oral cancer

Understanding personal risk of oropharyngeal cancer: risk-groups for oncogenic oral HPV infection and oropharyngeal cancer

Author: G D’Souza, T S McNeel, C Fakhry
Date: October 19, 2017
Source: Academic.oup.com

Abstract

Background

Incidence of human papillomavirus (HPV)-related oropharyngeal cancer is increasing. There is interest in identifying healthy individuals most at risk for development of oropharyngeal cancer to inform screening strategies.

Patients and methods

All data are from 2009 to 2014, including 13 089 people ages 20–69 in the National Health and Nutrition Examination Survey (NHANES), oropharyngeal cancer cases from the Surveillance, Epidemiology, and End Results (SEER 18) registries (representing ∼28% of the US population), and oropharyngeal cancer mortality from National Center for Health Statistics (NCHS). Primary study outcomes are (i) prevalence of oncogenic HPV DNA in an oral rinse and gargle sample, and (ii) incident oropharyngeal squamous cell cancer.

Results

Oncogenic oral HPV DNA is detected in 3.5% of all adults age 20–69 years; however, the lifetime risk of oropharyngeal cancer is low (37 per 10 000). Among men 50–59 years old, 8.1% have an oncogenic oral HPV infection, 2.1% have an oral HPV16 infection, yet only 0.7% will ‘ever’ develop oropharyngeal cancer in their lifetime. Oncogenic oral HPV prevalence was higher in men than women, and increased with number of lifetime oral sexual partners and tobacco use. Men who currently smoked and had ≥5 lifetime oral sexual partners had ‘elevated risk’ (prevalence = 14.9%). Men with only one of these risk factors (i.e. either smoked and had 2–4 partners or did not smoke and had ≥5 partners) had ‘medium risk’ (7.3%). Regardless of what other risk factors participants had, oncogenic oral HPV prevalence was ‘low’ among those with only ≤1 lifetime oral sexual partner (women = 0.7% and men = 1.7%).

Conclusions

Screening based upon oncogenic oral HPV detection would be challenging. Most groups have low oncogenic oral HPV prevalence. In addition to the large numbers of individuals who would need to be screened to identify prevalent oncogenic oral HPV, the lifetime risk of developing oropharyngeal caner among those with infection remains low.

Introduction

Human papillomavirus (HPV) is the most commonly sexually transmitted infection in the United States. HPV now causes ∼70% of all oropharyngeal squamous cell cancer (OPC) in the United States [1] and the incidence of HPV-related OPC (HPV-OPC) among men has more than doubled over the past 20 years [2]. Indeed, OPC is projected to be more common than cervical cancer in the United States by 2020 [3]. Given the ‘epidemic’ of HPV-OPC, there is interest in identifying specific groups that could benefit from screening, if effective tests were developed.

Sexual behaviors responsible for exposure to oral HPV infection are common (80% of the US population reports ever performing oral sex) [4]. Given the ubiquitous exposure to HPV infection and resulting anxiety [5], there is interest in identifying healthy individuals most at risk for development of OPC. As oncogenic oral HPV infection is the precursor to malignancy, identification of individuals with oncogenic oral HPV infection may point to individuals with premalignant disease. Such risk triage could both inform screening approaches and assist the public in understanding personal risk. This analysis therefore aims to understand how common HPV16, oncogenic HPV and HPV-OPC are in groups of people with different risk factor profiles.

Methods

Study population

This study included 13 089 people ages 20–69 years old who participated in National Health and Nutrition Examination Survey (NHANES) between 2009 and 2014 and had oral HPV DNA testing. Analyses involving number of oral sex partners were limited to ages 20–59, with data for number of oral sex partners, resulting in a sample size of 9425. Incidence and incidence-based mortality data from SEER 18 registries between 2009 and 2014 [6] were used with NCHS mortality data for projections of OPC risk.

HPV measurement

As previously described [7, 8] oral HPV DNA was tested in exfoliated cells collected from an oral rinse and gargle sample using PCR amplification using PGMY 09/11 consensus primers and line blot for the detection of 37 specific HPV types. Oncogenic oral HPV was defined as detection of any of the following 12 types: HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59 [9].

Analytic methods

Analyses of NHANES oral HPV data were weighted by Mobile Examination Center (MEC) exam sampling weights, and conducted using SUDAAN software (release 11.0.1, Research Triangle Institute) to account for survey sample design. Projected OPC risk was calculated using DevCan software [10].

To better understand subgroup risk, prevalence of oncogenic HPV and HPV16 were explored stratifying by multiple factors including sex, sexual behavior, age, and current smoking. Groups with similar prevalence were combined to create parsimonious risk stratification of people with similar prevalence.

Results

Oncogenic oral HPV and oral HPV16 infection are rare in the general US population. As expected, prevalence of infection is higher among men than women of every age group (oncogenic HPV; 6.0% versus 1.1%, P < 0.001; Table 1). Prevalence of oncogenic oral HPV is contrasted with risk of OPC in Table 1 by sex and age groups. While oncogenic oral HPV is detected in 3.5% of all adults age 20–69, the lifetime risk of OPC is low (37 per 10 000). For example, among men 50–59 years old, 8.1% have an oncogenic oral HPV infection, 2.1% have an oral HPV16 infection, yet 0.7% will ‘ever’ develop OPC in their lifetime; and risk of developing OPC in the next 10 (0.2%) or 20 (0.4%) years is even lower (Table 1).

Table 1.

Oral HPV prevalence by sex and age, compared with the risk of developing oropharyngeal cancer (OPC) in each group

    Risk spectrum: infection to cancer

 

NHANESa (prevalence)

 

SEERb (OPC risk: cases/100 people) 

 

Sex  Age  Oncogenic Oral HPV (%)  Oral HPV16 (%)  Lifetime (%)  Next 20 years (%)  Next 10 years (%) 
Men
20–29 4.8 1.1 0.7 0.01 <0.01
30–39 4.7 1.5 0.7 0.07 0.01
40–49 6.2 2.3 0.7 0.3 0.06
50–59 8.1 2.1 0.7 0.4 0.2
60–69 6.1 2.4 0.5 0.4 0.3
Total 6.0 1.9 0.7
Women
20–29 1.4 0.3 0.2 <0.01 <0.01
30–39 1.0 0.3 0.2 0.01 <0.01
40–49 0.8 0.1 0.2 0.05 0.01
50–59 1.6 0.5 0.2 0.08 0.03
60–69 0.7 0.1 0.1 0.10 0.05
Total 1.1 0.3 0.2
Men and women All 3.5 1.1 0.4

a- Weighted prevalence accounting for NHANES study design weights to reflect the general US population.

b- Estimates of OPC risk combine data on cancer occurrence from SEER with population data. OPC is shown as risk per 100 people to contrast with HPV prevalence. For reference in interpretation, 0.6% risk represent that 0.6 people out of the 100 (or 6 out of 1000, or 600 out of 100 000) would develop OPC.

