alcohol

Say No to Glow: Reducing the Carcinogenic Effects of ALDH2 Deficiency

Source: blogs.plos.org
Author: Catherine Chang et al.

Turning red after consuming alcohol may seem like a mere social inconvenience. Yet, behind this red complexion lies a far more serious problem. ALDH2 deficiency, more commonly known as Alcohol Flushing Syndrome or Asian Glow, is a genetic condition that interferes with the metabolism of alcohol. As a result, people with ALDH2 deficiency have increased risks of developing esophageal and head and neck cancers . Globally, this deficiency affects 540 million people — 8% of the world population. In East Asia (which includes Japan, China, and Korea), this is a much bigger problem, where 36% of the population is affected [1]. In our home, Taiwan, approximately 47% of the population carries this genetic mutation — the highest percentage in the world [2]!

Normally, ethanol is first converted to acetaldehyde (a toxic intermediate) by the enzyme alcohol dehydrogenase (ADH). A second enzyme, aldehyde dehydrogenase 2 (ALDH2), then converts toxic acetaldehyde into acetate, a compound which can be safely metabolized in the body. For people who carry wild type ALDH2*1, acetaldehyde can be broken down quickly. People with ALDH2 deficiency, however, have a point mutation which leads to the less efficient mutant ALDH2*2 [3], [4]. Enzymatic activity in ALDH2-deficient individuals can be as low as 4% compared to wild type [4], [5], [6], [7]. As a result, acetaldehyde accumulates and induces an inflammatory response that causes the skin to flush after drinking alcohol [8]. Turning red is the most obvious result of ALDH2 deficiency, but symptoms also include headaches, dizziness, hypotension, and heart palpitations [5], [9].

Acetaldehyde accumulates in ALDH2-deficient individuals. Ethanol is first converted to a toxic intermediate, acetaldehyde, by ADH, then converted to acetate by wild type ALDH2*1. The mutant form, ALDH2*2, cannot fully convert acetaldehyde into acetate, and toxic acetaldehyde accumulates as a result.

For people who are ALDH2-deficient and drink, acetaldehyde can accumulate to toxic levels. The International Agency for Research on Cancer classifies acetaldehyde associated with alcohol consumption as a Group 1 carcinogen [10]. Acetaldehyde levels over 50 μM are considered toxic and cause mutations in DNA, and studies show that the strongest effects are seen in the mouth [11], [12]. After consuming roughly 2 to 3 servings of alcohol (0.5-0.6 g alcohol/kg body weight), salivary acetaldehyde levels in ALDH2-deficient individuals reached over 100 μM, compared to normal levels of <20 μM without drinking [13], [14], [15], [16]. Because of the increased salivary acetaldehyde, people with ALDH2 deficiency are 2 to 8 times more likely to develop head and neck cancers (including oral cancer, pharyngeal cancer, laryngeal cancer, etc.), and 2 to 12 times more likely to develop esophageal cancer compared to people with normal ALDH2*1 [17-25].

Our ALDH2*1 probiotic candy significantly reduces acetaldehyde levels in simulated oral conditions. (A) The conversion of acetaldehyde to acetate by ALDH2 uses NAD+ and produces NADH. (B) Experimental setup. The candies were dissolved, the probiotic (Nissle) was lysed to release ALDH2 enzymes, and the supernatant was placed into artificial saliva. NADH concentration was measured by taking absorbance readings at 340 nm. (C) Enzymatic activity of ALDH2*1 and ALDH2*2 from the probiotic candies. A negative control of candy without Nissle was also included (gray). Under these conditions, the ALDH2*1 candies metabolized significantly more acetaldehyde compared to both the ALDH2*2 candies and the negative control. Error bars represent standard error.

To directly address the increased esophageal and head and neck cancer risks, we developed a probiotic (E. coli Nissle 1917) candy carrying recombinant human ALDH2*1 to maintain normal acetaldehyde levels in the mouths of ALDH2-deficient individuals. We tested the candy’s ability to break down acetaldehyde by measuring NADH, a byproduct of acetaldehyde metabolism. In simulated oral conditions, we observed a significant decrease in acetaldehyde levels when we added the contents of our ALDH2*1 candy (compared to the mutant ALDH2*2 or control candy). Through mathematical modeling, we also determined the exact amount of recombinant ALDH2*1 needed in each piece of candy. Our modeling shows that if a consumer eats our candy while drinking, the released ALDH2*1 will be able to combat the high salivary acetaldehyde levels and match the normally low levels found in wild type individuals.

 

Our final product, an ALDH2*1 probiotic candy!

Nearly half of Taiwan’s population is ALDH2 deficient. To combat the increased cancer risks associated with this deficiency, we developed and tested a method to regulate acetaldehyde levels in ALDH2-deficient individuals.

The TAS_Taipei iGEM Team have produced a full research article detailing their project. You can access that article here.

Note:Please note that the team’s full research article has not been peer-reviewed.

Authors: Catherine Chang, Tim Ho, Iris Huang, Justin Wu

References:
1. Brooks PJ, Enoch MA, Goldman D, Li TK, Yokoyama A. (2009). The alcohol flushing response: an unrecognized risk factor for esophageal cancer from alcohol consumption. PLoS Med. 24;6(3):e50.

2. Chang JS, Hsiao JR, Chen CH. (2017). ALDH2 polymorphism and alcohol-related cancers in Asians: a public health perspective. J Biomed Sci. 24(1):19.

