From the Departments of Thoracic/Head and Neck Medical Oncology, Biostatistics and Applied Mathematics, and Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, TX

Corresponding author: Li Mao, MD, Department of Thoracic/Head and Neck Medical Oncology, Unit 432, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030; e-mail: lmao@mdanderson.org

Purpose: Oral leukoplakia (OPL) is a heterogeneous oral lesion with an increased oral cancer risk. Current clinical parameters cannot predict the potential of malignant transformation in patients with OPL. We have shown that podoplanin, a lymphatic endothelial marker, is highly expressed in oral cancer and some oral premalignancies. The purpose of this study is to determine a role of podoplanin in predicting oral cancer development in patients with OPL.

Patients and Methods: Podoplanin expression was determined in 150 OPL patients with long-term follow-up using immunohistochemistry. Association between the protein expression patterns and clinicopathologic parameters including oral cancer development during the follow-up were analyzed.

Results: Fifty-six (37%) of the 150 OPL patients exhibited podoplanin expression in the basal and suprabasal layers and were classified as podoplanin positive. Podoplanin positivity was more frequent in older patients (P = .016), females (P = .020), and dysplastic lesions (P = .040). Patients with OPL that was podoplanin positive had significantly higher incidence of oral cancer than did those whose OPL was podoplanin negative (P = .0002). In the multivariate analysis using histology and podoplanin as cofactors, podoplanin was the only independent factor for oral cancer development (hazard ratio = 3.087; 95% CI, 1.530 to 6.231; P = .002). Importantly, oral cancer risk can be further stratified by considering both histology and podoplanin information.

Conclusion: Podoplanin is frequently expressed in OPL. Together with histology, podoplanin may serve as a powerful biomarker to predict the risk for oral cancer development in patients with OPL.

Supported in part by National Cancer Institute Grants No. PO1 CA52051, PO1 CA106451, P50 CA97007, and P30 CA16672, and by the Uehara Memorial Foundation (H.K.)

Authors’ disclosures of potential conflicts of interest and author contributions are found at the end of this article.

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¹ Departments of Head and Neck Surgery, ² Cancer Biology, and ³ Biostatistics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas

Expression of the epidermal growth factor (EGF) and activation of its receptor (EGFR), a tyrosine kinase, are associated with progressive growth of head and neck cancer. Expression of the vascular endothelial growth factor (VEGF) is associated with angiogenesis and progressive growth of tumor. The tyrosine kinase inhibitor NVP-AEE788 (AEE788) blocks the EGF and VEGF signaling pathways. We examined the effects of AEE788 administered alone, or with paclitaxel (Taxol), on the progression of human head and neck cancer implanted orthotopically into nude mice. Cells of two different human oral cancer lines, JMAR and MDA1986, were injected into the tongues of nude mice. Mice with established tumors were randomized to receive three times per week oral AEE788, once weekly injected paclitaxel, AEE788 plus paclitaxel, or placebo. Oral tumors were resected at necropsy. Kinase activity, cell proliferation, apoptosis, and mean vessel density were determined by immunohistochemical immunofluorescent staining. AEE788 inhibited cell growth, induced apoptosis, and reduced the phosphorylation of EGFR, VEGFR-2, AKT, and mitogen-activated protein kinase in both cell lines. Mice treated with AEE788 and AEE788 plus paclitaxel had decreased microvessel density, decreased proliferative index, and increased apoptosis. Hence, AEE788 inhibited tumor vascularization and growth and prolonged survival. Inhibition of EGFR and VEGFR phosphorylation by AEE788 effectively inhibits cellular proliferation of squamous cell carcinoma of the head and neck, induces apoptosis of tumor endothelial cells and tumor cells, and is well tolerated in mice. These data recommend the consideration of patients with head and neck cancer for inclusion in clinical trials of AEE788.

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Update from Marlene, December, 2006:

I’ve been in and out of the hospitals since my first surgery with one surgery after the other had 3 big lumps appear inside my mouth and a growth I thought was a wart on my nose. The doctor wanted to get the lumps out of my mouth and I asked him if while he did that, could he snip that thing off my nose. The lab results showed the lumps in my mouth were nothing, but the wart turned out to be cancer.