While prevalence of oncogenic oral HPV infection is low, the distribution of infections is not representative of the population (supplementary Table S1, available at Annals of Oncologyonline). Indeed 84% of oncogenic oral HPV infections in 20- to 69-year olds were among men. To elucidate why oncogenic oral HPV was more concentrated among certain groups, behavioral characteristics were considered. Performing oral sex and smoking are each strongly associated with detection of oncogenic oral HPV (Table 2) and HPV16 (supplementary Table S2, available at Annals of Oncology online). Oncogenic oral HPV prevalence is low (<2.5%) among both men and women who never performed oral sex. Prevalence of oncogenic oral HPV increased with number of lifetime oral sexual partners, up to 14.4% in men age 20–59 years old with ≥10 lifetime oral sexual partners (Table 2).

 

Table 2.

Oncogenic oral HPV prevalence by participant characteristics and behaviors

    Oncogenic oral HPV prevalencea(%)

 

 
Men  Women  All 
Characteristics (among those 20–69 years old)  No. of people  N = 6420  N = 6669  N = 13 089  P-valueb 
Sex
Women 6669 1.1 1.1 <0.0001
Men 6420 6.0 6.0
Currently smoke
No 10 041 4.5 0.9 2.6 <0.0001
Yes 3044 10.5 2.1 6.7
Age, in years
 20–29 2738 4.8 1.4 3.1 0.13
 30–39 2668 4.7 1.0 2.8
 40–49 2699 6.2 0.8 3.4
 50–59 2494 8.1 1.6 4.8
 60–69 2490 6.1 0.7 3.3
Race/ethnicity
 White non-Hispanic 5135 6.3 1.1 3.7 0.008
 Black non-Hispanic 2931 7.5 1.4 4.2
 Any race Hispanic 3347 4.5 1.3 2.9
 Other 1676 3.7 0.7 2.1
Ever oral sex (or man or woman)
 No 2453 2.3 0.2 1.1 <0.0001
 Yes 9272 6.5 1.4 4.0
Ever oral sex on a woman
 No 6660 3.6 1.0 1.4 <0.0001
 Yes 5095 6.4 3.5 6.2
Ever oral sex on a man
 No 7054 5.8 0.2 4.9 <0.0001
 Yes 4693 10.2 1.4 1.8
Number of partners performed oral sex on in lifetimec
 0 1661 2.4 0.2 1.2 <0.0001
 1 1877 1.2 1.0 1.1
 2–4 3165 4.8 0.7 2.5
 5–9 1363 3.9 2.5 3.3
 10+ 1359 14.4 3.0 11.1

a- Weighted prevalence accounting for NHANES study design weights to reflect the civilian non-institutionalized US population.

b-Wald F test (based on transforming the Wald χ2) for independence of row variable and oral HPV16, not accounting for sex (except where sex is the row variable).

C- Data on number of lifetime oral sex partners was not collected consistently in those 60 and older so is only presented among those 20–59 years old.

 

 

Oncogenic oral HPV prevalence was explored by sex, sexual behavior, and tobacco use to better understand groups that have higher and lower prevalence (Figure 1). Regardless of what other risk factors participants had, oncogenic oral HPV prevalence was low among those with only ≤1 lifetime oral sexual partner (women = 0.7% and men = 1.7%). Oncogenic oral HPV prevalence doubled among women with ≥2 versus 0–1 lifetime oral sexual partners (1.5% versus 0.7%, P = 0.02), but remained low among women with higher number lifetime oral sexual partners (Table 2). Oncogenic oral HPV prevalence was highest among men who currently smoked and had ≥5 lifetime oral sexual partners (14.9%, 95% CI = 11.4–19.1). Men with only one of these risk factors (i.e. either smoked and had two to four partners or did not smoke and had ≥5 partners) had ‘medium risk’, with 7.3% (95% CI = 5.8–9.1) oncogenic oral HPV prevalence (Figure 1). Findings were similar when considering oral HPV16 infection specifically.

 

What is my risk of oral HPV? Prevalence of oral HPV16 and any oncogenic oral HPV infection by risk group. In the ‘very low-risk’ group (among women with 0–1 lifetime oral sexual partners), oncogenic oral HPV was similar among smokers and nonsmokers (1.8% versus 0.5%, P = 0.26). In the ‘low-risk’ group of women, oncogenic oral HPV prevalence was 1.5% among women with two or more lifetime oral sexual partners. In the ‘low-risk’ group of men, oncogenic oral HPV prevalence was 1.7% among men with 0–1 lifetime oral sexual partners and was higher among men who did not smoke and had 2–4 lifetime oral sexual partners (4.1%, P = 0.0042). In the ‘medium risk’ group, oral HPV16 prevalence was 7.1% among men who smoke and had 2–4 partners and 7.4% among men who do not smoke and had 5+ partners (P = 0.87).

 

Discussion

This analysis highlights that the yield of oncologic oral HPV screening would be limited in most groups in the United States. With the increasing incidence of OPC, there is a need to understand how to identify individuals at risk of OPC. Oncogenic oral HPV detection is attractive as it samples the relevant epithelium in a non-invasive method, has relatively low cost and serves as a biomarker for HPV-OPC. However, for screening to succeed, a high prevalence population is needed to limit false positives, and balance the psychologic and physical harms of screening with the benefits.

From this analysis, it is clear that screening based upon oncogenic oral HPV detection would be challenging. Women across all categories have low prevalence of infection and low risk of OPC and therefore benefits of screening are unlikely to outweigh harms in this group. The higher prevalence of oncogenic oral HPV in men than women is thought be due to both a higher per partner risk of acquisition when performing oral sex [11, 12], and decreased clearance among men than women [11, 13]. While there are specific risk groups of men enriched for oncogenic oral HPV, most men have low prevalence of infection. Even among the elevated risk group, the majority of men do not have a prevalent oncogenic oral HPV. In addition to the large numbers of individuals who would need to be screened to identify prevalent oncogenic oral HPV, the lifetime risk of developing OPC among those with infection remains low [11, 14].

