk for Human Papillomavirus Infection in the United States. Ann Intern Med. 2024. doi:10.7326/M24-0421

2) If you're an adult, already know you have an HPV infection, and want to prevent being infected with another strain of the virus?
How likely is it for you to be infected with a different strain of HPV than you are currently infected with? It depends mostly on your social situation (i.e. your love life). How likely is it that you might run into a new partner who is infected and could transfer that infection to you? If you’re monogamous or simply no longer engaged in sexual activities, you should be all set. If you’re not, here are some things to think about. The HPV vaccine can prevent you from being infected with a different strain of HPV. There are hundreds of strains of HPV circulating around the world. Most aren't a health concern, although they can cause benign skin warts on your hands or feet. A few can cause genital warts. And a relatively small number of them can cause cancer. The current vaccine used in most countries is Merck’s Gardasil 9, which offers protection from the two most prevalent strains that cause genital warts (6 and 11) as well as seven “high-risk” strains that can cause cancer.

This might be a reason to get the vaccine. In case you were wondering, it is indeed possible to be infected with multiple strains at the same time. The vaccine could save you from getting genital warts or another cancer-causing strain. Keep in mind that being infected with a cancer-causing strain doesn’t mean you’ll get cancer from it. Most people won’t. One way we know this is because it’s estimated that some 14 million people in the US are infected with HPV every year. Compare that with the fact that some 35,000 people in the US will be diagnosed with an HPV-caused cancer each year (that’s in all tissues, not just oral cancer). This huge disparity in numbers tells us that not everyone will get an HPV cancer. It’s actually a relatively rare event.


3) You're an HPV cancer (or in the case of cervical cancer, have had a precancerous lesion), and want to lessen the chances of it turning into a new cancer.
If you’ve had an HPV cancer, this means that your immune system failed to mount a sufficient response to the virus. Most people who are infected with HPV clear that infection within two years. Some people fail to do so. It’s difficult to say if that means you won’t clear an infection with a different strain, but it seems reasonable to think that you might not. And just because you didn’t clear this second infection doesn’t mean the new strain will cause cancer (if it’s actually a cancer-causing strain). Again, most people infected don’t get cancer. The HPV virus is not sufficient on its own to cause cancer. Other changes need to take place inside your cells in order for an HPV-infected cell to become cancerous. And those changes may not happen within your cells.

Getting the HPV vaccine has been generally thought to NOT be capable of clearing existing HPV infections. Inside your cells, the virus can exist in several states. It can remain free floating in the cell, or it can actually integrate itself tightly and permanently into your DNA. It can cause cancer from either location. The antibodies generated in response to the vaccine won’t attack already infected cells. So what good would vaccination do? It turns out that it might actually prevent the spread of virus infected cells.

There are two types of data that support this idea, but do not prove it.

(1) Some people with HPV infections in their throats (specifically, strains 6 and 11, which are associated with genital warts, not cancer) develop RRP (recurrent respiratory papillomatosis), which is a rare disease where benign cancers form in the throat as a result of the HPV infections. Even after surgery to remove them, these tumors repeatedly arise in the throat, interfering with breathing and swallowing. It turns out that HPV vaccination with a vaccine that targets both strains 6 and 11 (Merck's Gardasil 9) can lessen the number of these throat recurrences, which means fewer surgeries to remove them over time.

Second,
(2) There is data showing that HPV vaccination of women who already have cervical intraepithelial neoplasia (a precursor to cervical cancer) led to a significant reduction in the number of women who still tested positive for cervical HPV infection months after vaccination, or developed cervical cancer.
Let's look at women with cervical pre-cancers, specifically ones designated as CIN2+. Cervical cancers are caused by the same strains of HPV as head and neck cancer, but their development is much faster. Many women will develop cervical cancer in their 20s and 30s, unlike HPV-caused head and neck cancers, which tend to occur more in the 40s-70s. CIN is cervical intraepithelial neoplasm, and 2+ refers to moderate to marked dysplasia (changes) in the cells. CIN2+ precancers often develop into full blown cervical cancer. They are usually treated by a process known as cervical conization (surgical excision). This is generally an effective treatment for pre-cancerous cervical lesions. Unfortunately, recurrence of the lesions can occur, especially among women with positive surgical margins, because all of the abnormal tissue may not have been removed. Might vaccination with the HPV vaccine (either before OR after the development of the cervical pre-cancer) reduce this recurrence rate? Doctors ran a clinical trial to answer this question, and here are the key results of this study:

Women who received the HPV vaccine after surgery (conization) experienced a 74% reduction in recurrent high-grade cervical lesions (CIN2+).
Women vaccinated during adolescence had a 62% reduction in recurrence risk for these cervical precancers.
Women who received the HPV vaccine immediately after surgery had a 89% reduction in recurrence in just 6 months, when relapse is most common.

The take home message: Regardless of timing, HPV vaccination has a beneficial long-term effect in lowering the risk of CIN2+ recurrence, and therefore cervical cancer as well. Whether a similar benefit of vaccination might occur for those undergoing treatment for HPV-caused head and neck cancer is simply not known. Cervical cancer is NOT head and neck cancer, even though both are caused by HPV. If you're thinking that the vaccine might prevent a recurrence of your HPV-caused oral cancer, this is something worth discussing with your medical team.

Petra, M. et al. Early and long-term effects of prophylactic and post-excision human papillomavirus vaccination on recurrent high-grade cervical intraepithelial neoplasia relative to margin status: a retrospective cohort study in the Czech Republic. The Lancet Regional Health Europe. Volume 55101337August 2025.
Here's an easier to read summary from the lead author.

In a similar study, researchers asked if HPV vaccination post CIN1 or CIN2-3 treatment would reduce the percentage of women who were still HPV+. During the 6-month follow-up period, HPV positivity rates were significantly lower for patients with CIN1 in the vaccinated group than for those in the unvaccinated group (18% vs 38%; P = .0169). The findings were consistent at the 15-month follow-up. During the 15-month follow-up period, HPV positivity rates were significantly lower for patients with CIN2-3 in the vaccinated group than for those in the unvaccinated group (8% vs 18%; P = .0353).
Vaccination showed a significant effect in reducing HPV positivity among women aged 40 years or older with CIN1 (P = .0100).
Palumbo, M et al Impact of Human papillomavirus 9-valent vaccine on viral clearance after surgical treatment: A single-center retrospective observational study. European Journal of Obstetrics and Gynecology 310 (2025) 113994.

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One other interesting thing about HPV infections is that they can be discordant in terms of the tissues affected. For example, if you have an oral HPV infection, you might think that means you also must have an HPV infection in your genitals. Turns out that’s not the case. You could have an infection in your mouth and not have one in your genitals. Or vice versa; you can have one in your genitals but not in your mouth (that obviously wouldn’t apply to the patients in this group). The virus doesn’t travel inside your body. And HPV infections are not limited to heterosexual couples. Same sex couples run these same risks as heterosexual couples do.

One question I don’t know the answer to: would being vaccinated inhibit your ability to spread HPV to partners? As far as I can tell, the answer is not known. A study was begun in 2020 to look into this, but it has not been completed as far as I can tell. Here’s the reference: MacCosham A, El-Zein M, Burchell AN, et al. Transmission reduction and prevention with HPV vaccination (TRAP-HPV) study protocol: a randomised controlled trial of the efficacy of HPV vaccination in preventing transmission of HPV infection in heterosexual couples. BMJ Open 2020;10:e039383. doi:10.1136/ bmjopen-2020-039383

For more information, read FAQ20 on this page of my website as well as the Epidemiology of HPV Cancers page.

Many of the folks on this page are aware that the standard treatment most people get for HPV+ head and neck cancers is a combination of radiation and chemotherapy (about 5 to 10% get surgery instead; some get all three treatments). The standard treatment can be very difficult to endure (just read the comments posted here every day) because the radiation and the chemo do damage to healthy tissues at the same time they are supposed to be getting rid of the cancer cells.

Could the same results be achieved by lowering the dose of radiation and/or chemo so that there’s less toxicity to the patient?

The answer to this question is complicated. First, what do we mean by “same results?” The standard measure of how effective cancer treatments are is something called the five-year survival rate. Essentially, this is calculated by asking: out of a group of 100 patients, how many would we find are still alive five years after their treatment? Different cancers have very different five-year survival rates. In the case of HPV+ head and neck cancers, the numbers are very good. About 90 to 95 of the 100 patients are currently expected to be alive after five years. And this doesn’t mean that 5 to 10 patients died of their cancer. It just means that they aren’t alive after five years (they could have died in a car crash or had a stroke). Compare this to pancreatic cancer, where the five-year survival rate is only about 5 patients alive out of 100 at five years.

What this means is that any “new” treatment for HPV+ head and neck cancers should achieve a five-year survival rate in this same range, about 90 to 95%, to be considered as good. So if a lower dose of radiation, for example, produced this result, it would likely become the new standard of care IF it had less “side effects” (which might mean fewer problems with swallowing, producing saliva, or tissue damage, for example). Ideally, it might achieve closer to a 100% response, but that’s not required if the lower dose has less “side effects” and causes collateral harm to the patient.

What happens if the new treatment clearly causes less “side effect” damage, but now shows a five-year survival rate of only around 80%? Now we are looking at trade off issues: patients would likely have less damage done, but now fewer people out of 100 will live as long as five years. Patients might be offered this choice, or they may not. And your willingness to try the reduced dose treatment might depend on your priorities.

Would you risk a greater chance of NOT surviving to have an easier to tolerate treatment? That’s a decision only a patient can make.

The fact that the standard measure is the “five-year survival rate” means that if one wants to do a clinical trial to see if a proposed “lower dose” treatment works as well (or better) than the standard of care, it might take more than five years to figure that out. Five years for the trial, plus time beforehand to recruit patients, and time afterwards to gather and generate the data. Along the way it may become apparent that patients are dying at a faster rate than with the standard of care treatment, at which point the trial would be stopped because it would be unethical to add more patients to the new reduced dose protocol. In the case of cancers with low survival rates, trials can stop early if it becomes clear that fewer patients are dying (put another way, the new treatment is better than the standard of care.