In 2005, I lost my job of 15 years due to downsizing, so my sons moved me to Kansas to live with them and I filed for disability. Soon after I moved, I started having trouble swallowing. Then it turned to painful inability to swallow. Antibiotic time again, but they did not help. The doctors checked and checked, but could not find anything; the CT scan came up clean. The squeaky wheel always gets the oil so I kept squeaking. I got aggravated and changed doctors after I joined Victory In The Valley in Wichita, Kansas. Executive director, Diane Thomi, was an oncology nurse for over 40 years and she suggested someone I should see. I changed doctors under her recommendation. The new doctor sent me for a PET scan and found cancer at the base of my tongue. He confirmed it with a biopsy. I started treatments of two pin pointed radiation treatments per day along with two different kinds of chemotherapy. I was on this regimen for about 3 months, and ended up in the hospital completely dehydrated for a week. I was very sick. I am still under care for this cancer. I just had another PET scan and a CT scan, one of which came back bad, so this month the doctor is doing another biopsy that will tell us once for all if the treatments got it all. If not, they will either cut my tongue open and install radiation seeds directly into my cancer, or I’ll have to go to Kansas City to have my tongue removed.
I have been in the best of moods, and I actually feel good so I’m trying not to get my hopes up too much. But, I can’t help feeling the cancer is gone. I now have 4 grandsons, the sweetest little guys you have ever seen. I babysit and we have a great time. I love those guys with all of my heart. You can contact Marlene directly at: marlene@livetodayandtomorrow.com. She also has a website dedicated to laryngectomy, oral and throat cancer: livetodayandtomorrow.com

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Approximately 90 percent of those diagnosed with oral cancer or pharyngeal cancer (including cancer of the mouth, tongue, lips, throat, parts for the nose, and larynx) are tobacco users.

What are the Risk Factors for Oral Cancers?

—Tobacco

All forms of tobacco increase a person’s risk of oral cancer. In fact, smokers are six times more likely to get an oral cancer than nonsmokers.

—Alcohol

Heavy, regular alcohol consumption is a risk factor for oral cancer. It’s estimated that 75 to 80 percent of those with oral cancer drink alcohol frequently.

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Like smokers, people who drink a lot of alcohol on a regular basis are also six times more likely to get an oral cancer than nondrinkers.

—Tobacco and Alcohol

The risk for oral cancer that each substance represents is compounded when they are used together.

—Gender

It appears that men contract oral cancer at twice the rate of women, due to the fact that they are more likely to smoke and drink heavily for longer periods of time than females.

—Age

After the age of 40, the risk of oral cancer increases, with 60 being the average age of diagnosis.

Other Risk Factors

—      Viral infections

—      Immunodeficiencies

—      Poor nutrition

—      Exposure to ultraviolet light (responsible for many cases of cancer to the lips)

—      Certain occupational exposures

It’s important to note that survival rates for oral cancers are 50 percent five years after diagnosis. The earlier oral cancer is detected, the better a person’s chances for survival are.

Signs and Symptoms of Oral Cancer

—      Sores in the mouth or on the lips that don’t heal and/or bleed easily.

—      A white or red patch of skin in the mouth or under the tongue that doesn’t go away.

—      A lump in the mouth, throat, or tongue.

—      A sore throat that doesn’t go away within a normal period of time.

—      Swallowing and/or chewing is difficult or painful.

If you have any of these symptoms, please see your doctor immediately.

Oral cancer screening is a normal part of dental checkups, so visit your dentist on a regular basis to get your teeth cleaned. It’s one of the best ways to catch oral cancer early.

Additional Oral Cancer Resources:

Diagnosed with Oral Cancer - Marlene’s Story

Oral and Head and Neck Cancer

Oral Cancer Photo Gallery

Most oral cancers could be avoided by not using tobacco and/or drinking heavily. If you fall into this risk category, use the information here as a springboard to help you get serious about quitting. Tobacco is a toxic killer and offers you nothing more than disease and ultimately, death.

Sources:

“FAQ Cancer of the Oral Cavity and Pharynx.” NOHSS. 23 May 2006. Centers for Disease Control.

“Oral Cancer.” 2006. American Cancer Society.

Updated: April 18, 2007

Oral Cancer

Oral Cancer Photo GalleryAn Oral Cancer Personal StoryOral and Head and Neck Cancer

Smoking and Cancer

Cigarette Smoking and CancerSmoking Related Cancer StatisticsSmoking and Ovarian Cancer

Smoking and Your Health

How Smoking Harms Us From Head to ToeSmoking and Degenerative Disc DiseaseSmoking and Pregnancy

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Using data from the California Cancer Registry, researchers examined the incidence rates of invasive oral squamous cell carcinoma (OSCC) from 1988 to 2001. They then categorized the cancer occurrences by anatomic site and the people who had cancer by ethnicity.