3. Larson HN, Weiner H, Hurley TD. (2005). Disruption of the Coenzyme Binding Site and Dimer Interface Revealed in the Crystal Structure of Mitochondrial Aldehyde Dehydrogenase “Asian” Variant. J Biol Chem. 280(34):30550-6.

4. Farrés J, Wang X, Takahashi K, Cunningham SJ, Wang TT, Weiner H. (1994). Effects of changing glutamate 487 to lysine in rat and human liver mitochondrial aldehyde dehydrogenase. A model to study human (Oriental type) class 2 aldehyde dehydrogenase. J Biol Chem. 13;269(19):13854-60.

5. Chen CH, Ferreira JCB, Gross ER, Mochly-Rosen D. (2014). Targeting Aldehyde Dehydrogenase 2: New Therapeutic Opportunities. Physiol Rev. 94(1):1-34.

6. Zhou J, Weiner H. (2000). Basis for half-of-the-site reactivity and the dominance of the K487 oriental subunit over the E487 subunit in heterotetrameric human liver mitochondrial aldehyde dehydrogenase. Biochemistry. 39(39):12019-24.

7. Gross ER, Zambelli VO, Small BA, Ferreira JCB, Chen CH, Mochly-Rosen D. (2015). A personalized medicine approach for Asian Americans with the aldehyde dehydrogenase 2*2 variant. Annu Rev Pharmacol Toxicol. 55:107-27.

8. Ijiri I. (1999). [Biological actions of acetaldehyde]. Nihon Hoigaku Zasshi. 53(3):285-95.

9. Lai CL, Yao CT, Chau GY, Yang LF, Kuo TY, Chiang CP, Yin SJ. (2014) Dominance of the inactive Asian variant over activity and protein contents of mitochondrial aldehyde dehydrogenase 2 in human liver. Alcohol Clin Exp Res. 2014 Jan;38(1):44-50.

10. International Agency for Research on Cancer. (n.d.). List of Classifications, Volumes 1-122. Retrieved from https://monographs.iarc.fr/list-of-classifications-volumes/ .

11. Yamaguchi H, Hosoya M, Shimoyama T, Takahashi S, Zhang JF, Tsutsumi E, Suzuki Y, Suwa Y, Nakayama T. (2012). Catalytic removal of acetaldehyde in saliva by a Gluconobacter strain. J Biosci Bioeng. 114(3):268-74.

12. Kocaelli H, Apaydin A, Aydil B, Ayhan M, Karadeniz A, Ozel S, Yilmaz E, Akgün B, Eren B. (2014) Evaluation of potential salivary acetaldehyde production from ethanol in oral cancer patients and healthy subjects. Hippokratia. 18(3): 269–274.

13. Homann N, Jousimies-Somer H, Jokelainen K, Heine R, Salaspuro M. (1997a). High acetaldehyde levels in saliva after ethanol consumption: methodological aspects and pathogenetic implications. Carcinogenesis. 18(9):1739-43.

14. Yokoyama A, Tsutsumi E, Imazeki H, Suwa Y, Nakamura C, Mizukami T, Yokoyama
(2008). Salivary acetaldehyde concentration according to alcoholic beverage consumed and aldehyde dehydrogenase-2 genotype. Alcohol Clin Exp Res. 32(9):1607-14.

15. Lachenmeier DW, Monakhova YB. (2011). Short-term salivary acetaldehyde increase due to direct exposure to alcoholic beverages as an additional cancer risk factor beyond ethanol metabolism. J Exp Clin Cancer Res. 30 (3).

16. Stornetta A, Guidolin V, Balbo S. (2018). Alcohol-Derived Acetaldehyde Exposure in the Oral Cavity. Cancers (Basel). 10(1). pii: E20.

17. Chao YC, Wang LS, Hsieh TY, Chu CW, Chang FY, Chu HC. (2000). Chinese Alcoholic Patients with Esophageal Cancer are Genetically Different from Alcoholics with Acute Pancreatitis and Liver Cirrhosis. Am J Gastroenterol. 95(10):2958-2964.

18. Yang SJ, Wang HY, Li XQ, Du HZ, Zheng CJ, Chen HG, Mu XY, Yang CX. (2007). Genetic Polymorphisms of ADH2 and ALDH2 Associated with Esophageal Cancer Risk in Southwest China. World J Gastroenterol. 13(43):5760-5764.

19. Yokoyama A, Muramatsu T, Omori T, Yokoyama T, Matsushita S, Higuchi S, Maruyama K, Ishii H. (2001). Alcohol and Aldehyde Dehydrogenase Gene Polymorphisms and Oropharyngolaryngeal, Esophageal and Stomach Cancers in Japanese Alcoholics. Carcinogenesis. 22(3): 433-439.

20. Matsuo K, Hamajima N, Shinoda M, Hatooka S, Inoue M, Takezaki T, Tajima K. (2001). Gene-Environment Interaction between an Aldehyde Dehydrogenase-2 (ALDH2) Polymorphism and Alcohol Consumption for the Risk of Esophageal cancer. Carcinogenesis. 22(6): 913-916.

21. Cui R, Kamatani Y, Takahashi A, Usami M, Hosono N, Kawaguchi T, Tsunoda T, Kamatani N, Kubo M, Nakamura Y, Matsuda K. (2009). Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhance esophageal cancer risk. Gastroenterology. 2009 Nov;137(5):1768-75.

22. Lee CH, Lee JM, Wu DC, Goan YG, Chou SH, Wu IC, Kao EL, Chan TF, Huang MC, Chen PS, Lee CY, Huang CT, Huang HL, Hu CY, Hung YH, Wu MT. (2007). Carcinogenetic impact of ADH1B and ALDH2 genes on squamous cell carcinoma risk of the esophagus with regard to the consumption of alcohol, tobacco and betel quid. Int J Cancer. 122(6):1347-56.