Clinical trials are indeed underway to find some radiation/chemo treatment plan that is less toxic AND has a similar, if not better, five-year survival rate. These trials obviously take a lot of time, and they also take a lot of money to do properly. That money would likely have to come from the government, the hospital, or wealthy donors because drug companies would not sponsor or pay for such a trial (there’s no financial benefit to them for doing so).

Bottom line: everyone would like to see a “kinder and gentler” treatment for this cancer, and clinical trials are underway, but getting a clear answer will take time.

You should also know that other types of therapies are being tested that might replace radiation/chemo treatments, but as yet none are as good or better than the standard of care. That's a topic for another day.

In the meantime, here's an excellent FREE review of where things stand with dose-deescalation therapies from the summer of 2023:
Allen Chen. De-Escalation Treatment for Human Papillomavirus–Related Oropharyngeal Cancer: Questions for Practical Consideration. ONCOLOGY Vol 37, Issue 7, 281-287 (2023)
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A report on the results from a key dose deescalation trial was released on Sept. 30, 2024. Sadly, the results were not good news for patients. Researchers looking to de-intensify radiation treatments for people with early-stage, HPV-associated oropharyngeal cancer to prevent long-term side effects halted a large, randomized Phase II/III trial after patients in the control arm reached a record high, two-year progression-free survival rate of 98%.

Result from the NRG Oncology HN005 trial were presented at the American Society for Radiation Oncology (ASTRO) Annual Meeting.
In this study, Dr. Sue Yom and her team at the University of California-San Francisco tested two lower-intensity treatment regimens against a control arm of more standard chemoradiation for people with HPV-associated, locoregionally advanced oropharyngeal squamous cell carcinomas. A total of 382 patients were randomly assigned to one of three treatment arms:

Usual radiation dosing (70 Gy total mildly accelerated over six weeks) combined with cisplatin chemotherapy
A reduced radiation dose (60 Gy total over six weeks) combined with cisplatin
A reduced radiation dose (60 Gy total mildly accelerated over five weeks) combined with an immunotherapy drug, nivolumab, in place of chemotherapy

All patients received intensity modulated radiation therapy, and most were male (90.6%), white (87.5%) and never-smokers (79.4%).
The Phase II trial was designed to trigger a futility analysis for each experimental arm after a predetermined number of patients experienced disease progression. These tests showed that neither de-intensified treatment approach met the threshold for non-inferiority compared to the standard treatment, however, and the trial was closed early.

Dr. Yom explained that a preplanned analysis would be triggered for futility when 11 events were reported between a combination of the control group and one of the experimental groups. The phase 3 trial would proceed either if one of the experimental groups did not trigger a futility analysis or at the end of phase 2.

The first futility analysis occurred at a median follow-up of 1.1 years, with nine of the 11 required PFS events occurring in group 2 and two in group 1. Group 2 was removed from the protocol, and randomization continued for groups 1 and 3. The second futility analysis was triggered, at a median of 1.7 years of follow-up, after 11 PFS events occurred, with nine of the 11 required events occurring in group 3. Dr. Yom said that accrual would have stopped at this point, but phase 2 accrual was already complete.

At a median follow-up of 2.2 years, the 2-year PFS was 98.1% in group 1 compared with 88.6% in group 2 and 90.3% in group 3. The 2-year locoregional failure rate was 0% in group 1, 6.5% in group 2, and 5.0% in group 3. The 2-year overall survival estimates are 99.0% in group 1, 98.0% in group 2, and 96.1% in group 3.

“These results set a new benchmark for PFS expectations in this population,” Dr. Yom said. “Deintensification studies going forward must evolve to be more selective and more effective if they are going to be competitive in a more challenging population.”

"In very rigorous testing, those experimental arms did not produce equivalent results to the control arm," said Dr. Yom.
"The experimental arms were close to meeting their expected goals, but the patients treated on the control arm had such incredible results that we had an ethical responsibility to halt the study. I believe we have to take stock of this new benchmark and that new trial designs for this disease will need to account for this result."

With a median follow-up of 2.2 years, the two-year PFS estimates were 98.1% following treatment on the control arm, 88.6% after reduced radiation with chemotherapy and 90.3% after reduced radiation with immunotherapy. The two-year overall survival estimates were 99%, 98% and 96.1%, respectively. "I think this study is a good reminder that patients with this disease have really outstanding cure rates after we treat them with contemporary chemoradiation," Dr. Yom said. "At this point, neither of the deintensification options we tested would be appropriate for standard of care use, because you would actually be changing some patients' chance for a cure."


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There are clinical trials being done that use PET scans done in the middle of treatment as a biomarker for deciding whether or not patients may respond equally well to a lower dose of radiation. We don't know yet whether or not this approach will pan out or not. One of these is described below.

This study looked at FDG-PET–Guided Deintensification of Radiotherapy in HPV+ cancer patients. Note: the data below is from a meeting abstract, not a published, peer reviewed journal article. Discuss this with your doctor if you are interested in learning more about this.

“FDG-PET may be a reliable predictive biomarker to selectively de-escalate the radiation dose in early-stage HPV-positive disease…. There were few locoregional recurrences,” Dr. Regan said.

The study enrolled 89 patients with stage I–II HPV-associated tumors with known avidity on FDG-PET imaging. All patients had a radiation plan for 70 Gy to gross disease and 56 Gy to elective nodal regions, to be given concurrently with carboplatin and paclitaxel. A mid-treatment PET was planned to assess response, which determined additional treatment. Those patients with at least a 50% reduction in metabolic tumor volume stopped treatment at 54 Gy to gross disease, whereas the others completed the entire course of 70 Gy. The primary endpoint was noninferiority of 2-year locoregional recurrence in the entire cohort, compared with an institutional historical control.

Primary Endpoint Met

Of the 84 patients who underwent mid-treatment evaluation, 48 continued to standard therapy, and 36 met criteria for de-escalation. At a median follow-up of 32 months, the study met its primary endpoint, demonstrating a 2-year locoregional recurrence rate of 6.8% for the entire population. By cohort, the 2-year locoregional recurrence rates were 4.6% for patients treated throughout with 70 Gy and 9.4% for those de-escalated to 54 Gy. “Of note, these rates represent only two and three locoregional failures each, respectively. The broad, overlapping confidence intervals preclude any definitive comparison of these two different cohorts,” Dr. Regan said. The 2-year progression-free survival rate was 87% with 70 Gy (four events, one likely treatment-related death) and 84% with 54 Gy (four events). After initial salvage therapy for the eight patients with recurrences (locoregional or distant), three of four treated with 54 Gy have no evidence of disease, and one is still on treatment, whereas with 70 Gy, two of four patients have no evidence of disease, one is on treatment, and one has died.

Weight Loss, Swallowing, and Quality of Life

Median weight loss from baseline to 3 months after radiotherapy was 23 lb in the standard-treatment group and 11 lb in the de-escalated group (P < .001), and the percentages lost were 12.6% and 6.0%, respectively (P < .001). A nasogastric tube was required by 16% and 11%, respectively (P = .5), and there was no appreciable change in the penetration-aspiration scale from baseline in either group. The University of Washington Quality-of-Life Total and Pain Subscale scores as well as the Functional Assessment of Cancer Therapy–Head & Neck Total and Cancer Subscale scores significantly improved at 1 month, above the minimal clinically important difference threshold (0.5 standard deviations), in the de-escalated cohort. Most patients in both cohorts returned to baseline at 1 year.

Full details can be found here. Note that these trials were NOT open to all patients. Particular criteria had to be met, as defined below.
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In 2024, a new study supported the idea of dose-deescalation treatment for HPV+ head and neck cancers.The MINT trial enrolled 58 patients with clinical stage I–III, HPV-positive oropharyngeal squamous cell carcinoma (or with a positive neck node with an unknown primary) who underwent surgery and selective neck dissection. Then, 54 patients were then stratified by pathologic risk into one of the following three treatment arms based on pathology:

Arm 1: high-risk pathology (extranodal extension and/or positive margins): De-escalated postoperative adjuvant chemoradiotherapy with cisplatin at 100 mg/m2 for one dose plus 42 Gy of radiotherapy over 21 fractions (n = 20)

Arm 2: intermediate-risk pathology (lymphovascular invasion, perineural invasion, at least two positive nodes, at least one positive node → 3 mm, T3 or N2 disease): De-escalated postoperative adjuvant radiotherapy with 42 Gy over 21 fractions (n = 30)

Arm 3: highest-risk pathology (cT3–pT4): Standard-of-care treatment with cisplatin at 100 mg/m2 for three doses plus 60 Gy of radiotherapy delivered concurrently (n = 4).
Dr. Thorstad reported the results of the two experimental arms involving de-escalated chemoradiotherapy (arm 1) and de-escalated radiotherapy (arm 2). The primary hypothesis was that de-escalated treatment would result in less weight loss, which is a quantitative surrogate of the severity of mucositis. Recurrence rate, progression-free survival, and overall survival were also endpoints. The recurrence rate was deemed acceptable if the 95% upper limit of the confidence interval (CI) was ≤ 20%.

Results With De-escalation. The data below is from a meeting abstract, not a published, peer reviewed journal article. Discuss this with your doctor if you are interested in learning more about this.

The mean percent weight loss during de-escalated postoperative adjuvant chemoradiotherapy was significantly less than in a similar historical cohort treated conventionally: 4.9% vs 7.4% (P = .0003). The mean percent weight loss during de-escalated radiotherapy was 3.18%, Dr. Thorstad reported.