They found that black men have the highest overall incidence rate of OSCC, and that blacks and whites have higher oral cancer rates than do Hispanics or Asians. They also found that the tongue was the most common site of OSCC for all ethnicities.

“From what we know of how the cancer develops, we can extrapolate that cultural habits and lifestyle choices are directly linked to the prevalence of oral cancer in certain groups,” said study co-author Dr. Satish Kumar, assistant professor, USC School of Dentistry’s Division of Diagnostic Sciences.

Researchers found that black and white men and Koreans had the highest rates of cancer of the tongue and the highest rates of cigarette smoking.

Chewing tobacco or areca nuts, which is common in South Asian cultures, may account for South Asians’ high likelihood of developing cancer in the inner cheek. The high rate of palatal cancer among Filipino women could be attributed to the common practice of reverse smoking (in which the lit part of the cigarette is concealed inside the mouth near the palate).

“If we are aware that certain subsets are getting a particular kind of oral cancer, we can develop educational materials tailored to that particular risk activity and that particular group,” said study co-author Dr. Parish Sedghizadeh, assistant professor of clinical dentistry, USC School of Dentistry’s Division of Diagnostic Sciences.

Please contact the ADA if you have questions about this article.

Click here to view archived ADA articles.

©2006 American Dental Association. All rights reserved. Reproduction or republication is strictly prohibited without the prior written permission from the American Dental Association.

1/07/08

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A tongue biopsy, gum biopsy, and microscopic examination of the lesion confirm the diagnosis of oral cancer.

Treatment

Surgical excision (removal) of the tumor is usually recommended if the tumor is small enough. Radiation therapy and chemotherapy would likely be used when the tumor is larger or has spread to lymph nodes in the neck. Surgery may be necessary for large tumors.

Rehabilitation may include speech therapy or other therapy to improve movement, chewing, swallowing, and speech.

Support Groups

The stress of illness can often be eased by joining a support group of people who share common experiences and problems. See cancer - support group.

Expectations (prognosis)

Approximately 50% of people with oral cancer will live more than 5 years after diagnosis and treatment. If the cancer is detected early, before it has spread to other tissues, the cure rate is nearly 75%. Unfortunately, more than 50% of oral cancers are advanced at the time the cancer is detected. Most have spread to the throat or neck.

Approximately 25% of people with oral cancer die because of delayed diagnosis and treatment.

Complications

—      Postoperative disfigurement of the face, head and neck

—      Complications of radiation therapy, including dry mouth and difficulty swallowing

Other metastasis (spread) of the cancer.

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Beck J, Eke PI, Dongming L, Madianos P, Couper D, Moss K, Elter J, Heiss G, Offenbacher S. Periodontal disease and coronary heart disease: Reappraisal of the exposure measures. Circulation 2005;112(1):19–24. View full text.*

Beltrán E, Beltrán RJ. Oral diseases and conditions throughout the lifespan. II. Systemic Diseases. General Dent 2004;52(2):107–114. View abstract on PubMed.

Blicher B, Joshipura K, Eke PI. Validation of self-reported periodontal disease: A systematic review. J Dent Res 2005;84(10):881–890. View full text.*

Dye BA, Tan S, Smith V, Lewis BG, Barker LK, Thornton-Evans G, et al. Trends in Oral Health Status, United States, 1988-1994 and 1999-2004. National Center for Health Statistics. Vital Health Stat 11(248); 2007. View full text. (PDF–1.8Mb)

Dye BA, Thornton-Evans G. A brief history of national surveillance efforts for periodontal disease in the United States.  J Periodontol 2007;78(7 Suppl):1380–1386. View full text.(PDF–103K)

Eke PI, Genco RJ. CDC periodontal disease surveillance project: background, objectives, and progress report.  J Periodontol 2007;78(7 Suppl):1366–1372. View full text. (PDF–305K)

Eke PI. Public health implications of periodontal infections in adults: Conference proceedings. J Publ Health Dent 2005;65(1):56–65.

Okoro CA, Balluz, LS, Eke PI, Ajani UA, Trine TW Town M, Mensah GA, Mokdad AH. Tooth loss and heart disease: findings from the Behavioral Risk Factor Surveillance System. Am J Prev Med 2005;29(5 Suppl 1):50–56. View abstract on PubMed.