These characteristics suggest that other tests will need to be combined or supplant present methods to accurately identify those with the greatest risk of OPC in the population. Serum HPV oncoprotein antibody tests are specific [15], but are even rarer than oral HPV16 infection [16], so may be impractical to use in most groups. An additional challenge for screening is that precursor lesions for HPV-OPC have not been found and the ability to detect lesions early in an ‘elevated-risk’ group is unknown.

With growing appreciation of the relationship between oral sex, infection, and cancer, some individuals have questions about their risk of having oncogenic oral HPV infection. To address concerns about infection among individuals with high number of oral sex partners or others concerned about their cancer risk, the infographic can be used to reassure that oncogenic oral HPV prevalence is low among most groups. This analysis has several imitations. Data on oral HPV infection were cross-sectional, with no information linking HPV and SEER data used for cancer risk. Comparing oncogenic oral HPV prevalence and OPC risk in this way informs potential future screening studies, and personal risk assessment. In summary, this analysis shows that screening based upon oncogenic oral HPV infection will not be useful and presents data to communicate to the layperson the low risk of infection and cancer.

Acknowledgements

The authors acknowledge Maura Gillison who led the testing for oral HPV in NHANES provided in the publicly available dataset. This dataset has provided investigators the opportunity to better understand the epidemiology of oral HPV infection in the United States. We also acknowledge the contributions of the Oral Cancer Foundation.

Funding

National Institute of Dental and Craniofacial Research (NIDCR) (R35 DE026631).

Disclosure

The authors have declared no conflicts of interest.

 

References

1 Saraiya M, Unger ER, Thompson TD et al. US assessment of HPV types in cancers: implications for current and 9-calent HPV vaccines. J Natl Cancer Inst 2015; 107(6): djv086

 

2 Jemel A, Simard EP, Dorell C et al. Annual Report to the Nation on the Status of Cancer, 1975-2009, featuring the burden and trends in human papillomavirus(HPV)-associated cancers and HPV vaccination coverage levels. J Natl Cancer Inst 2013; 105(3): 175-201.

 

3 Chaturvedi AK, Engels EA, Pfeiffer RM et al. Human papillomavirus and rising oropharyngeal cancer incidence in the United States. J Clin Oncol 2011;29(32): 4294-4301

 

4 D’Souza G, Cullen K, Bowie J et al. Differnece in oral sexual behaviors by gender, age, and race explain observed difference in prevalence or oral human papillomavirus infection. PLoS One 2014; 9(1): e86023

 

5 D’Souza G, Zhang Y, Merritt S et al. Patient experience and anxiety during and after treatment for and HPV-related oropharyngeal cancer. Oral Oncol 2016; 60: 90-95.

 

6 SEER Incidence and Incidence-Based Mortality Date, SEER 18 Regs (Excl Lousiana) 1973-2014; http://seer.cancer.gov/date/ (8 May 2017, date last accessed).

 

7 Gillison ML, Broutain T, Pickard RKL et al. Prevalence of oral HPV infection in the United States, 2009-2010. JAMA 2012;307(7): 693-703.

 

8 NHANES 2013-2014: Human Papillomavirus (HPV)- Oral Rinse Data Documentation, Codebook, and Frequencies:

https://wwwn.cdc.gov/Nchs/Nhanes/2013-2014/ORHPV_H.htm (2 May 2017, date last accessed).

 

9 IARC. Human Papillomavirus; http://monographs.iarc.fr/ENG/Monographs/vol100B/mono100B-11.pdf (23 May 2017, date last accessed)

 

10 Devcan: Probability of Developing or Dying of Cancer- Surveillance Research Program; https://surveillance.cancer.gov/devcan/ (8 May 2017, date last accessed).

 

11 D’Souza G, Wentz A, Kluz N et al.   Sex differnces in risk factors and natural history of oral human papillomavirus (HPV) infection. J Infect Dis 2016;213(12):1893-1896.

 

12 Chaturvedi AK, Graubard Bl, Broutian T et al. NHANES 2009-2012 findings: association of sexual behaviors with higher prevalence of oral oncogenic human papillomavirus infections in U.S. men. Cancer Res 2015; 75(12): 2468-2477.

 

13 Beachler DC, Sugar EA, Margolick JB et al. Risk Factors acquisition and clearance or oral human papillomavisur infection among HIV-infected and HIV-uninfected adults. Am J Epidemiol 2015; 181(1): 40-53.

 

14 Pierce Campbell CM, Kreimer AR, Lin H-Y et al. Long-term persistence of oral human papillomavirus type 16: the HPV infection in men (HIM) Study. Cancer Pres Res Phila Pa 2015; 8(3): 190-196.

 

15 Holzinger D, Wichmann G, Baboci L et al. Sensitivity and specificity of antibodies against HPV16 E6 and other early proteins for the detection of HPV16-driven oropharyngeal squamous cell carcinoma. Int J Cancer 2017; 140(12):2748-2757.

 

16 Beachler DC, Waterboer T, Pierce Campbell CM et al. HPV16 E6 seropositivity among cancer-free men with oral, anal or genital HPV16 infection. Papillomavirus res 2016; 2: 141-144.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

October, 2017|Oral Cancer News|

Lindsey Stirling Honors Her Late Father with Moving Routine on Dancing with the Stars: ‘I Felt Like I Was Dancing with My Dad’

Author: Karen Mizoguchi
Source: People.com
Date: October 9, 2017

Lindsey Stirling has had an incredibly tragic year. The violinist is mourning the loss of her father, Stephen, who died of throat cancer. And on Monday night’s episode of Dancing with the Stars, she honored him with her routine for Most Memorable Year Week, choosing 2017.

“I am the woman I am today because of you and I love you so much,” she said on the reality dancing competition series.

To celebrate her dad’s life, Stirling and pro partner Mark Ballas — who wore her father’s hat and scarf as part of his costume — performed a touching Viennese Waltz. “I felt like I was dancing with my dad,” said Stirling, who was awarded a 26/30 by judges.

“I feel like I got to thank my dad in a way I’ve never been able to before. I was really looking forward to this dance, I was terrified to do it and I’m really happy,” she said. “When you’re dancing about something that is so important that means so much to you doing something I’ve never done before, I just wanted it to be so special. And I feel like it was.”

In January, the YouTube star announced the sad news on Facebook, Twitter and Instagram, writing, “My dad passed away early this morning. There is nothing to say that could express my gratitude for this amazing, selfless man.”

She added, “But I love you daddy. I’m the woman I am today because of you.”

Along with the loving message, the America’s Got Talent alum shared a childhood photo of herself and her father.

In June 2016, Stirling’s father, a religious educator and author, detailed his battle with cancer on his website.