23. Wu M, Chang SC, Kampman E, Yang J, Wang XS, Gu XP, Han RQ, Liu AM, Wallar G, Zhou JY, Kok FJ, Zhao JK, Zhang ZF. (2013). Single nucleotide polymorphisms of ADH1B, ADH1C and ALDH2 genes and esophageal cancer: a population-based case-control study in China. Int J Cancer. 132(8):1868-77.

24. Huang CC, Hsiao JR, Lee WT, Lee YC, Ou CY, Chang CC, Lu YC, Huang JS, Wong TY, Chen KC, Tsai ST, Fang SY, Wu JL, Wu YH, Hsueh WT, Yen CJ, Wu SY, Chang JY, Lin CL, Wang YH, Weng YL, Yang HC, Chen YS, Chang JS. (2017). Investigating the Association between Alcohol and Risk of Head and Neck Cancer in Taiwan. Sci Rep. 7(1):9701.

25. Hiraki A, Matsuo K, Wakai K, Suzuki T, Hasegawa Y, Tajima K. (2007). Gene–gene and gene–environment interactions between alcohol drinking habit and polymorphisms in alcohol-metabolizing enzyme genes and the risk of head and neck cancer in Japan. Cancer Science. 98: 1087-1091.

September, 2019|Oral Cancer News|

Twitter lends insight to HPV-associated oral cancer knowledge

Source: www.oncnursingnews.com
Author: Brielle Benyon

The incidence of human papillomavirus (HPV)-associated oral cancer has risen in recent years, and the virus has now surpassed tobacco and alcohol use as the leading cause of the disease. In fact, while the HPV vaccine is typically associated with preventing cervical cancer, there have been more cases of HPV-associated oral cancer than there have been cervical cancer.1

While the link between oral cancer and HPV may be well-known to healthcare professionals, researchers at Howard University recently took to Twitter to get a glimpse into the public’s knowledge about the topic.

“By looking at the social media data, we wanted to know what people are hearing about oral cancer – especially HPV-caused oral cancer,” study co-author Jae Eun Chung, PhD, associate professor in the Department of Strategic, Legal & Management Communication at Howard University, said. “We wanted to see what the gaps are between the knowledge of the healthcare professionals and the public.”

The researchers collected 3,229 unique tweets over the course of 40 weeks using search terms such as “HPV or papilloma” and “mouth or oral or throat or pharyngeal or oropharyngeal.” They then used a program called nVivo 12.0 to conduct a content analysis that looked at certain phrasing, terms, and themes that commonly appeared.

More than half (54%; 1679 total) of the tweets had information about prevention, while 29% (910) were about the causes of oral cancer. Far fewer tweets were about treatment (5%; 141), diagnosis (3%; 97), symptoms (1%; 42), and prognosis (1%; 25).

Interestingly, the researcher discovered a prominence on the risk of HPV-associated oral cancer in men, with tweets that referred to males outnumbering tweets that referred to females in a 3:1 ratio. Also, the most popular hashtag used in the dataset was #jabsfortheboys, appearing in 89 tweets.

“There was a heavy emphasis on the risk of HPV-associated (oropharyngeal cancer) among men, which is different than what we see with HPV vaccination among girls,” Chung said. “That was very positive news to us, because HPV-associated (oral cancer) rates are higher among the male population and HPV vaccination rates are higher among girls.”

While spreading HPV vaccination and oral cancer is important on a global scale, the United States might have some catching up to do, as the 5 most mentioned Twitter users discussing the topic were located outside of the US–1 in New Zealand, 2 in Australia, and 2 in the United Kingdom.

“That’s kind of sad, because there are more Twitter users from the United States than from any other country,” Chung said.

Ultimately, Chung explained, these findings outlined an area where the country can benefit from more education and social media campaigns.

“In conclusion, this study provides some insight as to how the public makes sense of HPV-associated oral cancer,” she said. “More education and campaigns are needed, and US residents can benefit from more active involvement of US-based health education.”

Reference
1. Chung JE, Mustapha I, Gu X, Li J. Understanding public perception about human papillomavirus (HPV)-associated oropharyngeal cancer (OPC) through Twitter. Presented at: D.C. Health Communication Conference; Fairfax, Virginia; April 26-27, 2019.

‘Whitish patch’: increase in oral dysplasia in young adults

Source: www.medscape.com
Author: Kristin Jenkins

Most 8-year-olds with a wiggly tooth expect the Tooth Fairy to tuck some money under their pillow. In the case of one little Canadian boy, his wiggly tooth got him an incisional biopsy, a diagnosis of oral squamous cell carcinoma (OSCC), a partial maxillectomy, and a defect that was closed with local advancement flaps.

“This was the most unusual case we’ve seen,” said Marco A. Magalhaes, DDS, PhD, assistant professor of oral pathology and oral medicine in the Faculty of Dentistry at the University of Toronto in Ontario, Canada.

“OSCC predominantly affects patients 40 years of age and older,” write Magalhaes and colleagues in a case study report published in November 2016 in Oral Surgery Oral Medicine Oral Pathology Oral Radiology. “It is extremely rare in patients younger than 20 years of age.”