Page RC, Eke PI. Case definitions for use in population-based surveillance of periodontitis. J Periodontol 2007;78(7 Suppl):1387–1399. View full text

Tomar SL. Public health perspectives on surveillance for periodontal diseases. J Periodontol 2007;78(7 Suppl):1380–1386. View full text.

Special Topics

Beltrán-Aguilar ED, Beltrán RJ. Oral diseases and conditions throughout the lifespan. I. Diseases and conditions associated with tooth loss. General Dent 2004;52(1):21–27. View abstract on PubMed.

Beltrán-Aguilar ED, Malvitz, DM, Lockwood S, Rozier GR, Tomar SL. Oral health surveillance: past, present, and future challenges. J Publ Health Dent 2003;63(3):141–149. View abstract on PubMed.

Beltrán E, Beltrán RJ. Oral diseases and conditions throughout the lifespan. II. Systemic Diseases. General Dent 2004;52(2):107–114. View abstract on PubMed.

Beltrán E, Cherrett H, Holodell M, Jaramillo F, Robison V. Tanzania Site Assessments, March 2006. Refugee Camps. Dar es Salaan, Tanzania, Faculty of Dentistry, Muhinbill University, Tanzania Dental Association, 2006:1–41. View full text. (PDF–2Mb)

Beltrán-Neira RJ, Beltrán Aguilar ED. Taxonomy in dental education. J Dent Educ 2004;68:978–984. View abstract on PubMed.

Gooch BF, Griffin SO, Malvitz DM. The role of evidence in formulating public health programs to prevent oral disease and promote oral health in the United States. J Evidence-Based Dental Practice 2006:6(1):85–89. View abstract on PubMed.

Maas W. Access to care: what can the United States learn from other countries. Comm Dent Oral Epid 2006;34(3):232–240. View abstract on PubMed.

Riley JL III, Tomar SL, Gilbert GH. Smoking and smokeless tobacco: increased risk for oral pain. J of Pain 2004;5:217–222. View abstract on PubMed.

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In the case of preventive services guidelines, implementation needs to go beyond traditional dissemination and promotion efforts to recognize the added patient and clinician barriers that affect preventive care. These include clinicians’ ambivalence about whether preventive medicine is part of their job, the psychological and practical challenges that patients face in changing behaviors, lack of access to health care or of insurance coverage for preventive services for some patients, competing pressures within the context of shorter office visits, and the lack of organized systems in most practices to ensure the delivery of recommended preventive care.

Dissemination strategies have changed dramatically in this age of electronic information. While recognizing the continuing value of journals and other print formats for dissemination, the Agency for Healthcare Research and Quality will make all U.S. Preventive Services Task Force (USPSTF) products available through its Web site. The combination of electronic access and extensive material in the public domain should make it easier for a broad audience of users to access U.S. Preventive Services Task Force materials and adapt them for their local needs. Online access to U.S. Preventive Services Task Force products also opens up new possibilities for the appearance of the annual, pocket-size Guide to Clinical Preventive Services.

To be successful, approaches for implementing prevention have to be tailored to the local level and deal with the specific barriers at a given site, typically requiring the redesign of systems of care. Such a systems approach to prevention has had notable success in established staff-model health maintenance organizations, by addressing organization of care, emphasizing a philosophy of prevention, and altering the training and incentives for clinicians. Staff-model plans also benefit from integrated information systems that can track the use of needed services and generate automatic reminders aimed at patients and clinicians, some of the most consistently successful interventions. Information systems remain a major challenge for individual clinicians’ offices, however, as well as for looser affiliations of practices in network-model managed care and independent practice associations, where data on patient visits, referrals, and test results are not always centralized.