“The pain in my throat persists. (That pain is likely the residual result of radiation and chemotherapy. In other words, I now suffer from the cure, now that the disease has fled.  Ironic.),” he wrote about his illness, which he was diagnosed for in late 2015.

The father of five wrote his final Facebook post. “As I prepare to write the next chapter of my life, I am not afraid. God be with you ’til we meet again,” he said.

October, 2017|Oral Cancer News|

Treatment That’s Easy to Swallow in HPV+ Throat Cancer

Source: Medscape.com
Author: Nick Mulcahy
Date: September 27, 2017

SAN DIEGO, California ― Daniel Ma, MD, of the Mayo Clinic in Rochester, Minnesota, treats a lot of relatively young patients with human papillomavirus (HPV)-related oropharyngeal cancers who are cured by various standard combinations of surgery, radiation therapy and chemotherapy and then have “another 30 to 40 years of life ahead of them.”

But that life expectancy can be marred by the “potentially life-altering side effects” of standard treatment, including dry mouth, loss of taste, and, in about one half of patients, difficulty swallowing, he said.
These patients inspired the genesis of Dr. Ma’s phase 2 study of an “aggressive dose de-escalation” of adjuvant radiation in this setting, he said.

The investigators evaluated experimental radiation doses of 30 to 36 Gy, which is a 50% reduction from the current standard of 60 to 66 Gy.

At a median of 2 years’ follow-up among 80 patients, the treatment de-escalation has resulted in locoregional control rates comparable to historical controls, low toxicity, and, perhaps most notably, no decrement in swallowing function or quality of life, Dr. Ma reported here at the American Society for Radiation Oncology (ASTRO) 2016 Annual Meeting.

The toxicity and swallowing results are “the most exciting data,” Dr. Ma told a standing-room-only crowd at a meeting session today.

“It’s the first clinical trial in head and neck cancer to demonstrate no injury to swallowing function after radiation,” he told Medscape Medical News. In other words, patients’ ability to swallow was no worse post treatment. In fact, patients’ ability to swallow improved slightly at 1 year following radiation therapy compared to pretreatment (P = .03).

“It’s an exciting concept. Everyone’s going to want to hear more about it,” said Thomas Galloway, MD, of Fox Chase Cancer Center in Philadelphia, Pennsylvania, who was asked for comment about the trial.

The answer is not yet known, but the 2-year results from Dr. Ma are encouraging.

Two-year data indicate that after de-escalated treatment, the rate of locoregional tumor control was 95%, which is comparable to results with standard radiation (60 Gy) from the Radiation Therapy Oncology Group (RTOG) 0234 trial.

In the Mayo Clinic trial, three patients experienced local recurrence, and one patient experienced a nodal recurrence.

Fox Chase’s Dr. Galloway also observed that, in the new trial, patients received 30 Gy delivered in 1.5 Gy twice a day over 12 days (along with weekly docetaxel, 15 mg/m2, days 1 and 8). Twelve days is a lot shorter than the standard 6 weeks for 60-Gy therapy, but the twice-daily schedule may not be suitable for all patients, he pointed out.

De-escalation radiation therapy is experimental, but a phase 3 study that seeks to confirm the approach, known as the DART-HPV trial, is now underway.

“This is not incremental change,” he told Medscape Medical News. “It’s a stark change from the current standard of care.”

Dr. Galloway and Dr. Ma both said that HPV-positive head and neck cancers are necessitating change, because patients with these cancers are younger and healthier than patients without the virus, whose cancers are typically caused by smoking and alcohol consumption.

Some HPV-positive patients are now being treated without surgery. “What the perfect recipe for treatment is, no one knows for sure,” Dr. Galloway told Medscape Medical News about treatment combinations.

Paul Harari, MD, of the University of Wisconsin, Madison, said the HPV-positive head and neck cancers, including oropharyngeal cancers, “warrant different treatment approaches.” Standard treatment is toxic ― “make no mistake about it,” Dr Harari commented while acting as moderator at a press conference featuring the dose de-escalation trial.

However, cutting the radiation therapy dosage, he said, prompts a “tense question: can you maintain the cure rate?”

 

More Study Details, Including Toxicity

About half of the study patients, all of whom had oropharynx squamous cell carcinoma, had the above-described 2-week-long treatment schedule. But 43 patients had extracapsular extension, a marker of aggressive disease, and thus received an additional radiation boost to the affected areas, for a total dose of 36 Gy.

Data for both groups of patients were combined in the statistical tallies.

All of the study patients had no evidence of residual disease following surgery and a minimal smoking history (eg, less than one pack per day for 10 years or less). The median patient age was 60.5 years. All patients had stage III or IV disease.

There was also a “very dramatic reduction” in side effects, compared with standard treatment, said Dr. Ma. No patients required percutaneous endoscopic gastrostomy (PEG); by contrast, with traditional radiation therapy, one fifth to one third of patients undergo PEG.

The PEG feeding tube is inserted through the abdomen into the stomach. Typically, one fifth to one third of patients will receive such a feeding tube during standard treatment for oropharyngeal cancers, he said.

The rate of grade ≥2 toxicities 2 years post radiation therapy was 10%. Again, this compared favorably with 55% rate reported in RTOG 0234.

No patients had grade 3+ toxicity at 1 or 2 years following treatment.

All 14 patients (18%) who experienced cumulative grade 3+ toxicity did so within 3 months of treatment, and all cases resolved by 6 months post treatment. One patient experienced acute grade 4 toxicity related to a chemotherapy reaction, which quickly resolved.

Patient quality of life either improved or did not change following treatment, except with regard to xerostomia. Patients reported worse salivary flow following treatment (P < .0001).

Dr. Ma, his coinvestigators, Dr Galloway, and Dr. Harari have disclosed no relevant financial relationships.

American Society for Radiation Oncology (ASTRO) 2017 Annual Meeting. Abstract LBA-14, presented September 26, 2017.

 

 

 

 

September, 2017|Oral Cancer News|

Don’t start, be smart: Local, Reno Rodeo competitor advocates being tobacco-free

Source: mynews4.com
Author: Kenzie Bales
Date: June 13th, 2017

RENO, Nev. (News 4 & Fox 11) — As a country phenomenon, Garth Brooks once said, “It’s bulls and blood, it’s dust and mud, it’s the roar of a Sunday crowd. It’s the white in his knuckles, the gold in the buckle, he’ll win the next go ’round. It’s boots and chaps, it’s cowboy hats, it’s spurs and latigo, it’s the ropes and the reins, and the joy and the pain and they call the thing rodeo.”