The clinical, radiographic, and histologic findings in this young patient were distinctive. Although the diagnosis and treatment were challenging, the clinical course was favorable at follow-up, the authors said. This case illustrates the fact that even pediatric patients can be at risk for OSCC. Magalhaes said that he and other dentists are concerned about the rising number of OSCC cases in patients who are in their 20s and 30s. These patients have no known risk factors and are often without symptoms. Many are diagnosed with high-grade oral epithelial dysplasia (OED) that rapidly progresses to cancer, Magalhaes told Medscape Medical News.

“When you look at the distribution of cases of oral dysplasia or carcinoma, you see that they tend to occur in older males in their 50s with a history of smoking and a low risk of [malignant] transformation,” he explained.

“What we are seeing in practice, however, is a lot of dysplasia in younger individuals without risk factors. These cases are the most concerning,” he commented.

At the time of presentation, patients may say, “I’m not sure why I’m here, but I saw a whitish patch in my mouth,’ ” said Magalhaes.

Others may be asymptomatic and have “absolutely no concerns,” he pointed out. “Unfortunately, this story is becoming more common.”

Nonhealing Sore in Mouth
Oral cancer usually presents as a nonhealing sore that is often painful. OED can be more difficult to diagnose because it manifests as a faint whitish or red patch anywhere in the oral cavity.

The gums, tongue, soft palate, and the inside of the cheeks can be affected. Most commonly, the floor of the mouth is affected.

Currently, Magalhaes and colleagues are conducting a review of more than 3000 cases of dysplasia in Ontario to determine group distribution, pattern, and, potentially, risk factors.

Although oral cancer has multiple causal factors, Magalhaes noted that smoking is “by far” the most significant and well-recognized risk factor. Heavy alcohol consumption is also a well-known risk factor. Human papillomavirus accounts for 5% to 6% of oral cancers, he noted.

A regular dental checkup is important, and early detection is critical for survival, Magalhaes emphasized.

For high-grade OED, the risk for progression to frank carcinoma is 18% to 30%, he noted. For moderate-grade OED, the risk is 10% to 15%, and for low-grade oral dysplasia, it is 1% to 4%.

“Physicians should reinforce to their patients the importance of dental checkups at least twice a year,” Magalhaes said. “This alone would increase the chances of early lesion detection.”

Review of Biopsy Specimens
A recent review of 63,483 biopsy specimens submitted by dentists to the Toronto Oral Pathology Service (TOPS) primarily from 2005 through 2015 bears this out. The review, led by Magalhaes, was published online April 25 in the Journal of the American Dental Association.

TOPS is operated by the Faculty of Dentistry at the University of Toronto and is one of the largest oral pathology services in Canada, noted Magalhaes, who works there.

The results show that generally, the incidence of OED (2679 cases) and OSCC (828 cases) in Ontario remained stable from 2005 to 2015. It also showed that when it comes to early detection of oral lesions, dentists have seriously stepped up their game. During the 10-year period, detection of OED by dentists increased 3.8-fold. The number of OSCC cases they detected doubled. OSCC accounted for about 10% of all oral cancers in the province in 2015.

“These biopsy specimens were submitted mostly by specialists in oral and maxillofacial surgery, periodontics, endodontics, and oral and maxillofacial pathology and oral medicine,” the authors write.

“However,” they continue, “informal discussion with clinicians who submitted the biopsy specimens has indicated that the initial detection of the mucosal abnormality was often accomplished by the general practice dentist, dental hygienist, or both, who referred the patient to specialists for evaluation, biopsy, and case management.”

The study also shows that potentially malignant lesions made up 4.68% of all cases and that OED accounted for 90%. An increased awareness of early lesions with malignant potential can result in early diagnosis and decreased morbidity and mortality from OSCC, the researchers say.

Both dentists and patients appear to be maintaining a high index of suspicion, according to Magalhaes.

“Dentists are increasingly aware of the presence of these early lesions and are either biopsying them themselves or sending them for biopsy,” he explained. “We’ve also noticed that patients are more aware of mouth changes and are asking dentists about lesions that they have identified.”

During a routine dental checkup, an examination for early signs of oral cancer is performed. This includes inspection of the lymph glands in the neck and a check of all mucosal surfaces in the oral cavity for signs of ulcers or red or white patches.

The severity of OED determines treatment, noted Magalhaes. In cases of low-grade OED, the lesion is monitored every 6 months, and a repeat biopsy is performed if warranted. A high-grade OED that is accessible and relatively well contained is treated with complete surgical excision. This is followed by monitoring two or three times a year. When the lesion is diffuse, affects 60% of the oral cavity, or extends into areas that are difficult to access without significant morbidity, the patient is closely monitored with examinations four times a year, he said.

Source:
J Am Dent Assoc. Published online April 25, 2019. Abstract

Oral Surg Oral Med Oral Pathol Oral Radiol. 2016 Nov;122:e179-e185. Full text

April is Oral Cancer Awareness Month: Self-exams, early detection can save lives

Source: www.prnewswire.com
Author: press release

Because early detection of oral cancer offers a greater chance of a cure, the American Association of Oral and Maxillofacial Surgeons (AAOMS) is reminding the public during Oral Cancer Awareness Month of the importance of performing monthly self-exams.

AAOMS promotes self-exams and screenings every April with the Oral Cancer Foundation, which predicts about 53,000 new cases of oral cancer will be diagnosed in 2019 in the United States – leading to more than 9,000 deaths.

“A monthly self-exam takes only minutes and could potentially save your life,” said AAOMS President A. Thomas Indresano, DMD, FACS. “If done on a regular basis, you’re increasing the chances of identifying changes or new growths early. The survival rate for oral cancer is between 80 and 90 percent when it’s found at early stages of development.”