At a median follow-up of 50 months, there were 2 recurrences (distant alone) in the 20 patients in arm 1 (de-escalated chemoradiotherapy) at 12 and 19 months after treatment. There was one recurrence (both regional and distant) in the 30 patients in arm 2 (de-escalated radiotherapy) at 22 months. The one death in arm 2 was a patient known to be disease-free 3 months earlier, he added.

These events amounted to recurrence rates of 10% in arm 1 (95% CI = 1.2%–31.7%) and 3.3% in arm 2 (95% CI = 0.1%–17.2%). At 4 years, 90.0% and 90.1%, respectively, were progression-free, and 100% and 94%, respectively, were alive. “Note the 95% confidence interval in arm 2 was < 20% as an upper limit [for significance], but we did not achieve that in arm 1, possibly because of the low patient numbers,” Dr. Thorstad commented. “We are looking at a future trial to increase the confidence with the arm 1 [approach] and perhaps at randomly assigning patients from arm 2 to an even lower radiotherapy dose.”

Thorstad WL, Jackson RS, Oppelt P, et al: Long-term efficacy of risk-directed, de-escalated post-operative adjuvant therapy for surgically resected locally advanced, human papillomavirus-positive oropharynx squamous-cell carcinoma: A non-randomized, multi-arm phase 2 trial. 2024 Multidisciplinary Head and Neck Cancers Symposium. Abstract 14. Presented March 1, 2024.
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The second study looked at FDG-PET–Guided Deintensification of Radiotherapy in HPV+ cancer patients.

“FDG-PET may be a reliable predictive biomarker to selectively de-escalate the radiation dose in early-stage HPV-positive disease…. There were few locoregional recurrences,” Dr. Regan said.

The study enrolled 89 patients with stage I–II HPV-associated tumors with known avidity on FDG-PET imaging. All patients had a radiation plan for 70 Gy to gross disease and 56 Gy to elective nodal regions, to be given concurrently with carboplatin and paclitaxel. A mid-treatment PET was planned to assess response, which determined additional treatment. Those patients with at least a 50% reduction in metabolic tumor volume stopped treatment at 54 Gy to gross disease, whereas the others completed the entire course of 70 Gy. The primary endpoint was noninferiority of 2-year locoregional recurrence in the entire cohort, compared with an institutional historical control.

Primary Endpoint Met

Of the 84 patients who underwent mid-treatment evaluation, 48 continued to standard therapy, and 36 met criteria for de-escalation. At a median follow-up of 32 months, the study met its primary endpoint, demonstrating a 2-year locoregional recurrence rate of 6.8% for the entire population. By cohort, the 2-year locoregional recurrence rates were 4.6% for patients treated throughout with 70 Gy and 9.4% for those de-escalated to 54 Gy. “Of note, these rates represent only two and three locoregional failures each, respectively. The broad, overlapping confidence intervals preclude any definitive comparison of these two different cohorts,” Dr. Regan said. The 2-year progression-free survival rate was 87% with 70 Gy (four events, one likely treatment-related death) and 84% with 54 Gy (four events). After initial salvage therapy for the eight patients with recurrences (locoregional or distant), three of four treated with 54 Gy have no evidence of disease, and one is still on treatment, whereas with 70 Gy, two of four patients have no evidence of disease, one is on treatment, and one has died.

Weight Loss, Swallowing, and Quality of Life

Median weight loss from baseline to 3 months after radiotherapy was 23 lb in the standard-treatment group and 11 lb in the de-escalated group (P < .001), and the percentages lost were 12.6% and 6.0%, respectively (P < .001). A nasogastric tube was required by 16% and 11%, respectively (P = .5), and there was no appreciable change in the penetration-aspiration scale from baseline in either group. The University of Washington Quality-of-Life Total and Pain Subscale scores as well as the Functional Assessment of Cancer Therapy–Head & Neck Total and Cancer Subscale scores significantly improved at 1 month, above the minimal clinically important difference threshold (0.5 standard deviations), in the de-escalated cohort. Most patients in both cohorts returned to baseline at 1 year.

Regan SN, Rosen BS, Suresh K, et al: FDG-PET-based selective de-escalation of radiotherapy for HPV-related oropharynx cancer: Results from a phase II trial. 2024 Multidisciplinary Head and Neck Cancers Symposium. Abstract 16. Presented March 1, 2024.

The short answer is: we simply don’t know. Let me start off by saying that most of the people here are not going to actually have a choice about this. Most people are going to get standard photon (X-ray) treatments (sometimes called external beam therapy) if it’s decided that their cancer needs irradiation to eliminate it. It’s been the standard treatment for a long time, often in combination with chemo. But there’s a new kid on the block: proton beam radiation. I’m not going to focus on the physics here to explain the differences, but basically proton radiation can provide more destructive energy to the tumor. Use the link below if you’d like to learn more.

X-ray machines are (relatively) small. Think how small the ones are at the dentist’s office. The ones used on head and neck cancer patients are much more sophisticated, with mechanisms that allow them to move in three dimensions using a computer-controlled beam that hits exactly where the radiation oncologist wants it to hit with the rays. In contrast, proton beam machines are enormous. They, too, are computer controlled and can direct the beam in a very precise manner. Building them is very expensive, which is one reason why there are so few of them, and why proton radiation treatments costs more than X-ray irradiation. Where I live, the one proton radiation facility in the city went bankrupt (but never stopped operating) a few years ago.

So why did they develop proton beam therapy treatments? The idea is that the beam can be controlled in a way that’s more precise than with X-rays, specifically in how deep the rays penetrate. The idea is to try to limit the damage caused by rays hitting normal tissues after passing through the tumor. This should lead to a better quality of life. There is some data that’s been developed that suggests that the proton beam really is less destructive of normal tissue than standard X-ray therapy. As I explain below, that may or may not be a good thing.

Here’s the dilemma, and it’s essentially the same one I covered in dose de-escalation trials. With radiation, there are two competing issues. Can you do less damage to tissues you don’t want to hit? That’s important for your quality of life, but more important (at least to many of us) is whether or not the radiation beam will destroy all parts of the tumor.

Once again, the five-year survival rate is the key measure of success here. The proton beam may cause less short term damage to surrounding tissues, but that may come at the cost of being less effective in killing all of the cancer cells. That in turn could reduce overall survival rates for patients. Clinical trials are being done with the proton machines to compare them to X-rays, but we just don’t know yet if they can provide an equal or (hopefully) better survival benefit while reducing off target damage. Yes, once again it’s about potential trade offs.

In the US, most people have their cancer treatments paid for by health insurance that they get through their jobs. The health insurance companies generally will pay for therapies that have been demonstrated to have an actual health benefit and are the “standard of care.” At this point many of these companies regard proton therapy as “experimental” in treating head and neck cancers, and therefore they won’t pay for it. Wealthy patients may decide they want to pay for it on their own out of pockets (if recommended by their doctors), but many people will not be able to afford this. Patients without health insurance are in a bad situation period when it comes to cancer (or any other) healthcare treatment. If and when proton radiation shows that it really is better than photon (X-rays), it will likely become the standard of care, and health insurance companies should pay for it then.

Bottom line: we don’t yet know whether or not proton will supplant photon as the radiation of choice. And since it’s they’re so expensive, proton machines will still be in limited supply for some time.

Those of you wanting more information can look at this page of my website that explained head and neck cancer treatment options.
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NOTE: As of June 2024, new guidelines have been issued by the American Society of Radiation Oncology for how radiation is to be used in treating HPV+ oropharyngeal patients.

"The American Society for Radiation Oncology convened a task force to address 5 key questions on the use of RT for management of HPV-associated OPSCC. These questions included indications for definitive and postoperative RT and chemoradiation; dose-fractionation regimens and treatment volumes; preferred RT techniques and normal tissue considerations; and post-treatment management decisions. The task force did not address indications for primary surgery versus RT. Recommendations were based on a systematic literature review and created using a predefined consensus-building methodology and system for grading evidence quality and recommendation strength.

Results
Concurrent cisplatin is recommended for patients receiving definitive RT with T3-4 disease and/or one node >3 cm, or multiple nodes. For similar patients who are ineligible for cisplatin, concurrent cetuximab, carboplatin/5-fluorouracil, or taxane-based systemic therapy are conditionally recommended. In the postoperative setting, RT with concurrent cisplatin (either schedule) is recommended for positive surgical margins (PSM) or extranodal extension (ENE). Postoperative RT alone is recommended for pT3-4 disease, >2 nodes, or a single node >3 cm. Observation is conditionally recommended for pT1-2 disease and a single node ≤3 cm without other risk factors. For patients treated with definitive RT with concurrent systemic therapy, 7000 cGy in 33 to 35 fractions is recommended, and for patients receiving postoperative RT without PSM and ENE, 5600-6000 cGy is recommended. For all patients receiving RT, intensity modulated RT over 3-D techniques with reduction in dose to critical organs-at-risk (including salivary and swallowing structures) is recommended. Reassessment with positron emission tomography-computed tomography (PET-CT) is recommended approximately 3 months following definitive RT/chemoradiation, and neck dissection is recommended for convincing evidence of residual disease; for equivocal PET-CT findings, either neck dissection or repeat imaging is recommended."

Here's a link to the actual guidelines, which are intended for physicians.

The concept here is pretty straightforward. Develop a blood test that can figure out if you do, or do not, have any HPV+ cancer cells in your body. This information can then be used to determine if you need more treatment, or if you have been effectively “cured” by the treatment you’ve already had. To be useful, the test must be highly accurate.

So the key question here is: how accurate is the test? When you’re making cancer treatment decisions, it needs to be not just good, not just great, but pretty darn near perfect. And the test could give a wrong answer in one of two ways: it could say that cancer cells are present when they’re actually not (a false positive), or it could say that you are cancer free when you’re not (a false negative).

Relying on either of these wrong results would be problematic, which is a polite way of saying disastrous for a patient. With a false positive, you may get additional treatments that you didn’t really need (not to mention some anxiety as well). With a false negative, you would walk away from having additional treatments when you actually did need them, and the cancer cells would continue to grow in your body, and that’s not going to end well. It’s this clear need for incredible, ultra-dependable accuracy that makes developing such a test very difficult.