2017 Reno Rodeo competitor Cody Z Kiser has been riding and roping for as long as he can remember.

Born and raised to Carrie and P.D. Kiser in Carson City, Nevada, Cody started riding bulls as a Dayton High School student.

A horrific injury would set Kiser back, but by no means did it keep him from chasing his dreams.

Kiser says a bull stepped on his face and crushed all the bones in the left side of his face. After recovering, Kiser transitioned from bull riding to bareback bucking horses and hasn’t looked back since.

If traveling to rodeos all the time wasn’t enough to keep someone completely preoccupied, Cody competed while pursuing a Bachelor’s Degree in Civil Engineering at the University of Nevada, Reno.

After testing the waters in the engineering field for awhile, Kiser decided it was time to chase his lifelong dream and give rodeo his full attention.

During his endeavors as a cowboy, Cody was fortunate enough to establish a partnership with the Oral Cancer Foundation.

Everyone knows it is terrible for you, yet they still do it.

He says that being tobacco-free is something he advocates for because he understands the huge health risks that come along with it.

I have seen the impact it can have on a human’s health and it is something that I want no part of, and if I can help others from starting it, then I am happy.

Kiser says he is always willing to answer questions pre-existing tobacco users may have, but by no means is he trying to tell people how to live their life.

A big goal of his: to show people that you don’t have to smoke or chew to be a real cowboy or to be successful in the sport you love. Primarily focusing on kids, Kiser hopes to spread the movement to younger generations who haven’t picked up the bad habit yet.

The sport is hard enough on your body, no sense in making in harder on yourself.

Kiser says he strays away from just throwing facts and statistics at people, but rather making a positive, memorable impact and associating with people without the use of tobacco.

After partnering with the OCF three years ago, the cowboy says that he has had nothing but positive feedback and calls himself the “luckiest guy in the world.”

If you are interested in watching Cody Kiser compete in the 2017 Reno Rodeo, you can catch him on Father’s Day, Sunday, June 18 (making his dad, a former bucking horse rider proud) or Monday, June 19.

June, 2017|Oral Cancer News|

Study reveals high environmental cost of tobacco

Source: www.cnn.com
Date: May 31st, 2017
Author: Jacopo Prisco

Details of the environmental cost of tobacco are revealed in a study released Wednesday by the World Health Organization, adding to the well-known costs to global health, which translate to a yearly loss of $1.4 trillion in health-care expenses and lost productivity.

From crop to pack, tobacco commands an intensive use of resources and forces the release of harmful chemicals in the soil and waterways, as well as significant amounts of greenhouse gases. Its leftovers linger, as tobacco litter is the biggest component of litter worldwide.

“Tobacco not only produces lung cancer in people, but it is a cancer to the lungs of the Earth,” said Dr. Armando Peruga, who previously coordinated the WHO Tobacco Free Initiative and now works as a consultant. He reviewed the new report for the WHO.

Commercial tobacco farming is a worldwide industry that involves 124 countries and occupies 4.3 million hectares of agricultural land. About 90% of it takes place in low-income countries, with China, Brazil and India as the largest producers.

Because tobacco is often a monocrop — grown without being rotated with other crops — the plants and the soil are weak in natural defenses and require larger amounts of chemicals for growth and protection from pests.

“Tobacco also takes away a lot of nutrients from the soil and requires massive amounts of fertilizer, a process that leads to degradation of the land and desertification, with negative consequences for biodiversity and wildlife,” Peruga said.

The use of chemicals directly impacts the health of farmers, 60% to 70% of whom are women. This is especially prominent in low- and middle-income countries, where some compounds that are banned in high-income countries are still used.

300 cigarettes = one tree

Farming also uses a surprisingly large amount of wood, rendering tobacco a driver of deforestation, one of the leading causes of climate change.

About 11.4 million metric tonnes of wood are utilized annually for curing: the drying of the tobacco leaf, which is achieved through various methods, including wood fires. That’s the equivalent of one tree for every 300 cigarettes, or 1.5 cartons.

This adds to the impact of plantations on forest land, which the study describes as a significant cause for concern, citing “evidence of substantial, and largely irreversible, losses of trees and other plant species cause by tobacco farming.”

Deadly gases

In 2012, 967 million daily smokers consumed approximately 6.25 trillion cigarettes worldwide, the WHO estimates.”That means about 6,000 metric tones of formaldehyde and 47,000 metric tonnes of nicotine are released into the environment,” Peruga said.

Tobacco smoke contains about 4,000 chemicals, at least 250 of which are known to be harmful. It also contains climate-warming carbon dioxide, methane and nitrous oxides. “The combination of greenhouse gases from combustion is equivalent to about 1.5 million vehicles driven annually,” Peruga said.

Secondhand smoke is particularly deadly: It contains twice as much nicotine and 147 times more ammonia than so-called mainstream smoke, leading to close to 1 million deaths annually, 28% of them children.

Some of these pollutants remain in the environment (and our homes) as “third-hand smoke,” accumulating in dust and surfaces indoors, and in landfills. Some, like nicotine, even resist treatment, polluting waterways and potentially contaminating water used for consumption, the study notes.

Non-biodegradable litter

Tobacco litter is the most common type of litter by count worldwide.

“We calculate that two-thirds of every cigarette ends up as litter,” Peruga said.

The litter is laced with chemicals including arsenic and heavy metals, which can end up in the water supply. Cigarette butts are not biodegradable, and tossing one on the ground is still considered a socially acceptable form of littering in many countries.

The WHO estimates that between 340 million and 680 million kilograms of tobacco waste are thrown away every year, and cigarette butts account for 30% to 40% of all items collected in coastal and urban clean-ups.

“In addition to that, there are 2 million tons of paper, foil, ink and glue used for the packaging,” Peruga said.

A way forward?

Even though smoking is declining globally, it is increasing in some regions, such as the eastern Mediterranean and Africa. China is a world leader both in production (44%) and consumption, with 10 times more cigarettes smoked than in any other nation.

Every stage of the production of a cigarette has negative effects on the environment and the people who are involved in manufacturing tobacco products, even before the health of smokers and non-smokers is affected.

Although governments worldwide already collect $270 billion in tobacco taxes a year, the WHO suggests that increasing tax and prices is an effective way of reducing consumption and help development priorities in each country, adding that by collecting 80 cents more per pack, the global tax revenue could be doubled.

“Tobacco threatens us all,” WHO Director-General Margaret Chan said in a note. “It exacerbates poverty, reduces economic productivity, contributes to poor household food choices, and pollutes indoor air.”