Oral and maxillofacial surgeons (OMSs) encourage a six-step oral cancer self-exam that involves looking and feeling inside the mouth for suspicious sores and feeling the jaw and neck for lumps. Using a bright light and a mirror:

  1. First remove any dentures.
  2. Look and feel inside the lips and the front of the gums.
  3. Tilt the head back to inspect and feel the roof of the mouth.
  4. Pull the cheek out to inspect it and the gums in the back.
  5. Pull out the tongue and look at its top and bottom.
  6. Feel for lumps or enlarged lymph nodes in both sides of the neck, including under the lower jaws.

Oral cancer symptoms may include one or more of the following if they are persistent and not resolving:

  • Red, white or black patches in the soft tissue of the mouth.
  • A sore in the mouth that fails to heal within two weeks and bleeds easily.
  • An abnormal lump or hard spot in the mouth.
  • A painless, firm, fixated mass or lump felt on the outside of the neck that has been present for at least two weeks.
  • Difficulty in swallowing, including a feeling food is caught in the throat.
  • Chronic sore throat, hoarseness or coughing.
  • A chronic earache on one side.

The risk factors for oral cancer include smoking and tobacco use, alcohol consumption and the human papillomavirus (HPV).

“About 25 percent of oral cancer patients have no known risk factors,” Dr. Indresano said. “It’s important that everyone perform a monthly self-exam. And if you have any of the symptoms for more than two weeks, promptly contact an oral and maxillofacial surgeon. OMSs are experts in diagnosing and surgically treating oral cancer.”

April, 2019|Oral Cancer News|

Early detection, treatment helps conquer oral cancer

Source: www.newsbug.info
Author: Bob Moulesong

According to the Oral Cancer Foundation, almost 50,000 cases of oral cancer will be diagnosed in the U.S. in 2018. The American Cancer Society reports that 10,000 people will die from the disease this year. Half of all people diagnosed with oral cancer will be alive in five years, according to both sources.

While those are disquieting statistics, Region physicians say routine checkups and early diagnosis improve the odds.

Oral cancer
Oral cancer includes cancers of the lips, tongue, cheeks, floor of the mouth, hard and soft palate, sinuses, saliva glands, and throat.

“People we see usually come to us for a lesion or ulcer found in the mouth or throat,” says Dr. Akta Kakodkar, an ear, nose and throat specialist with Community Healthcare System. “Some of them experience no pain but notice a growth or patch of discolored tissue in their mouth, cheek or gum.”

Kakodkar, who with her husband and fellow Community ENT physician, Dr. Kedar Kakodkar, treats oral cancer patients, is quick to point out that not every lesion, ulcer or mouth sore is cancer.

“We see hundreds of nervous patients who have bacterial or fungal infections,” she says. “Treatment with antibiotics or antifungal medications clear up many of these lesions. There are also many white and red patches that clear up on their own.”

The only way to know is a thorough examination.

Types and risk factors
“Most cases of oral cancer are linked to use of tobacco, alcohol and betel nuts, or infection with HPV,” Kakodkar says. “There are major risks associated with tobacco use, whether it’s smoking or chewing.”

There are two main types of oral cancer. Most prevalent is squamous cell carcinoma, accounting for more than 90 percent of cancers that occur in the oral cavity and oropharynx. Slow-growing verrucous carcinoma makes up more than 5 percent of oral cavity tumors.

First steps
Kakodkar says prevention is the best defense. “Your primary care physician may examine your head, neck, mouth and throat for abnormalities,” she says.

Self-exam may uncover a lesion or sore. “Remember, many of these are very treatable and are not cancer,” Kakodkar says. “But don’t wait. Cancer never goes away by itself.”

When Kakodkar discovers a suspicious lesion, she recommends a biopsy: “Depending on several variables, we might do the biopsy in clinic, or we may do it in a hospital setting.”

Once the results return, a plan of action can be established. “Usually, the next steps include imaging, such as a CT scan,” she says. “We also order a PET scan, which tells us what stage the cancer is in and whether or not it has spread.”

Treatment
Kakodkar says she prefers to go straight to surgery. “Many oral cancers are still small and local,” she explains. “Removing them completely is the best way to stop the spread of the cancer.”

Depending on the type and stage of the cancer, radiation and/or chemotherapy may be used.

“I want people to know that surgery for oral cancer is frequently a simple procedure,” Kakodkar says. “Oral cancer is frequently found early due to its visibility. Almost 90 percent of cancer patients in stage 1 or 2 recover and survive.”

A dental checkup
“Oral cancer screening is crucial during a dental examination,” says Dr. Ami Pandya, dentist at Family Dental Care in Valparaiso. “Recognizing abnormal tissue in a patient’s mouth could indicate precancerous tissues, and when identified early could save your life.”

A dentist will perform a thorough head and neck exam, which includes an oral cancer screening. “Dentists will complete extraoral examinations by palpating your jaw line to feel for any suspicious lumps that are not routinely present in these areas,” Pandya says.

A dentist will examine the intraoral tissues of your mouth and look for any suspicious lesions. “We examine the patient’s tongue, the floor of their mouth, and their gingival tissue,” Pandya says. Red and/or white patches can become cancerous.

Many doctors including Pandya have begun using VELscope, a light-based technology to detect precancerous tissues. It’s a wireless hand-held device that scans tissue, with abnormalities showing up as a dark black color.

“VELscope can detect abnormalities before they have a clinical presentation,” Pandya says. “It’s an incredible aid with oral cancer screening.”