Another thing to think about is the sensitivity of the test. How many cancer cells do there need to be for the test to detect them? Keep in mind that the average human body has about 30 TRILLION cells in it. So finding a small number of cancer cells is a very daunting task. There’s one other key point to keep in mind about a positive test that is really, truly positive. The test tells you that you have cancer cells in your body, but it doesn’t tell you WHERE they are. In your tonsil? Lymph node? Lung? Knowing you have cancer cells is good, but finding out where these cells are lurking can be a challenge. Why? Because the sensitivity of tests that show where cancer cells are located (i.e. PET scan) may be less sensitive than the NavDx test that tells you the cancer cells are hanging out somewhere. In order to attack this small number of cancer cells (with surgery or radiation, for example), you need to know where they are. This dilemma could be resolved by retesting you from time to time with the NavDx test, and when the numbers have gone up sufficiently (whatever that amount is), then doing a PET scan once more. While you’re waiting you might be living in a state of high anxiety.

Let’s spend a moment to look at the NavDx test. It works by quantifying fragments of tumor-specific DNA shed by cancer cells into the blood. This simply means it’s looking for HPV+ cancer cells, not just cancer cells in general. The test would not find kidney or stomach or prostate cancer if you have it (but it should find cervical cancer cells since that cancer is also caused by HPV). Here's a link to the Naveris website, the company that markets the NavDx test, if you want to read more about it there.

A study was done that ended in 2024 that looked at whether or not the NavDx could be clinically used to identify patients who had “minimal residual disease” (that’s another way of saying a small number of cancer cells somewhere in the body). The study ended early because of a failure to meet the primary endpoint of the study. That means that the test failed to find people who had small numbers of cancer cells. A second clinical study is still ongoing that is evaluating the utility of the NavDx test in identifying patient who might qualify for “de-escalation of radiotherapy and chemotherapy in patients with positive margins (< 3 mm) or extracapsular extension."

A really good review of the relative usefulness (or not) of the NavDx test was published in June 2024. This article also provides good information as to why the authors feel the test is not ready for prime time. Here's what the article had to say:

Different studies analyzed by the review found that the likelihood of the NavDx test coming back positive in patients who had a true cancer recurrence (likely measured by biopsy) was in the range of 29.3% to 87.3%. What this means is that the test failed to identify cancer in 15% to 70% of patients that actually had a true cancer recurrence. That's not good. The test faired much better at identifying negative patients, with a strong predictive value of about 93.3% to 98.5%. That sounds pretty good UNTIL you factor in the relative rate of recurrence. That was only about 7% in the studies looked at. What that means is that a test that was essentially worthless (that is, a fake test that measured nothing, or no test at all) would have a predictive value of identifying negative patients of 93%. The actual test is only slightly better than an imaginary test in determining if patients are truly negative.

Another question is whether or not the test can find cancer recurrences earlier than it would otherwise have been detected. The answer was about 1.6 to 1.8 months, meaning without the NavDx test the cancer would have been found by other methods less than two months later. Does that "finding the cancer earlier" translate into better outcomes (that is, longer survival times) for patients? Unfortunately it does not. The test also does not seem to be very sensitive at finding “minimal residual disease”. Essentially, that's a very few cancer cells compared to an actual tumor. It needs to be bigger in size for the test to detect it.

The authors concluded: "no evidence exists that detecting recurrent head and neck cancer earlier is associated with improved long-term survival or quality of life. Thus, there is no consensus about whether posttreatment imaging should be performed in asymptomatic patients, and the National Comprehensive Cancer Network does not recommend routine posttreatment imaging. Earlier detection of recurrent disease may not be beneficial and may even be harmful. For example, chemotherapy treatment based on the blood-based biomarker cancer antigen–125 in recurrent ovarian cancer was not associated with improved survival but rather poorer quality of life."

There are certain circumstances where the test may have some utility. It may be helpful when imaging or biopsy tests don't provide a clear answer.

"In conclusion, the TTMV-HPV DNA assay (that is, the NavDx test) currently lacks sufficient sensitivity to replace imaging or tissue biopsies or detect clinically occult” [hidden or concealed] “disease in most cases destined to develop recurrence. Therefore, caution should be exercised when considering the use of TTMV-HPV DNA (again, the NavDx test) in routine clinical decision-making (eg, when considering de-escalation of adjuvant therapy). For now, we believe that the use of TTMV-HPV DNA as an integral biomarker for decision-making should be reserved for clinical trials. Ultimately, prospective randomized clinical trials of TTMV-HPV DNA–based surveillance (again, the NavDx test) that examine whether the use of these assays improves overall survival or quality of life are needed before the assay should be adopted into routine practice."

Lee, N.Y. et al Assessing the Evidence for Circulating Tumor HPV DNA in Patients With Oropharyngeal Cancer. AMA Oncol. Published online June 27, 2024. doi:10.1001/jamaoncol.2024.1821

Another study was published in Dec. 2024 that also raised questions about the clinical utility of the NavDx test.

155 patients with HPV-positive oropharyngeal cancer and were undergoing curative-intent treatment were part of this study. Pretreatment plasma and/or tumor tissue were tested for tumor tissue modified viral HPV DNA (NavDx test) from HPV subtypes 16/18/31/33/35.. Post-treatment plasma was assessed periodically using the NavDx test. Tests that were positive or indeterminate led to imaging. The primary goal was to determine the proportion of recurrences first detected by the NavDx test. Results: Median follow-up was 23 months, with median 6 post-treatment NavDx tests for 155 subjects. Fifteen subjects (9%) had recurrences. Among these, 6 (40%) were ‘early true-positives’, for whom NavDx detection predated and prompted the imaging and clinical workup that diagnosed recurrence (median lead-time=132 days; range=47-280). Another 5 subjects (33%) were ‘confirmatory true-positives’, for whom the NavDx test confirmed suspicious standard-of-care imaging findings. Finally, 4 subjects (27%) with recurrence had undetectable NavDx tests at diagnosis (‘false-negatives’). False-negatives had low or undetectable pretreatment NavDx test results, and 2/4 had non-HPV16 genotypes. Finally, 3 subjects had prolonged detectable NavDx tests without disease (‘false-positives’); all had immunologic comorbidities. Overall, sensitivity of the NavDx test for recurrence was 73%. Among 117 subjects with HPV16 and detectable pretreatment positive NavDx tests, sensitivity was higher (91%) Conclusions: NavDx surveillance facilitates early detection of many HPV-positive OPC recurrences, with highest sensitivity for HPV16 and detectable pretreatment TTMV. Clinical implementation should be carefully informed by the limitations described herein being false negatives as well as false positives.


Rettig, E. et al. Prospective Trial of Biomarker-Guided Surveillance for HPV-positive Oropharynx Cancer Using Plasma Tumor Tissue Modified Viral HPV DNA. Clinical Cancer Res (2024)
https://doi.org/10.1158/1078-0432.CCR-24-3053

The NavDx test is not the only test that has been or is being developed to detect circulating HPV+ cancer cells. You can find a sampling of some of the other not-ready-for-prime-time tests in FAQ2 on this page of my website.

Bottom line: at present the NavDx test has some utility, but it’s not accurate enough yet that a doctor would rely solely on this test to determine that one is really cancer free. It’s this clinical uncertainty that prevents this test from being as helpful as people would like it to be. Hopefully the test gets better. Check with your doctor if you have more questions about this. The NavDx test is being covered by Medicare as of Nov. 30, 2023.

More details about this and other HPV+ cancer screening tests can be found on this page of my website (look both at this main page, and at the info in FAQ2 here).

Note that the NavDx test was designated as an Advanced Diagnostic Laboratory Test in April 2024. This designation is not related to the accuracy or other characteristics of the test. Rather, it simply means that the provider of the test has been designated the sole provider of that test, and the designation is related to payment costs and reimbursements. So it's a financing thing, not a science issue.

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A 2024 study looked at the utility of preoperative circulating tumor tissue-modified viral human papillomavirus DNA (TTMV-HPV DNA) levels in predicting human papillomavirus (HPV)–associated oropharyngeal squamous cell carcinoma (HPV+ OPSCC) disease burden.

This was a small study of only 70 patients who were scheduled for TORS to remove their tumors. The researchers found that pre-operative levels of TTMV-HPV DNA were quite variable, and did not appear to be associated with tumor size or other tumor characteristics.

Lam, D. et al. Preoperative Circulating Tumor HPV DNA and Oropharyngeal Squamous Cell Disease. JAMA Otolaryngol Head Neck Surg. Published online April 4, 2024. doi:10.1001/jamaoto.2024.0350
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The NaxDx test is just one of a number of tests that are in development to allow the earliest detection of cancer. A new one that has come on the scene is the MyHPVScore, which was created by the University of Michigan, and is offered to patients there. Like the NavDx test, the MyHPVScore test measure circulating DNA in the blood that comes from HPV+ tumors. Whether this test is as good as, better than, or worse than the NavDx test is unknown because they have not been tried side by side, and details about the accuracy of the MyHPVScore test have not been published. This new test is said to be able to detect circulating tumor DNA from six of the strains of HPV that together make up 99% of human HPV cancers. Patients who test positive with the MyHPVScore for recurrence undergo additional monitoring but still require secondary confirmation through imaging and clinical surveillance to begin treatment.
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Another new test is the HPV-DeepSeek test, which uses a more complex technology and which claims to provide greater selectivity (99%) and specificity (99%) than the other two tests. It is not yet commercially available yet. It actually can detect HPV+ head and neck cancers BEFORE they are clinically diagnosed. Here's a paper describing how it works:
Das, E. et al Circulating tumor human papillomavirus DNA whole genome sequencing enables human papillomavirus-associated oropharynx cancer early detection.
JNCI: Journal of the National Cancer Institute, djaf249, https://doi.org/10.1093/jnci/djaf249

—————————————————————————————————————————————————————————————————————————Some other tests use blood, some use urine, some use other body fluids. Researchers are hoping that their tests can help identify as many as 50 different types of cancer with a single blood test. The article below describes a number of these other tests in development, for those of you who are interested in the subject. The article does a very nice job outlining the pitfalls and problems that need to be overcome before these are ready to be widely used on patients. “It’s safe to say that the technology is not well enough developed to be marketed,” Ruth Etzioni, PhD, a biostatistician at the Fred Hutchinson Cancer Center’s Public Health Sciences Division, said in an interview.