May, 2017|Oral Cancer News|

Padres Hall of Famer Randy Jones Battling Throat Cancer

Source: 10news.com
Author:
Mark Saunders
Posted: Jan 26, 2017

SAN DIEGO – Legendary San Diego Padres pitcher Randy Jones is battling throat cancer, the team’s website announced Thursday.

Jones was reportedly diagnosed in November 2016 and has been undergoing radiation and chemotherapy treatments since December at Sharp’s Hospital.

“I feel positive,” Jones said told the Padre’s Bill Center. “They caught it early. It’s all in the throat and not in the lymph nodes. I’m beating this thing.”

Jones said he used chewing tobacco as a player and has smoked cigars throughout his adult life.

“I’ve completed 90 percent of my treatment,” Jones told Center. He added that his physicians have said his cancer is linked to tobacco use. He also said his cancer is low-risk.

Since his playing days he has remained heavily involved with the team. He is a spokesperson for the team and a local radio and television personality.

The Friars drafted Jones in 1972, during the 5th round of the amateur draft.

Jones pitched for the Padres from 1973-1980. He recorded a 3.42 ERA and 735 strikeouts through his career. He was the first Padre to win the National League Cy Young Award and the first Padre to start an All-Star Game.

He was a National League all-star in 1975 and 1976, when he led the NL in ERA in 1975 and led in wins in 1976.

Jones’ number was retired by the team in 1997 and two years later, he was a member of the Padre’s first Hall of Fame class.

 

“This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.”

January, 2017|Oral Cancer News|

FDA Warns Against So-Called “Cancer Cure”

Source: http://www.curetoday.com/articles/fda-warns-against-socalled-cancer-cure

Published: 01/13/2017

Author: BRIELLE URCIUOLI

The US Food and Drug Administration (FDA) just added another agent, PNC-27, to the growing list of drugs that falsely claim to treat or cure cancer.

An FDA lab recently found the bacteria Variovorax paradoxus in PNC-27, a product that is claiming to treat and cure all cancers, claiming to affect lung cancer as affectively as head and neck cancer. Though no illness or serious adverse events were reported to the FDA, contact with contaminated samples can lead to life-threatening infections, especially in vulnerable populations, such as young children, elderly people, pregnant women and people who have weakened immune systems, according to a statement released by the FDA.

“In general, consumers should be cautious of products marketed and sold online claiming to treat, cure or prevent any disease. Products claiming to treat, cure or prevent disease, but are not proven safe and effective for those purposes not only defraud consumers of money, they can lead to delays in getting proper diagnosis and treatment of a potentially serious condition,” Kristofer Baumgartner, FDA spokesperson, said in an interview with CURE.

PNC-27 is being dosed in multiple ways, such as a nebulized solution, intravenous solution, vaginal suppository or rectal suppository.

The FDA is urging people not to purchase or use PNC-27, which is neither FDA evaluated or approved. Patients should consult with their licensed health care providers before deciding on a treatment plan, and if they have already taken PNC-27, they should see their doctor as soon as possible, and report any adverse events to the FDA’s MedWatch Adverse Event Reporting Program.

As a matter of policy, the FDA cannot discuss any ongoing trials in detail, Baumgartner said. – See more at: http://www.curetoday.com/articles/fda-warns-against-socalled-cancer-cure#sthash.YgMC7JgV.dpuf

 

“This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.”

January, 2017|Oral Cancer News|

NCI-Designated Cancer Centers Issue Statement in Support of New CDC Recommendations on HPV Vaccination

Source: The ASCO Post
Posted: 1/11/2017

The 69 National Cancer Institute (NCI)-designated cancer centers have issued a joint statement in support of recently revised recommendations from the Centers for Disease Control and Prevention (CDC) to improve national vaccination rates for human papillomavirus (HPV).

According to the CDC, incidence rates of HPV-associated cancers have continued to rise, with approximately 39,000 new HPV-associated cancers now diagnosed each year in the United States. Although HPV vaccines can prevent the majority of cervical, anal, oropharyngeal, and other genital cancers, vaccination rates remain low across the United States, with just 41.9% of girls and 28.1% of boys completing the recommended vaccine series.

New Recommendations

The new guidelines from the CDC recommend that children under age 15 should receive 2 doses of the 9-valent HPV vaccine at least 6 months apart. Adolescents and young adults older than 14 should continue to complete the 3-dose series.

Research shows there are a number of barriers to overcome to improve vaccination rates, including a lack of strong recommendations from physicians and parents not understanding that this vaccine protects against several types of cancer. In an effort to overcome these barriers, NCI-designated cancer centers have organized a continuing series of national summits to share new research, discuss best practices, and identify collective action toward improving vaccination rates.

The original joint statement, published in January 2016, was the major recommendation from a summit hosted at The University of Texas MD Anderson Cancer in November 2015, which brought together experts from the NCI, CDC, American Cancer Society, and more than half of the NCI-designated cancer centers.

The updated statement is the result of discussions from the most recent summit, hosted this past summer by The Ohio State University Comprehensive Cancer Center. Nearly 150 experts from across the country gathered in Columbus to present research updates and plan future collaborative actions across NCI-designated cancer centers.

 

“This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.”

January, 2017|Oral Cancer News|

Immunotherapies Form New Frontier in Treating Head and Neck Cancers

Source: OncLive.com

Date: January 2nd, 2017

In August 2016, the FDA approved pembrolizumab (Keytruda) for patients with platinum-refractory squamous cell carcinoma of the head and neck (SCCHN).1 Not only was it the first immunotherapy approved for head and neck cancer (HNC), but it marked the first new drug approval for HNC in the United States in 20 years.

“Now we have an agent that really changes the paradigm—a new class of treatment—and we are seeing amazing benefit in some patients,” said Tanguy Seiwert, MD, during an OncLive Peer Exchange® panel held during the 2016 European Society for Medical Oncology (ESMO) Annual Meeting.

Less than a month later, the menu of immunotherapy options expanded as the FDA approved nivolumab (Opdivo) for the treatment of patients with recurrent or metastatic SCCHN with disease progression on or after a platinum-based therapy.

During the Peer Exchange, the panelists provided an overview of the immunotherapy terrain in HNC, a discussion that was filled with considerable hope and excitement. “When we try immunotherapies in the second-line setting, we see objective responses—sometimes deep, clinically meaningful, extremely durable responses—and we’re beginning to think that maybe, on some occasions, we may be able to cure patients with relapsed metastatic head and neck cancer,” said Kevin Harrington, MD, PhD. This is especially remarkable since such patients have generally had a survival of ≤1 year.