Pandya recommends an annual VELscope examination for low-risk adults. Higher risk patients should get a VELscope exam each appointment.

Under the VELscope, cancer shows up as black, says Dr. Ami Pandya

If the dentist detects an abnormality, he or she informs the patient, noting the size, color and location of the lesion. A two-week follow-up is standard. “Oftentimes, these lesions resolve,” Pandya says. If it doesn’t resolve after two weeks, the patient is referred for further evaluation.

Note: This article originally ran on nwitimes.com.

November, 2018|Oral Cancer News|

Patients with HPV-positive oropharynx cancer should receive chemoradiation

Source: medicalxpress.com
Author: provided by European Society for Medical Oncology

Patients with human papilloma virus (HPV)-positive throat cancer should receive chemoradiotherapy rather than cetuximab with radiotherapy, according to late-breaking research reported at the ESMO 2018 Congress in Munich.

“Many patients have been receiving cetuximab with radiotherapy on the assumption that it was as effective as chemotherapy with radiotherapy and caused less side effects but there has been no head-to-head comparison of the two treatments,” said study author Prof Hisham Mehanna, Chair, Head and Neck Surgery, Institute of Cancer and Genomic Sciences, University of Birmingham, UK.

Throat cancer is rapidly becoming more common in Western countries. For example in the UK, incidence was unchanged in 1970 to 1995, then doubled in 1996 to 2006, and doubled again in 2006 to 2010.The rise has been attributed to HPV, a sexually transmitted infection. Most throat cancer was previously caused by smoking and alcohol and affected 65-70 year-old working class men. Today HPV is the main cause and patients are around 55, middle class, working, and have young children.

HPV-positive throat cancer responds well to a combination of cisplatin chemotherapy and radiotherapy, and patients can survive for 30-40 years, but the treatment causes lifelong side effects including dry mouth, difficulty swallowing, and loss of taste. Patients deemed unable to tolerate chemotherapy, for example because of poor kidney function or older age, receive cetuximab, an epidermal growth factor receptor (EGFR) inhibitor, and radiotherapy.

This study compared side effects and survival with the two treatments in 334 patients with HPV-positive throat cancer enrolled from 32 centres in the UK, Ireland, and the Netherlands. Patients were randomly allocated to radiotherapy and either cisplatin or cetuximab. Eight in ten patients were male and the average age was 57 years.

During the two-year study there were ten recurrences and six deaths with cisplatin compared to 29 recurrences and 20 deaths with cetuximab. Patients on cisplatin had a significantly higher two-year overall survival rate (97.5%) than those on cetuximab (89.4%; p=0.001, hazard ratio [HR] 4.99, 95% confidence interval [CI] 1.70-14.67). Cancer was over three times more likely to recur in two years with cetuximab compared to cisplatin, with recurrence rates of 16.1% versus 6.0%, respectively (p=0.0007, HR 3.39, 95% CI 1.61-7.19).

There were no differences between groups in the overall number of side effects, or of acute or late severe (grade 3-5) toxic events including dry mouth and difficulty swallowing. There were significantly more serious adverse events such as renal and haematological problems with cisplatin than with cetuximab.

Mehanna said: “Cetuximab did not cause less toxicity and resulted in worse overall survival and more cancer recurrence than cisplatin. This was a surprise—we thought it would lead to the same survival rates but better toxicity. Patients with throat cancer who are HPV positive should be given cisplatin, and not cetuximab, where possible.”

Commenting on the study for ESMO, Dr. Branislav Bystricky, Head, Medical and Radiation Oncology Department, University Hospital Trencin, Slovakia, said: “It was believed that cetuximab causes less side effects and was therefore a good option for HPV-positive throat cancer patients who are young and expected to survive for several decades, as well as those less able to tolerate chemotherapy. This study shows that the best treatment choice for patients with HPV-positive throat cancer is cisplatin and radiotherapy. This combination gives ‘double’ the benefit since it is more effective in terms of survival and does not worsen all grade toxicity compared to cetuximab with radiotherapy.”

Bystricky noted that the results were in agreement with interim findings of the US National Cancer Institute’s RTOG 1016 trial, which is scheduled to report this month. He said: “We now have two studies showing that these patients should not be given cetuximab. Future research should examine whether genotyping for the KRAS-variant can select a group of patients that will benefit from cetuximab treatment with radiotherapy.”

October, 2018|Oral Cancer News|

New risk factor for mouth cancer uncovered

Source: www.medicalnewstoday.com
Author: Tim Newman, fact checked by Paula Field

In some regions, mouth cancer incidence has risen. A recent study investigates a new risk factor for mouth cancer. In certain parts of the world, over the past couple of decades, mouth cancer rates have soared. For instance, in the United Kingdom, rates of mouth cancer have increased by 68 percent. They rose from eight cases per 100,0000 in 1992–1995 to 13 cases per 100,000 in 2012–2014.

In the United States, mouth cancer and mortality rates have declined overall. However, when examined at a state level, the data reveal a more complex picture. For instance, mouth cancer deaths have risen significantly in Nevada, North Carolina, Iowa, Ohio, Maine, Idaho, North Dakota, and Wyoming.

Some known risk factors for mouth cancer include smoking tobacco, drinking alcohol, human papillomavirus (HPV), and chewing betel quid, which is a mix of natural ingredients wrapped in a betel leaf that is popular in some parts of Southeast Asia.

In India, mouth cancers are the most common cause of cancer-related deaths in men aged 30–69 years old. Scientists think that chewing betel quid could be responsible for many of these deaths.