Rita Rubin. Questions Swirl Around Screening for Multiple Cancers With a Single Blood Test. Journal of the American Medical Association. March 15, 2024. doi:10.1001/jama.2024.1018

Here's a more recent article from mid-2024 that covers much of the same territory. Blood based cancer screening still presents risks, and the overall benefits are unfortunately still unclear.
Sanket S. Dhruva and Rita F. Redberg Blood tests for cancer detection aren’t yet ready for prime time.

Much more information about the NavDx test, including a number of other studies can be found in FAQ #2 on the Screening for HPV Cancers page of this website. Look in the area below the Header "Commercial Screening Tests for HPV-caused Cancers"
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Some of you may have wondered: if they have a NavDx for HPV oral cancers, why don't they have a similar test for HPV driven cervical and other gynecological cancers? The answer is: they now do! The NavDx+Gyn™ test for early detection of HPV-Driven gynecologic cancers. I haven't seen any info to say how this test differs from the standard NavDx test, but it's likely to be very similar, if not actually identical.

We’ve all been there. We finish our treatments and then anxiously anticipate our first (and subsequent) appointments hoping for good news (but also fearing bad news). Scanxiety (anxiety related to what scans will show) is something that I expect most of us have experienced somewhere on our journeys. It’s perfectly natural to be worried as to whether or not your treatment will confer on you the “holy grail” from the mouths of your doctor: your status is NED; no evidence of disease. I hope you all get to experience hearing those words.

Even after getting a good report, many of us will remain anxious going forward. Suppose the cancer comes back? What if the scan missed something? Both of these things are indeed possible (though not common), and this leaves us feeling unsettled and concerned about what the future might bring.

As a result of this anxiety, many of us want to have frequent follow up exams from out medical teams. And this leaves people wondering why it is that these exams happen so infrequently once most of us are past the first year or two. Part of our thinking is: even if a follow up exam finds something, I know it will be caught earlier rather than later, and that will lead to a better outcome. So why is it that you don’t get PET/CT scans, or even physical exams, more than once a year?

There are two major reasons for this. In the case of PET/CT scans, they are both very expensive (so insurance companies won’t want to pay for them), and they also expose you to a great deal of radiation. Radiation damage to your body is cumulative, and the more you get, the more problems that may arise somewhere down the road. A PET/CT scan can expose you to as much radiation as 250 chest X-rays, so these are only done when medically necessary. The PET part of the PET/CT scan raises costs quite a bit since they require the preparation and administration of (slightly) radioactive glucose molecules.

There’s one other reason that we don’t get regularly scheduled scans or physical exams more that once a year past the first year or two. That reason may surprise you: it’s because these exams rarely find recurrences. In fact, this happens so infrequently that some have called for a stop to doing these yearly follow up exams. Maybe now you’re thinking: wait a minute, that doesn’t make sense. I know people who have had recurrences, and of course we read about them from time to time in posts to this group. Yes, recurrences can and do happen. The key point is: recurrences are most often found when someone experiences some perceived change in their bodies; not in the yearly exams.

Maybe swallowing feels a little harder. Maybe there’s a small hard lump on the neck that’s felt. Maybe you find your voice is hoarse all the time. In each of these circumstances, the change drives the patient to schedule an exam with their doctor. These are the situations where recurrences are found. So if you had an exam four months ago that was clear, but now find something that is a bit off, go ahead and schedule an exam to check it out. Don’t wait another eight months for your next scheduled exam. The bottom line is that recurrences are most often found from self-surveillance, not routinely scheduled follow up exams. So stay vigilant for any perceived changes, and if you detect something, contact your doctor. If you are not experiencing anything unusual, then in most cases it means that everything really is OK. And even if you do experience something that feels different, it doesn’t mean that your cancer is back. After all, there are many things that can cause your voice to become hoarse that are NOT associated with cancer. Your doctor will help you figure out just what is going on with your body. If you can, try not to worry.

“Don’t worry” is an easy thing to say, but not so easy to do. I’ve been there, done that. One of the best pieces of advice I got about this is from Tammy von Keisenberg, who likes to remind people “don’t borrow sorrow from tomorrow.” Yes, bad things can happen in the future, but if you’re doing (relatively) OK, enjoy it! Don’t let fear of future problems prevent you from living your life to the fullest!

FYI researchers are working to develop blood or saliva tests that are sensitive enough to find recurrences without the need of scans or physical exams. Those of you who are interested in learning more about why regularly scheduled follow up exams may not be necessary or helpful can read this article: https://onlinelibrary.wiley.com/doi/abs/10.1002/hed.25425

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How much screening does it actually take to uncover a single case of HPV+ oral cancer recurrence? A lot!

A recent study looked at this question.
"Of the p16+ OPSCC patients (n = 214), 23 had confirmed recurrence (11%). Standard work-flow model determined 72 imaging studies and 2198 physical examinations with FL were needed to detect one recurrence."

Costs for screening each patient for five years were estimated to be ~$69,000.

Lin, M.G. et al Novel HPV Associated Oropharyngeal Squamous Cell Carcinoma Surveillance DNA Assay Cost Analysis. Laryngoscope (2023) FREE download. https://doi.org/10.1002/lary.30701

The issue of cancer recurrence quite naturally comes up all the time. We all fear it (I was terrified of it), and hope that with every scan and physical exam, nothing is found.
The overall recurrence rate for HPV+ oropharyngeal cancers is actually fairly low, around 10%. That means the vast majority of us will never have a recurrence.
The farther out you get from treatment, the less your chances are for having a recurrence.
How are most recurrences found?
Is it from scans? No.
Is it from the NavDx test. No.
The vast majority (81%) of recurrences are found through symptom changes. Only about 8% show up in scans first. It's for this reason that I suggest people focus inward. Lean into how you are feeling. Know your body. If something seems different (e.g. a cough that doesn't stop; a lump in your neck; pain in your throat; difficulty swallowing), or doesn't feel right, that's the time to reach out to your doctor and get it checked out. Got a scan coming up in four months but you're having symptoms? Don't wait. Get it checked out now. I'm eight years out from treatment, and I check my neck for lumps every day. Only takes a few seconds, and then I get back to whatever it is I'm doing.

You can read more about it here: Shah, R. et al Detection, Patterns, and Outcomes of Recurrent HPV-Positive Oropharyngeal Squamous Cell Carcinoma. doi:10.1001/jamaoto.2024.3237

Before diving into the role that HPV plays in cancer, let’s start by taking a look at how cancers form in general. Cancer is a genetic disease, that is, it’s caused by mutations to the DNA inside your cells. These mutations keep some of the proteins inside your cells from working the way they were meant to work, because the instructions for making these proteins are encoded in your DNA. These mutations occur in a variety of ways. Some happen as part of the normal process of cell division (it’s actually designed by nature to NOT be a perfect process). Some mutations are caused by DNA damaging agents, such as chemicals (called carcinogens) or radiation from X-rays or other sources. Mutations in our DNA tend to accumulate over time as we age. Older folks have many more DNA mutations inside their cells than babies do, which is why the rates of developing different cancers are much higher in older people. This helps explain why of the approximately two million cancer cases diagnosed in the US every year, only 15,000 are cancers in children (that's 0.75 percent). Sometimes these mutations cause cells to continuously divide; the normal brakes on this process are disrupted by the genetic alterations. When this happens, the cells eventually will form a tumor.

How many of these genetic alterations or mutations are needed to transform a normal cell into a cancer cell? This is a highly variable process. Some of these alterations are extremely powerful and only a single mutation can result in a cell becoming transformed and turning cancerous. The more usual course is that a substantial number of these genetic alterations are required to turn a normal cell cancerous. Could be 25. Could be closer to 50, or maybe even a hundred. Every tumor is like a snowflake; no two are alike. Different mixes of genetic alterations can lead to the transformation process. Some of these combinations are more transformative than others. There are some well-known mutations (genetic alterations) that are seen in many cancers; these alterations may serve as targets that anti-cancer drugs are meant to attack. As cancers divide and grow, they tend to add additional mutations that make the tumors that much more difficult to treat.

These mutated (or altered genes) receive a lot of attention from cancer researchers. Scientists want to know if any of the changes are necessary to cause cancer (that is, without that change, cancer won’t develop) as well as if they are sufficient (if the change occurs, then the cell will definitely become cancerous). HPV actually fails both of these tests. The vast majority of cancers (such as breast, brain, bladder, kidney, or colon cancer) do NOT contain any HPV. This tells us it’s not always needed to cause cancer. HPV infection is also not sufficient on its own to cause cancer. How do we know this? It’s because only a small percentage of HPV-infected people go on to develop cancer. Most never do. So HPV alone is clearly not sufficient to cause cancer on its own, although it clearly can contribute to the process.

Most of you know that many cases of head and neck cancers are NOT caused by HPV (instead, they’re associated with excessive smoking and/or drinking). Even though they’re the same kind of cancer (squamous cell carcinoma), these non-HPV head and neck cancers are actually considered a separate disease from those head and neck cancers caused by HPV. These non-HPV cancers are treated in exactly the same way, but it turns out that the HPV-caused head and neck cancers are actually much more treatable (and curable) than those cancers NOT caused by the virus. Exactly why this happens isn’t well understood. HPV infection, even though it helps to make the cells cancerous, also makes them more susceptible to the killing effects of chemo and/or radiation.