The panelists concurred that the care of patients with HNC will evolve significantly over the next 5 to 10 years, as the tip of the immunotherapy iceberg is just starting to be scratched. During the Peer Exchange, they provided a rationale for using immunotherapies in HNC, including human papillomavirus (HPV)-positive and HPV-negative disease; outlined key immunotherapy studies; and offered their thoughts on the future of immunotherapies in HNC, including use of biomarkers to guide therapy and the opportunity to improve response by using combination treatments.

“Next-generation sequencing efforts are beginning to shed light on the hidden complexities of these tumors, leading to the identification of multiple molecular subtypes,” said Ezra Cohen, MD, who served as moderator for the session. “As key differences between tumors, with and without HPV infection, are beginning to emerge, the challenge is to find ways to use this information to personalize treatment for individual patients.”

Rationale for Immunotherapy in HNC

In patients with locally advanced HNC, HPV status has generally determined outcomes, with HPV-positive patients having a good prognosis and higher likelihood of cure, and HPV-negative patients having a poorer prognosis and a lower likelihood of cure.

However, outcomes with conventional therapy in recurrent metastatic disease have been poor across the board, especially in the setting of platinum- refractory disease, indicating a tremendous unmet need. Before pembrolizumab was approved in this setting, the recommendation was to use a taxane, such as methotrexate or cetuximab (Erbitux), as a single agent, but the outcomes have been unsatisfactory. In contrast, immunotherapy studies have shown promising results in these patients, with HPV-negative patients also benefiting.

“The rationale for [using immunotherapies] for HPV-positive tumors may be the virus, as well as mutations, and for HPV-negative tumors, it’s likely the mutation load,” said Seiwert. He explained that HPV-negative tumors are often smoking-associated tumors and, therefore, have high mutation loads, a factor that has been associated with good response to immunotherapy, whereas HPV-positive tumors resemble melanoma, with significant inflammation, another factor associated with good response.

Although efficacy was found to be the same for HPV-positive and HPV-negative tumors in KEYNOTE-012, which was the study that led to pembrolizumab’s approval for HNC, some CheckMate-141 subanalyses suggest there might be slightly more activity in HPV-positive patients, noted Seiwert.

Despite such findings, he said, “HPV status should not actually dissuade us one way or the other from using immunotherapy—it’s clearly active in both HPV-negative and HPV-positive tumors.” And, as Harrington pointed out earlier in the discussion, since nothing else works well in the second-line setting, “why not try it?”

Key Pembrolizumab Studies

The panelists proceeded to provide an overview of several instrumental pembrolizumab studies, including the KEYNOTE-012 expansion study and KEYNOTE-055 studies, and of the phase III CheckMate-141 study, which paved the way for nivolumab’s approval.2-4 They also discussed a subanalysis of CheckMate-141 presented at ESMO that demonstrated good patient-reported outcomes following nivolumab therapy, lending further support to its use in SCCHN.5

KEYNOTE-012 Expansion Study

The phase Ib KEYNOTE-012 expansion study administered 200 mg of pembrolizumab intravenously once every 3 weeks to 132 patients with recurrent or metastatic SCCHN, irrespective of their programmed death-ligand 1 (PD-L1) or HPV status.2 Primary endpoints included overall response rate (ORR), and safety and secondary endpoints included progression-free survival (PFS), overall survival (OS), and PD-L1 expression’s impact on response.

Pembrolizumab was well tolerated, and yielded a clinically meaningful ORR with evidence of durable responses; median duration of response was not reached. The ORR was 18% by central imaging vendor review and 20% by investigator analysis. A statistically significant increase in ORR was observed for PD-L1–positive versus PD- L1–negative patients (22% vs 4%, respectively; P = .021).

At 6 months, PFS and OS rates were 23% and 59%, respectively. “And we have patients living far beyond what we usually expect for metastatic disease…we now have patients who have completed 2 years of treatment in a setting with a median life expectancy of about 6 months,” revealed Seiwert, who is involved with the study.

Pembrolizumab was also well tolerated. Grade ≥3 events occurred in 9% of patients. “[This is] within the range of toxicities that we have seen in other studies,” said Viktor Grünwald, MD. “Because we’re approaching a very sick and morbid patient population, we might expect different toxicity outcomes, so I think it’s very reassuring that we’re seeing the same amount of toxicity as in other studies,” he explained.

While checkpoint inhibitors are generally well tolerated and have favorable toxicity profiles, the panelists warned that severe side effects can occur and careful patient monitoring is required. A key concern they discussed is pneumonitis.

“Although it only occurs in about 1% to 2% of patients, you must screen for it because it’s life threatening,” said Seiwert. “If somebody says, ‘I am short of breath’ or ‘I have a little bit of a cough,’ I scan them right away to look for it,” he said, explaining that immediate treatment with high-dose steroids is warranted.

KEYNOTE-055 Preliminary Results

KEYNOTE-055 enrolled 172 patients with recurrent or metastatic SCCHN to receive pembrolizumab 200 mg every 3 weeks after progression on platinum plus cetuximab. The preliminary analysis, which reported on 92 evaluable patients, was initially presented at the 2016 American Society of Clinical Oncology (ASCO) Annual Meeting.3 Primary endpoints include ORR and safety.

As with KEYNOTE-012, pembrolizumab was found to be well tolerated and to have significant antitumor activity, with 17% to 18% response rates. Evaluation of the full study cohort will include analyses of HPV status and response by anatomic site. “I think that’s the story we’re seeing for pembrolizumab in head and neck cancer—patients are already being treated in single-arm clinical studies, which is somewhat unusual, but reflects the speed of knowledge that we’re gaining that is leading to approvals,” said Grünwald.

Nivolumab also had a lower incidence of treatment-related adverse events (TRAEs) than IC. Any grade TRAEs occurred in 59.3% and 77.5% of patients on nivolumab or IC, respectively. Grade 3/4 TRAEs occurred in 13.6% and 35.1% of patients, respectively, indicating the treatment is well tolerated, which also translated to improvements in quality of life in the patient-reported outcomes study.5

“A very detailed analysis of patient-reported outcomes using 3 well-validated questionnaires showed nivolumab was able to maintain good patient-re- ported outcomes in terms of their quality of life, their functioning, and their symptom scores, whereas IC showed serious detriment in those scores,” said Harrington.

In the study,5 patients treated with nivolumab had delayed worsening of functioning and symptoms compared with IC at approximately 4 months of follow-up, with patients receiving nivolumab reporting longer maintenance of function and less pain, fatigue, and dyspnea on treatment, as compared with those receiving IC.