New risk factor for mouth cancer
Although scientists have confirmed some risk factors, there is still much to learn about how and why mouth cancer affects certain individuals and not others. Recently, scientists set out to investigate another potential risk factor: air pollution.

The researchers, funded by the Ministry of Science and Technology in Taiwan, published their findings this week in the Journal of Investigative Medicine.

In particular, the team focused on the impact of fine particulate matter, also known as PM2.5. These are particles of liquid or solid matter that measure 2.5 micrometers in diameter or under. Scientists already knew that PM2.5 has a negative impact on cardiovascular and respiratory health, but they wanted to find out whether exposure to higher levels of PM2.5 might also increase mouth cancer risk.

To investigate, they collated information from 482,659 men aged 40 years old or above. All participants had attended health services and given information about smoking and chewing betel quid.

The scientists next gathered data from 66 air quality-monitoring stations across Taiwan. By referring to the participants’ health records, the scientists could estimate each person’s exposure to PM2.5.

Risk increased by 43 percent
The researchers collected the data in 2012–2013. During this time, 1,617 men developed mouth cancer. As expected, both tobacco smoking and chewing betel quid increased mouth cancer risk. After taking a range of influencing factors into account, the scientists demonstrated that exposure to PM2.5 also increased mouth cancer risk.

The scientists compared PM2.5 levels of below 26.74 micrograms per cubic meter (ug/m3) with those above 40.37 ug/m3. They associated the higher levels of PM2.5 with a 43 percent increase in the risk of developing mouth cancer. According to the authors:

“This study, with a large sample size, is the first to associate mouth cancer with PM2.5. […] These findings add to the growing evidence on the adverse effects of PM2.5 on human health.”

Alongside PM2.5’s relationship with mouth cancer, the authors identified a correlation between higher levels of ozone and an increased risk of developing the disease.

The next challenge will be to understand how particulate matter might cause mouth cancer. Although this will require more detailed studies, some theorize that carcinogenic compounds found in PM2.5, including polycyclic aromatic hydrocarbons and heavy metals, might be part of the answer.

Because these particles have such a small diameter, the body absorbs them relatively easily, potentially causing damage as they travel through the body.

However, the authors also remind us to be cautious — this is an observational study, so it cannot definitively prove that pollution causes mouth cancer. Also, it is not clear exactly how much PM2.5 enters the mouth.

This interaction needs further investigation, but the large size of the current study makes their conclusions worthy of follow-up.

October, 2018|Oral Cancer News|

Head and neck cancer: An overview of head and neck cancer

Source: www.curetoday.com
Author: staff

Meryl Kaufman, M.Ed., CCC-SLP, BRS-S, and Itzhak Brook, M.D., M.Sc., board members of the Head and Neck Cancer Alliance, discuss the prevalence of cancers of the head and neck, emphasizing the potential risk factors and importance of prevention.

Transcript:
Meryl Kaufman, M.Ed., CCC-SLP, BRS-S: Welcome to this CURE Connections® program titled “Head and Neck Cancer: Through the Eyes of a Patient.” I’m Meryl Kaufman, a certified speech-language pathologist and founder of Georgia Speech and Swallowing LLC. I am joined today by Dr. Itzhak Brook, a professor of pediatrics and medicine at Georgetown University School of Medicine, who was diagnosed with throat cancer in 2006. Together we will discuss the prevalence of head and neck cancer, what unique challenges patients may face and how one can adjust to life after receiving treatment for their disease. Dr. Brook and I also serve as board members on the Head and Cancer Alliance.

Dr. Brook, let’s talk about head and neck cancer in general. What’s the difference between head and neck cancer associated with the traditional risk factors, such as smoking and drinking, and HPV-related head and neck cancers?

Itzhak Brook, M.D., M.Sc.: The traditional head and neck cancer is related to smoking and alcohol consumption. It’s usually associated with a high rate of laryngeal cancer. And HPV-related cancer is a relatively new arrival on the scene of head and neck cancer, and it’s associated with a condition of infection by a venereal disease. The virus HPV is usually associated with a posterior tongue cancer or an oropharyngeal cancer.

Meryl Kaufman, M.Ed., CCC-SLP, BRS-S: Exactly, yes. So the HPV viruses typically in the oropharynx, the tonsil and the tongue basis are certainly rising in incidence as compared with the traditional head and neck cancers, which are decreasing in incidence. In fact, it’s anticipated that in the year 2020, the HPV-related oropharyngeal cancers are going to surpass HPV-related cervical cancers, which are typically what you think of with the HPV virus. So that is a new patient population, but the good news is that the survival rates are better for the HPV-related head and neck cancers versus the non-HPV-related cancers. Can you speak a little bit about the incidence of the two?

Itzhak Brook, M.D., M.Sc.: The incidence of head and neck cancer is not as high as others like colon cancer, breast cancer in women or lung cancer, but it’s around the ninth or 10th cause of cancer in the world in this country. In countries where there is smoking and alcohol consumption, it’s a higher rate. HPV is usually happening in younger people, in the late 30s or early 40s. And fortunately, we hope that it could be prevented by vaccination. Although it’s approved that it can, it’s not yet available because the incubation period for the cancer, as you may call it, takes 20, 30 years, so we don’t really know. Fortunately, even though HPV is very common, the occurrence of HPV-related cancer is very, very rare.