Tumors may simply stay in one place, or they may acquire additional mutations that allow the tumor cells to break off from the main mass and travel (via the bloodstream or the lymphatic system) to distant locations. There, the cells may get stuck and begin the division process all over again and form a new tumor. This process is known as cancer metastasis and is a bad development because cancers are much easier to attack if they are located in a single place.

So how does HPV cause cancer? Cancer-causing strains of HPV enter our cells and can do one of two things. If your immune system doesn’t clear the infection, the viral particles can simply float around and just hang out in your cells. Alternatively, they can actually insert themselves into the DNA inside our cells in a process known as integration. Sometimes the virus may hang out for long periods of time before it integrates into our cells. Once this happens, the integrated virus begins to make some of the proteins that are contained within its own genetic structure. Exactly where the virus integrates into our DNA also plays a role in whether or not the virus can cause cancer. At least two of these viral proteins, E6 and E7, appear to play a role in transforming a normal cell into a cancer cell. There is also data that the E4 protein made by the virus suppresses antiviral immunity, making it harder for your body to get rid of the virus.

As a result of this, a number of biopharma companies are creating drugs to disable these proteins, which may render the cells non-cancerous and leave them open to attack by the immune system. These drugs wouldn’t work on non-HPV cancers, but if they are effective, they should be able to be used to fight all of the HPV-caused cancers, including anal and cervical cancer. I keep track of these clinical trials and will let people know if these actually pan out. It would be a great advance to have another option beside surgery, chemo, and radiation.

The short answer is no. This topic is a bit complicated, but I will explain. There are many different types or strains of HPV that cause cancer. The two most prominent are HPV 16 and HPV 18, with 16 being the most common in the US. This is determined by using a technique known as PCR on a biopsy sample from the tumor. These PCR tests take time to run and get results. So doctors often use something called a surrogate marker (see below) to infer that a cancer is likely to be caused by HPV. However, being p16+ is NOT the same as being HPV 16 positive.

During surgery, biopsy samples are sent to the pathology lab, where they use a different technique called staining to determine what kind of cancer it is, and if it is likely to be caused by an HPV infection (without doing the PCR test, which can't be done quickly). So the pathologists use what's called a surrogate marker, which is something that essentially suggests that the cancer is caused by HPV but without directly measuring it. We use surrogate markers all the time. If you see someone smiling or appear to be laughing when you watch TV with the sound muted, that smiling and laughing is a surrogate marker for something funny being experienced by the people you are looking at. That there are actual jokes occurring can be inferred by the surrogate marker of the smiling and laughing. p16 is used as a surrogate marker for cancers being caused by HPV because it is quick and easy to measure..

p16 refers to a protein (hence the p for protein) named p16, which is completely different from HPV 16 (the virus), but if cells are stained and shown to be p16+, that suggests that the cancer is being caused by some strain of HPV (could be 16, or 18, or another strain). It is very unfortunate that p16 is so similarly named to HPV strain 16. The hospital will often do a follow up PCR to confirm that the tumor really is HPV+, because there are times when tumors are p16+ but are actually HPV negative. Put another way, the surrogate marker leads us to a wrong conclusion.

Does being p16+ guarantee or prove that you are HPV+? The answer is no. There can be a lack of concordance between these two measurements. A new paper in 2023 confirmed that a substantial number of p16-positive patients are actually HPV-negative when tested for HPV DNA or RNA. Why does that matter? It's because the study found that for the one in ten of patients who have discordant HPV results, they saw significantly worsening outcomes compared to those who tested negative in both tests.

In those cases, 5-year overall survival were:
81% among double positive tests,
53% for patients with p16-/HPV+ test
54% for patients with p16+/HPV- tests for patients

Your doctor can explain this further.

Reference: Mehanna, H. et al. Prognostic implications of p16 and HPV discordance in oropharyngeal cancer (HNCIG-EPIC-OPC): a multicentre, multinational, individual patient data analysis. The Lancet Oncology Feb. 2023
DOI: https://doi.org/10.1016/S1470-2045(23)00013-X (Free Download)

The survival numbers we often see are not a "cure" rate. They are five-year survival rates, which is a standard measure of cancer survival. It allows doctors to compare different types of cancer for lethality. What that means is: for every 100 patients, what percentage of them are still alive five years later? That number incorporates exactly what it says: still alive after five years. If it's not 100%, It doesn't mean that those people died of cancer. They could have had a heart attack. Or been hit by a bus. Or overdosed on pills.

The median age of diagnosis for HPV+ oropharyngeal cancers in one study was about 61 for both men and women, so this is not a young group. For this disease, depending on the source you use, that five-year survival rate is around 90%, which is really good for cancer. For pancreatic cancer, that number is closer to 5%. If you get checked out at that five year appointment and the doc finds NED (no evidence of disease), then you're a survivor. If you don't go back to the doc for the five year appointment, you are still a survivor, but your status (NED) is simply unclear because no one looked for evidence. Many doctors don't use the word "cured" anymore because they can't back that word up with any data that will guarantee that status. And as with everything in life, your mileage may vary because we are all unique individuals. Our genes are different, as are our immune systems and our lifetime exposure to toxic chemicals. So hang in there and hope for the best, and when you get there, enjoy your NED status. Life offers no guarantees, and the diagnosis is life changing, but you have to have hope going forward.

The answer to this question is probably not. This is a bit of a complex issue, as explained below. Blood transmission of the HPV virus has not been a big concern in the biomedical community. For example, blood donations are not currently screened for HPV, and the American Red Cross (and other Red Cross societies) do not prevent HPV-positive individuals from donating blood. This may simply reflect that fact that doctors know that around 90% of people are going to be infected by HPV sometime during their lifetime via sexual contact, so therefore there is little reason to try to prevent spread via blood donation.

Survivors of HPV cancers are at a slightly increased risk of developing a second HPV-caused cancer. This could indicate that the virus has spread in the body, but it could also mean that the person is infected with two different cancer-causing strains of HPV, and those infections just happen to be in separate places. The only way to really answer this question is to do genetic sequencing of the virus from different body sites, and see if the exact same sequence is found at multiple sites. Even then, this would not guarantee that the virus has spread, because the person could have been infected at multiple locations during the initial infection.

You can develop different HPV infections at different sites in your body. A study was done in men to look at their acquisition of HPV strains at different anatomic sites over time. The researchers looked at a large group of men or evidence of for sequential genital to oral infection with one of nine HPV types (HPV 6, 11, 16, 18, 31, 33, 45, 52, 58); and also for sequential, same-type oral to genital infection. They observed a significantly higher incidence of an oral HPV infection among men with a prior genital infection of the same type for any of the 9 HPV types. Overall findings suggest that HPV infections at one site could raise the risk of a subsequent genital or oral HPV infection of the same type in men. Exactly how this happens is unclear, nor is the potential role of a partner in this transmission defined.

Dickey BL, et al Sequential acquisition of human papillomavirus infection between genital and oral anatomic sites in males. International Journal of Cancer July 7, 2021

A paper was recently published suggesting that blood transmission may be possible for papilloma viruses using animal models. The study came about after an observation made in 2005 where blood samples from a group of HIV-positive children were also found to be positive for HPV. Because of the age of the children, it's highly unlikely that they acquired HPV via the usual sexual transmission mode of viral transfer. The researchers wondered if the HPV virus could have come from blood transfusions, which some of the children had undergone. Researchers showed using two different animal models that HPV could be transmitted via blood. Whether or not this holds true for humans remains to be determined. It's still believed that most, if not all, HPV infections are sexually transmitted.

Cladel, N.M. et al, Papillomavirus can be transmitted through the blood and produce infections in blood recipients: Evidence from two animal models. Emerging Microbes & Infections (2019). DOI: 10.1080/22221751.2019.1637072.

Infection through other body fluids like sperm or saliva is considered to be rather unlikely. However, the virus may spread during oral sex if mucous membranes in the mouth touch areas of skin of your partner that have been infected with HPV.

Transmission from the mother to baby via nursing has also been looked at in a couple of small studies. In one study it appeared that the virus might be transmitted via milk in a very small percentage of cases, but it appears to be rare. Milk from lactating women in Australia was examined in a separate study and a few samples were found to be HPV positive. Breast feeding of babies is still encouraged by virtually all organizations, so this is something that women should not be overly concerned about. About 40% of pregnant women in the US have an HPV infection, and HPV could be detected in 10% of placentas. Only 7% of neonates had HPV at birth, and no infection persisted at 6 months.
Khayargoli, P.et al Human Papillomavirus Transmission and Persistence in Pregnant Women and Neonates. JAMA Pediatr. Published online May 22, 2023. doi:10.1001/jamapediatrics.2023.1283

This question comes up often. Sadly, the short answer is no. The thought of having to endure these harsh “standard of care” treatments drives many patients to consider other remedies. Yes, the standard treatments are rough for many people. You can see this in the comments posted here nearly every day. Some people would much rather try other things, including CBD oil, “natural” cures, homeopathy (which simply doesn’t work), dietary supplements, and any number of other agents, including trendy things like ivermectin and hydroxychloroquine instead of the “standard of care”. None of these will cure your cancer.

Can I prove that these alternatives don’t work? I can’t because I haven’t rigorously tested them in a carefully done clinical trial to determine if they really are effective. The question you really want to be asking is: Is there any solid, reliable evidence that any of these treatments actually do work? It’s highly unlikely that you’ll be able to find any such information. Instead, you’ll find bold claims and hype-filled anecdotal stories (“my cousin had that cancer, took those pills that he bought online, and now he’s cured!”) instead of actual hard data. There are many different kinds of supplements you can buy from online websites, on Amazon, from neighborhood “healers”, or in stores that sell nutritional supplements. Most of them will have a legal disclaimer on the package that will say something like this:

“These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.”