“So not only do we have clear evidence that these drugs can work in terms of improving survival and delivering meaningful responses, but they do so with fewer episodes of treatment-related toxicity and disease-associated morbidity,” said Harrington.

Future of Immunotherapy in HNC

The panelists noted that use of biomarkers and combination therapies are key areas of future development for HNC. Both areas are already being examined in clinical trials and have relevance across the vast HNC spectrum, from those with minimal disease to those with previously treated advanced disease, potentially offering a curative pathway to more patients.

“It’s fantastic to have drugs that work in second-line relapsed metastatic or first-line metastatic setting, but what I want and what patients want is to be cured at the time they first present with their disease so they never have treatment in relapsed metastatic setting,” said Harrington.

Biomarkers

Although biomarkers such as PD-L1 expression are already being used and can help identify patients who are more likely to respond, high PD-L1 expression does not guarantee response, nor does no or low PD-L1 expression ensure lack of response or lack of durable response.

Subsequently, use of pembrolizumab and nivolumab is without use of this biomarker for patient selection. “While [a PD-L1 assay] can help inform patients of their likelihood to respond, it is not an assay that can select patients,” said Seiwert, who is working to identify novel biomarkers.

“I’ve been involved in looking at a novel biomarker called interferon gamma signature, which can be assayed quite easily with a rapid turn-around, and seems to perform somewhat better than PD-L1 expression,” said Seiwert. “It seems to have a high negative predictive value, and it may eventually allow us to exclude some patients who have no chance of having benefit, but it needs further validation.” He said that other biomarkers are also under investigation, including mutational load, immunogenic mutations, and dynamic biomarkers, but all are still experimental.

“What we really need is a biomarker that would predict progressive disease,” said Grünwald. “To me, that would be much more usable than an assay that just allows us to say to patients ‘your chance of response is 30%.’ I see biomarkers as having the potential to guide development of treatment algorithms,” he said.

Combinations

Currently, PD-L1–targeted agents have seen the greatest development, and studies are starting to suggest that response with these agents can be enhanced when they are combined with other treatments, including chemotherapy, CTLA-4 blockade, and radiotherapy. “About 70% of HNCs have some level of PD-L1 expression—some level of inflammation—but we only see responses in 15% to 18% of patients, so the pool of patients who might benefit from combinations is huge,” said Seiwert.

He noted that the melanoma and lung cancer settings have already shown combining PD-1 inhibitors with chemotherapy or a second checkpoint inhibitor to be particularly promising in the front line, and he suspects one or both combinations will eventually receive approval in these settings and warrant serious investigation for patients with SCCHN.

“Some of our patients do not benefit from a checkpoint inhibitor, and we can’t identify these patients in advance, but giving them chemotherapy might buy us time,” he said. “It’s almost like a pharmacodynamic effect, where we have more time for the immunotherapy to work, and maybe, also make the immune system stronger and expose antigens.”

In the locally advanced setting, animal studies have shown promise combining chemoradiotherapy with immunotherapy, but results of a small study presented at ESMO revealed some dosing challenges in humans.6

In the study, 18 patients with various forms of intermediate- or high-risk SCCHN received ipilimumab, an anti–CTLA-4 antibody, in addition to standard intensity-modulated radiotherapy with cetuximab. Dermatologic immune-related adverse events limited dosing. “There are some safety hints that it may not be a piece of cake getting through radiotherapy, and maybe cetuximab might not be the optimal part now, but I think there is still a lot of promise combining radiochemotherapy with immunotherapy,” said Grünwald. “It could be a future way in how we successfully treat early forms of localized SCCHN.”

Combining checkpoint inhibition with radiation is another intriguing combination, and one that has the potential to act like an in situ vaccination that can lead to abscopal responses (ie, responses at distant sites), noted Harrington, something he has, thus far, only observed rarely with radiation.

“The idea behind combining checkpoint inhibition and radiation is that we could use the confluence of the two different mechanisms to make abscopal responses more predictable and more effective at a distant site, while engendering an immunologically relevant response that allows us to treat macroscopic metastatic disease while also getting rid of micrometastatic disease that could lead to metastatic failure,” he said.

Although immunotherapy combinations are showing promise in SCCHN and other cancers, the panelists warned that they should only be attempted as part of clinical trials. “There are still a lot of question marks about combinations, so they must be done as part of a clinical trial,” said Seiwert. Not only are toxicities and immunosuppressive effects best managed in clinical trials, but trials are essential in advancing these therapies and identifying the next breakthroughs in the field, he said.

 

“This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.”

January, 2017|Oral Cancer News|

We Now Know Exactly How Many DNA Mutations Smoking Causes

Every 50 cigarettes you smoke gives you one extra DNA mutation per lung cell.

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Source: The Verge
Author: James Vincent

A common tactic for people trying to give up smoking is to quantify exactly how much damage — financial or physical — each cigarette or pack of cigarette does. How much does smoking cost you per month, for example, or how much shorter is your life going to be for each drag you take? Well, a new study into the dangers of smoking now lets us measure this damage right down to the number of mutations in your DNA.

A research team led by scientists from Los Alamos National Laboratory compared tissue samples from 1,063 non-smokers and 2,490 smokers, examining each individual’s DNA to look for mutations. They found that for every 50 cigarettes smoked, there is one extra DNA mutation for each cell in the lungs. Over the course of a year, this means that someone who smokes a pack a day (20 cigarettes) has 150 extra mutations per cell in the lung, 97 per larynx cell, 23 per mouth cell, 18 per bladder cell, and six per liver cell.

These changes to the cells aren’t dangerous in themselves, but each one has the potential to turn into a cancerous growth. “Smoking is like playing Russian roulette: the more you play, the higher the chance the mutations will hit the right genes and you will develop cancer,” Ludmil Alexandrov, the co-lead author of the study, told the New Scientist. “However, there will always be people who smoke a lot but the mutations do not hit the right genes.”

The reason for all these extra mutations is found in tobacco smoke — a substance that contains some 7,000 different chemicals, over 70 of which are known to cause cancer. How exactly different types of cell mutations lead to cancer is less clear, and the team from Los Alamos are hoping next to drill down further into this line of research and find out the probabilities that any individual DNA mutation will turn into cancer.

The good news for smokers, though, is that it’s never too late to quit. Although smoking causes regular DNA mutations, as soon as people give up cigarettes, the mutations stop too. One UK study from 2004 found that those who quit smoking at age 30 nearly eliminate the risk of dying prematurely, while those who quit at 50 halve it. For people trying to give up, those are certainly some more comforting odds.

 

This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

November, 2016|Oral Cancer News|