Meryl Kaufman, M.Ed., CCC-SLP, BRS-S: Correct. In terms of the vaccination for the HPV virus, I agree, the proof certainly isn’t definitively out there yet, but the vaccine protects against the strain of virus that ultimately can lead to head and neck cancer. So the thought is that by preventing the contraction of the virus, hopefully we can also prevent these head and neck cancers, which is why the American Academy of Pediatrics and the CDC (Centers for Disease Control and Prevention) recommend that children between the ages of 11 and 12, female and males, are vaccinated prior to sexual debut in the hopes of preventing these cancers down the road, certainly. So yes, head and neck cancer does account for about 6 percent of all cancers worldwide, with about 500,000 cases worldwide. And in the United States, we anticipate about 65,000 a year, I believe, and they do occur more frequently in men, almost twice as often in men than in women and typically in people over the age of 50 in the traditional head and neck cancers. But certainly, there is a change in that with the introduction of the HPV-related cancers. Can you talk a little bit about prevention in terms of things that we can do to prevent the risky behaviors?

Itzhak Brook, M.D., M.Sc.: Of course, with the traditional cancers, it can be prevented by not smoking or drinking alcohol in high quantities. But there’s the behavioral changes that men and women can change that can reduce the risk of acquiring it. It’s a sexually transmitted disease. Oral sex has been the No. 1 cause, so you think of condoms or men using them also when having oral sex may prevent it.

September, 2018|Oral Cancer News|

With oral cancer on the rise, dentists can play an important role

Source: http://exclusive.multibriefs.com
Author: Tammy Adams

Today’s dental professionals routinely see and deal with many issues and conditions that were not so common just a few short decades ago. For example, there has been a marked increase in the incidence of oral cancer in the United States, sparking the need for regular oral cancer screening as part of a preventive dental checkup. This additional screening is now routinely performed in many dental practices across the nation.

The American Cancer Society estimates that around 50,000 Americans are infected with oral cancer each year. In past generations, oral cancer was mostly linked to smoking, alcohol use or a combination of the two. But even as smoking rates have fallen, oral cancer rates have risen (especially in men), and researchers have concluded that this is likely caused by the human papillomavirus (HPV), a sexually transmitted disease.

Early diagnosis makes a difference
Oral cancer is often only discovered when the cancer has metastasized to another location, most commonly the lymph nodes of the neck. Prognosis at this stage of discovery is significantly worse than when it is caught in a localized intraoral area.

According to the Oral Cancer Foundation, the best way to screen for HPV-related oral and oropharyngeal cancer is through a visual and tactile exam given by a medical or dental professional, who will also perform an oral history taking to ask about signs and symptoms that cover things that are not visible.

Most of the symptoms of a developing HPV-positive infection are discovered by asking questions, using a test, a light or other device.

ADA supports dental industry with this growing challenge
In 2017, a panel of experts convened by the American Dental Association (ADA) Council on Scientific Affairs published a clinical practice guideline called the “Evidence-Based Clinical Practice Guideline for the Evaluation of Potentially Malignant Disorders in the Oral Cavity.”

The goal of this guideline is to inform dentists, orthodontists and other dental professionals about triage tools for evaluating lesions, including potentially malignant disorders, in the oral cavity. If you’re a dentist or an orthodontist, the ADA offers the following considerations concerning the diagnosis of oral and oropharyngeal cancers:

  • Clinicians should obtain an updated medical, social and dental history as well as perform an intraoral and extraoral conventional visual and tactile examination in all adult patients.
  • For patients with suspicious lesions, clinicians should immediately perform a biopsy of the lesion or refer the patient to a specialist.
  • Salivary and light-based tools are not recommended for evaluating lesions for malignancy.

If you are a dental professional and want to learn more about the dental industry’s role in addressing the rising occurrence of oral cancer, visit the ADA’s Oral and Oropharyngeal Cancer page.

April, 2018|Oral Cancer News|

Be your own advocate

Source: www.wvnews.com
Author: Mary McKinley

The importance of dental care goes beyond cavities — it’s also about preventing cancer. The week of April 8 is National Oral, Head and Neck Cancer Awareness Week, and your dentist or dental hygienist may be your first line of defense against oral cancer.

More than 50,000 Americans are expected to be diagnosed with oral or oropharyngeal cancer (cancer of the back of the throat, including the base of the tongue and the tonsils) in 2018, and 350 will be diagnosed in West Virginia alone.

Routine dental exams can detect cancer or pre-cancers during the early stages. If you notice a persistent sore or pain, swelling or changes in your mouth, or red or white patches on the gums, tongue, tonsils or lining of the mouth, visit a doctor or dentist so they can examine your mouth more closely.

Some people diagnosed with oral cancer have no risk factors, so it’s important for everyone to keep those dental appointments.

If you use tobacco, drink alcohol in excess, or have the human papillomavirus (HPV), you have an increased risk for oral cancer. Oral cancer is more common in older adults, particularly men, but oropharyngeal cancer is on the rise in middle-aged, nonsmoking white men between the ages of 35 and 55. The majority of these types of cancer cases are caused by HPV.

Take charge of your health and reduce your risk of oral cancer. If you smoke or chew tobacco, quit now (it’s never too late). Moderate your alcohol consumption to no more than one drink a day for women or two for men.

If you have children, make sure they receive the HPV vaccine, which is recommended for all girls and boys ages 11 and 12; a “catch-up” vaccine is also available for young women up to age 26 and most young men up to age 21.

You can be your own best advocate. Check the inside of your mouth in the mirror each month, and speak up to your dentist or dental hygienist if you notice any changes that concern you.

Ask about cancer screenings when making your dental appointments. And to learn more about cancer prevention, be sure to visit www.preventcancer.org.

April, 2018|Oral Cancer News|