This statement is there to protect the seller from being sued by consumers (or their heirs) when the product turns out to be ineffective. There are different types of claims that products can make. The following info is from the Edible Chemistry consulting website:

“Nutritional claims: These are statements about the general effects dietary supplements, vitamins, and minerals have on diseases known to be caused by nutrient deficiency. For example, “vitamin C prevents scurvy.” These claims do not need to be approved by the FDA (US Food and Drug Administration). But the label must also state how many cases of the disease occur in the United States. In this example, consumers must weigh the risk of getting scurvy against the potential risks of the supplement itself.

Claims of wellbeing: These are just that – statements such as “makes you feel better.” These claims do not require pre-approval by the FDA.

Health claims: These are statements about known health benefits of certain compounds. For example, risk-reduction claims such as “folate may reduce the chance of pregnant women delivering an infant with neural tube defects” fall into this category. The FDA must pre-approve all health claims, and requires that they be supported by evidence from scientific studies. Remember that risk-reduction claims are not the same as prevention claims.

Structure or function claims: These are the most confusing claims made to consumers. They are claims about the effect of the dietary supplement on the structure or function of the body. The FDA published a ruling in January 2000 that explained exactly what kinds of structure or function claims OK for dietary supplements are.

Dietary supplements may not make any claims regarding the treatment of disease. But the following descriptions and examples are considered structure or function claims that are OK for dietary supplements:
The product’s mechanism of action (“works as an antioxidant”)
The product’s effects on cellular structure (“helps membrane stability”)
The product’s effects on the body’s physiology (“promotes normal urinary flow”)
The product’s effects on chemical or lab test results (“supports normal blood glucose”)
Claims of maintenance (“helps maintain a healthy circulatory system”)
Other non-disease claims (“helps you relax”)
Claims for common conditions and symptoms related to life stages (“reduces irritability, bloating, and cramping associated with premenstrual syndrome”)””

Here’s my main takeaway: it’s easy for people to make claims about their products, but much, much harder to collect solid proof that supports that claim. A product may claim to supercharge your immune system, but it can’t promote claims that doing so will help treat, prevent, or cure any disease unless they can actually prove it. These claims are made simply to transfer the money in your wallet into the pockets of the sellers. Many of them are no better than the “snake oil salesmen” from early in the last century.

Be wary of any dietary supplement or other product that claims to prevent, treat, or cure any type of cancer. Such claims can only be made for products such as pharmaceuticals or treatments that have been proven (by doing multiple clinical trials) that they do what they claim to do. And while we’re on the subject of drugs, no, pharma companies don’t have cures for cancer that they are hiding from the public. Ask yourself: why wouldn’t they sell them, and who are they saving them for?

For more details, see this info from the Food and Drug Administration.

A new research paper showed that people who chose to take non-conventional treatments (e.g. vitamins/homeopathy/unapproved drugs/CBD oil) for a number of survivable cancers (nonmetastatic breast, prostate, lung, or colorectal cancer) instead of the “standard of care” were twice as likely to die from their cancers as those who chose the “standard of care.”

Complementary Medicine, Refusal of Conventional Cancer Therapy, and Survival Among Patients With Curable Cancers. Johnson, S.B. et al

JAMA Oncol. 2018;4(10):1375-1381. doi:10.1001/jamaoncol.2018.2487

In the US healthcare system (and maybe others as well), patients and their caregivers need to be their own best advocates. You have to stand up for yourself to get the care you deserve.

Our system is large, overly complex, and often maddening. There are many moving parts. It would be great if everything worked smoothly all the time, but that’s not what happens in the real world. Papers get misplaced. Names get left off lists. Folks fail to pass along information they promised to pass along. It’s because of this I suggest patients make sure that their needs are being met. If that’s not happening, you need to speak up and take action. Here are a few examples:
If someone tells you that you’ll get a call tomorrow about scheduling something, and three days later you’ve heard from no one, reach out. Call a member of your team and tell them you were told that you’d get a call, and it didn’t happen. Can they please look into this to find out why? If another couple of days pass without a callback, call them again. Don’t wait and assume that everything is OK. Follow up.

If you’re meeting with a member of your medical team, and they tell you something you don’t understand, just tell them “I didn’t understand that. Would you please explain it to me again in a different way?” If you still don’t understand it, ask the question again. Try to either write down (or record on your smartphone) what’s said, so that you can review it later if you forget, or if you want to share it with someone else. For cancer patients, we often stop hearing what’s being said after scary words like “surgery” “chemo” or “radiation” enter our ears. That's why it's often a good idea to have your caregiver or a friend with you at your appointments with your doctors. They may hear what you miss.

If there’s something that you think it’s important for your team to know so that you get the best care possible, make sure to tell them what that is. This is not the time to be shy, or to think they would have asked about the issue if it was important. Speak up. Make your needs known.

Wishing you all the best with getting the care you truly deserve.

Insurance companies frequently deny preauthorization claims, or they outsource them to a company that will deny them. This saves them money, but can cost you your life. If your doctor feels that any of your claims are being unfairly denied, please make sure that they file appeals. These often work out.

The idea of "starving" cancer by avoiding sugar is a common misconception. While it's true that cancer cells consume more glucose than normal cells, simply cutting out sugary foods from your diet is not an effective way to starve tumors.

Here's why:
1) Your body maintains a baseline blood glucose level: Even if you completely eliminate sugar from your diet, your body will still produce glucose from other sources to maintain necessary blood sugar levels.
2) All cells need glucose: Both healthy and cancerous cells require glucose for energy. Your body will prioritize providing glucose to cells that need it, including cancer cells.
3) Complex relationship: The link between sugar and cancer is more complex than simply "sugar feeds cancer".

However, there are important considerations regarding sugar consumption and cancer:
1) Indirect effects: High sugar intake can lead to obesity, which is a known risk factor for several types of cancer.
2) Insulin and IGF-1: Excessive sugar consumption can lead to high insulin levels and increased production of insulin-like growth factor 1 (IGF-1), which may promote cancer cell growth.
3) Metabolic pathways: Some studies suggest that high-sugar diets may activate certain metabolic pathways that could promote cancer growth and progression.

Instead of trying to "starve" cancer by eliminating sugar, experts recommend:
1) Balanced diet: Focus on a balanced diet rich in fruits, vegetables, whole grains, and lean proteins.
2) Moderation: Limit intake of added sugars and refined carbohydrates.
3) Healthy weight: Maintain a healthy body weight, as obesity is a clear risk factor for cancer.
4) Overall lifestyle: Consider your overall lifestyle, including physical activity and stress management, in addition to diet.

In conclusion, while completely avoiding sugar is not an effective strategy to "starve" cancer, moderating sugar intake as part of a balanced diet and healthy lifestyle may help reduce cancer risk and support overall health.

This decision is a highly personal one. Let me just share a few thoughts on this subject. Scan results in the US are almost always sent to patients when the results are available via an online patient portal. I highly recommend that you use great caution in accessing these results. Why is that? It's because scan and other results are written in highly technical language and they can be very difficult for anyone besides oncologists and radiologists to interpret properly. You may see something that sounds dangerous when in fact it's actually something benign. The results of a scan can be life changing. You really do need professionals to provide context for the results, so think twice before accessing your patient portal to view scan results online. I suggest waiting until you can actually meet with your doctors before looking at these. This isn't just my recommendation. See Rowe, D.G, and Goodman, C.R. Unintended Consequences of Patient Portal Access. JAMA Oncol. Published online April 10, 2025. doi:10.1001/jamaoncol.2025.0415

You may be asking yourself: why are they sharing these results with me if they are so difficult to interpret? It's because it's required by law in the US. The 21st Century Cures Act, known as the Cures Rule, took effect in April of 2021, and it requires clinicians to give patients real-time access to their health data via patient portals.
Proceed with caution!

The short answer is: we don't really know for certain. Note that whether or not cannabis can cause head and neck cancers is a separate question from asking if cannabis drives the growth of existing cancers. Research in this area is, in a word, messy. Determining doses used by patients depends on the survey questions asked as well as the truthfulness and recollection of the patients, as well as the content of the active ingredients in whatever it is they consumed. There is no way to know this. Smoking a joint could have very different effects than having an edible. Smoking anything (tobacco or marijuana) is likely to be carcinogenic at some level, but determining what that is is not known.

Recent research provides increasingly strong evidence that frequent or heavy marijuana use, especially “cannabis use disorder”, is associated with a significantly increased risk of developing head and neck cancers. The relationship appears particularly pronounced for daily users and those with cannabis dependence. Head and neck cancers in this setting are not separated out as either HPV+ or HPV-. Adults with “cannabis use disorder” are 3.5 to 5 times more likely to develop head and neck cancers compared to non-users, independent of age, gender, ethnicity, and even after accounting for tobacco and alcohol use. The increased risk was observed across various types of head and neck cancers, including oral, laryngeal, and oropharyngeal cancers. Having said this, note that earlier case-control studies and pooled analyses (pre-2020) did not find a significant association between infrequent or moderate marijuana use and head and neck cancer risk (see below). For oropharyngeal cancer patients (most of whom will be HPV+), an increased frequency of cancers in marijuana users may also be influenced by the fact that they may have had more sex partners, which is a known driver for HPV-caused head and neck cancers.

A mechanism by which THC can promote the growth of HPV+ head and neck cancers was described by researchers at the University of San Diego in this paper. Note that the data obtained was from cell lines and molecular analyses, and the growth of tumors in people may not be affected in the same way.
Liu, C. Cannabinoids Promote Progression of HPV-Positive Head and Neck Squamous Cell Carcinoma via p38 MAPK Activation . Clin Cancer Res (2020) 26 (11): 2693–2703. https://doi.org/10.1158/1078-0432.CCR-18-3301

A newer paper from this same group came to the opposite conclusion for cannabidiol. This compound inhibited the growth and migration of HPV+ H&N squamous cell carcinoma cells.
Sen, P. et al CBD promotes antitumor activity by modulating tumor immune microenvironment in HPV associated head and neck squamous cell carcinoma. Front. Immunol., 21 May 2025

As I said above, this is a complicated story.

Those who are casual cannabis users may not have that same level of risk of either developing a head and neck cancer, or influencing the growth of that cancer. Again, it is also difficult to separate the irritating and possibly carcinogenic effects of cannabis smoke from the effects of active compounds like THC. Put another way, ingesting gummies may or may not be as harmful as smoking a joint. Laboratory research has identified a biological mechanism by which THC, the psychoactive component of marijuana, can accelerate tumor growth in HPV-related head and neck cancers. Lots of substances that can stimulate or inhibit the growth of tumor cells in the laboratory do not have the same effects on tumors in people. We simply don’t know exactly how THC affects the growth of existing tumors. As with many biological systems, the dose may matter greatly.

Balancing these studies out are research papers that reach different conclusions. One very small study found that marijuana use had no effect on survival of HPV+ oral cancer patients. A different study generated data that suggested that "moderate" marijuana use actually reduced the risk of developing head and neck squamous cell carcinoma (HPV+ and HPV- patients were not broken out in that study).

Considerations and Limitations

Dose and Frequency: The strongest associations are seen with frequent, daily use or cannabis use disorder. Infrequent or occasional use has not consistently shown a significant increase in risk. Smoking in general, whether tobacco or marijuana, is likely to be an irritant and could contribute to the development and growth of some cancers.
Confounding Factors: While recent large studies have attempted to control for tobacco and alcohol use, which are well-established risk factors, completely disentangling these effects remains challenging. As mentioned above, the number of sex partners is a known risk factor for HPV+ oropharyngeal cancer.
Mechanism: The risk appears to be linked to the inhalation of cannabis smoke, which, like tobacco smoke, contains carcinogenic compounds and may cause inflammation and DNA damage in the tissues of the mouth and throat. THC within the smoke, or in gummies, may also promote the growth of cancer cells. Gummies have not been directly tested to see if they are problematic or not.

Bottom line: We simply don’t know if marijuana use is a key contributor to the growth of existing HPV+ cancers, or even if it can contribute to the development of these cancers. The answer to both of those questions may depend on the dose as well as the delivery route. This is an excellent question to raise with your care team if you have concerns. Taking gummies for a short period of time to get you through your treatment or recovery period is different than being a daily marijuana smoker for years. Heavy or daily marijuana use, especially when it meets criteria for "cannabis use disorder", is associated with a substantially increased risk of developing head and neck cancers. Whether this extends to the active substances in marijuana is an open question that can only be answered with more research.

A clinical study is going to start in 2025 to try and determine if cannabis negatively affects wound healing in head and neck cancer patients. Researchers funded by the Presbyterian Health Foundation will do the study at the University of Oklahoma , which will include 220 adult patients undergoing surgery for head and neck cancer and reconstruction after the tumor removal. Many surgeries can compromise swallowing and breathing. This is a prospective study: patients will be followed for six months from the time of their treatment – rather than retrospectively looking at patient data. In addition, patients’ self-reporting of cannabis use will be biochemically verified through blood tests, which adds strength to the study. The study is not designed to answer if cannabis drives the growth of HPV+ or - head and neck cancers, and is also not designed to look at the effects of cannabis on the majority of patients who get chemo +/- radiation.

Sadly, the answer may be yes. In addition to causing cancer, a meta-analysis being presented on March 31 at the American College of Cardiology’s (ACC's) Annual Scientific Session in Chicago suggests that it also poses a significant risk of cardiovascular disease.

For the University of Connecticut review, researchers analyzed 7 studies conducted from 2011 to 2024 that included the HPV status and cardiovascular outcomes of 249,366 patients over follow-up times of 3 to 17 years. Three each were from the United States and South Korea, and 1 each was from Brazil and Australia.

The researchers examined the relationship between HPV and cardiovascular disease, coronary artery disease, and high blood pressure in pooled study cohorts. Some analyses adjusted for potential confounding factors such as smoking and diabetes.

Relative to HPV-negative participants, HPV patients had a 40% higher risk of cardiovascular disease and twice the risk of coronary artery disease, but no increased rate of high blood pressure. After adjusting for factors such as sociodemographics, medical history, lifestyle, family history, and use of blood pressure–lowering drugs, HPV patients had a 33% higher risk of cardiovascular disease. "The biological mechanism has not been determined but is hypothesized to be related to chronic inflammation," lead author Stephen Akinfenwa, MD, of UConn, said in the ACC press release. "We would ultimately like to see if reducing HPV via vaccination could reduce cardiovascular risk."
Clinicians should closely monitor HPV patients' hearts. "We always talk about cardiovascular risk factors like smoking, high blood pressure and so on, but we know that about 20% of cardiovascular disease cannot be explained by these conventional risk factors," he said. 

Don't eat fresh pineapple!!! The irritating sensation you feel on your tongue when eating pineapple is primarily caused by an enzyme called bromelain. Bromelain is a protease, meaning it breaks down proteins—including those in the protective mucosal lining of your mouth and tongue. As bromelain digests these proteins, it can cause a tingling, burning, or sore feeling.
In addition to bromelain, pineapple is also naturally acidic, which can further aggravate the irritation once the protective barrier in your mouth is weakened. Some sources also note that pineapples contain needle-like calcium oxalate crystals called raphides, which may contribute to the sensation by physically irritating the mouth lining and allowing bromelain and acids to penetrate more easily. The irritation is temporary—your mouth heals quickly, and the effect disappears soon after you stop eating the fruit. Cooking or processing pineapple (such as canning) destroys bromelain, so these forms of pineapple are less likely to cause discomfort

There tests are available, such as this one from MicroGenDx (there may be other ones as well). I can’t comment on the accuracy or reliability of the test. The company suggests that the test would be appropriate for people with a history of HPV or oral cancer, or at high risk of an oral HPV infection, or may have been exposed to HPV, or just want to protect their health. I don’t really think it’s very useful for any of these things. Why not? Because the information isn’t actionable. What would you do if you found out you were HPV positive? Only about 1% of oral HPV infections lead to oral cancer, but worry created by a positive test result could be very problematic for some people. The better solution is to simply pay more attention to your oral health. If you feel something is amiss in your mouth at some point, and it doesn’t go away in a couple of weeks, go see your healthcare provider and get it checked out. Remember that only about one-third of oral cancers are caused by HPV. The HPV test won’t find any evidence of these other oral cancers because that is not what it is designed to do.

This seems like it would be a very good thing to do. Remove the other tonsil at the same time to make sure that it never becomes cancerous. Doctors ran a clinical trial to answer the question, and what they found might surprise you. Turns out it’s a bad idea to take out the second tonsil at the same time. Why? Because it led to an increase in a number of health problems. From the study: “In this cohort study, 158 patients undergoing bilateral transoral surgery had a higher postoperative hemorrhage rate, postoperative emergency department visit/hospitalization rate, and length of stay. There were no differences in swallowing outcomes or survival between the 2 approaches; contralateral tonsil second primary tumor rates were low.” Other studies have also shown that the risk of developing a tumor in the second tonsil is very low.

Peterson, A.M. et al Unilateral vs Bilateral Transoral Robotic Surgery for HPV-Positive Tonsillar Squamous Cell Carcinoma. JAMA Otolaryngol Head Neck Surg Published Online: July 10, 2025 doi: 10.1001/jamaoto.2025.1833

This question is a bit tricky to answer. In general, the answer would be no. Skin cancer is generally caused by UV radiation from the sun, not the HPV virus. There are many different types of HPV, each tending to infect cells in a particular tissue and part of the body. The strains of HPV found mostly on the skin—beta-HPV—are considered innocuous viruses on your skin; they don't typically integrate into the DNA of skin cells and cause problems. This contrasts them with the alpha types of HPV, known to integrate into the DNA of mucous membrane cells and directly cause cancer of the genitals, anus, cervix, and head and neck.

The thinking about these beta HPV cancers changed when researchers at the NIH examined a 34-year-old woman who came in for evaluation and treatment of recurrent cSCC (cutaneous squamous cell carcinoma) on her forehead. "She had undergone multiple surgeries and a round of immunotherapy to try to remove or kill the tumor, but it repeatedly grew back. Her local doctors thought this was due to an inherited inability to repair DNA damaged by UV radiation plus an impairment in immune cells called T cells. The tumor was one of many progressively worsening HPV-related diseases the woman was experiencing.
Through a sophisticated genetic analysis, the NIH researchers discovered that a beta-HPV had integrated into the cellular DNA of the woman’s well-established tumor and was extensively producing viral proteins there. This contradicted the prevailing theory that beta-HPV only facilitates the establishment of cSCC without integrating into cellular DNA and plays no role in maintaining the cancer. Further genetic analysis of the woman’s cells showed they were fully capable of repairing DNA damage from UV radiation, suggesting the virus alone had caused cSCC.
To understand how beta-HPV could take the unusual steps of integrating into the woman’s skin-cell DNA and multiplying there unchecked, the investigators studied the woman’s inherited immune disorder. They found that her genetic mutations greatly hampered T cells from activating in response to skin-cell infection by beta-HPV. This suggested that the immune disorder itself was responsible for the woman’s worsening HPV-related diseases, including the beta-HPV cSCC on her forehead, and that treating this disorder might cure all of them."
The NIH investigators developed a personalized plan to give the woman a stem cell transplant to replace the defective T cells of her immune system with healthy ones. Afterward, all her HPV-related diseases including the recurrent, aggressive cSCC resolved and have not recurred during the more than three years since the transplant. This confirms that the woman’s inherited disorder had prevented her T cells from keeping beta-HPV in check, allowing the virus to directly cause and sustain cSCC.
The key feature here is that the woman had an immune disorder. Without this, she would NOT have developed this HPV skin cancer. More details here.