COMPOSITION OF GROUP THAT AUTHORED THE GUIDELINE

Task Force Members*: Alfred O. Berg, MD, MPH, Chair, USPSTF (Professor and Chair, Department of Family Medicine, University of Washington, Seattle, WA); Janet D. Allan, PhD, RN, CS, Vice-chair, USPSTF (Dean, School of Nursing, University of Maryland Baltimore, Baltimore, MD); Ned Calonge, MD, MPH (Acting Chief Medical Officer, Colorado Department of Public Health and Environment, Denver, CO); Paul Frame, MD (Tri-County Family Medicine, Cohocton, NY, and Clinical Professor of Family Medicine, University of Rochester, Rochester, NY); Joxel Garcia, MD, MBA (Deputy Director, Pan American Health Organization, Washington, DC); Russell Harris, MD, MPH (Associate Professor of Medicine, Sheps Center for Health Services Research, University of North Carolina School of Medicine, Chapel Hill, NC); Mark S. Johnson, MD, MPH (Professor of Family Medicine, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, NJ); Jonathan D. Klein, MD, MPH (Associate Professor, Department of Pediatrics, University of Rochester School of Medicine, Rochester, NY); Carol Loveland-Cherry, PhD, RN (Executive Associate Dean, School of Nursing, University of Michigan, Ann Arbor, MI); Virginia A. Moyer, MD, MPH (Professor, Department of Pediatrics, University of Texas at Houston, Houston, TX); C. Tracy Orleans, PhD (Senior Scientist, The Robert Wood Johnson Foundation, Princeton, NJ); Albert L. Siu, MD, MSPH (Professor of Medicine, Chief of Division of General Internal Medicine, Mount Sinai School of Medicine, New York, NY); Steven M. Teutsch, MD, MPH (Senior Director, Outcomes Research and Management, Merck & Company, Inc., West Point, PA); Carolyn Westhoff, MD, MSc (Professor of Obstetrics and Gynecology and Professor of Public Health, Columbia University, New York, NY); and Steven H. Woolf, MD, MPH (Professor, Department of Family Practice and Department of Preventive and Community Medicine and Director of Research Department of Family Practice, Virginia Commonwealth University, Fairfax, VA)

*Member of USPSTF at the time this recommendation was finalized. For a list of current Task Force members, go to www.ahrq.gov/clinic/uspstfab.htm.

FINANCIAL DISCLOSURES/CONFLICTS OF INTEREST

The U.S. Preventive Services Task Force (USPSTF) has an explicit policy concerning conflict of interest. All members and Evidence-based Practice Center (EPC) staff disclose at each meeting if they have an important financial conflict for each topic being discussed. Task Force members and EPC staff with conflicts can participate in discussions about evidence, but members abstain from voting on recommendations about the topic in question.

From: Harris RP, Helfand M, Woolf SH, Lohr KN, Mulrow, CD, Teutsch SM, Atkins D. Current methods of the U.S. Preventive Services Task Force: a review of the process. Methods Work Group, Third U.S. Preventive Services Task Force. Am J Prev Med 2001 Apr;20(3S):21-35.

GUIDELINE STATUS

This is the current release of the guideline.

This release updates a previously published guideline: U.S. Preventive Services Task Force. Guide to clinical preventive services. 2nd ed. Baltimore (MD): Williams & Wilkins; 1996. Chapter 16, Screening for oral cancer. p. 175-80.

GUIDELINE AVAILABILITY

Electronic copies: Available from the U.S. Preventive Services Task Force (USPSTF) Web site.

Print copies: Available from the Agency for Healthcare Research and Quality (AHRQ) Publications Clearinghouse. For more information, go to http://www.ahrq.gov/news/pubsix.htm or call 1-800-358-9295 (U.S. only).

AVAILABILITY OF COMPANION DOCUMENTS

The following are available:

Evidence Reviews:

— Screening for oral cancer: a brief evidence update for the U.S. Preventive Services Task Force. Rockville (MD): Agency for Healthcare Research and Quality (AHRQ), 2004 Feb. 4 p.

Electronic copies: Available from the U.S. Preventive Services Task Force (USPSTF) Web site.

Background Articles:

—      Woolf SH, Atkins D. The evolving role of prevention in health care: contributions of the U.S. Preventive Services Task Force. Am J Prev Med 2001 Apr;20(3S):13-20.

—      Harris RP, Helfand M, Woolf SH, Lohr KN, Mulrow, CD, Teutsch SM, Atkins D. Current methods of the U.S. Preventive Services Task Force: a review of the process. Methods Work Group, Third U.S. Preventive Services Task Force. Am J Prev Med 2001 Apr;20(3S):21-35.

—      Saha S, Hoerger TJ, Pignone MP, Teutsch SM, Helfand M, Mandelblatt JS. The art and science of incorporating cost effectiveness into evidence-based recommendations for clinical preventive services. Cost Work Group of the Third U.S. Preventive Services Task Force. Am J Prev Med 2001 Apr;20(3S):36-43.

Electronic copies: Available from U.S. Preventive Services Task Force (USPSTF) Web site.

The following are also available:

— The guide to clinical preventive services, 2006. Recommendations of the U.S. Preventive Services Task Force. Rockville (MD): Agency for Healthcare Research and Quality (AHRQ), 2006. 228 p. Electronic copies available from the AHRQ Web site.

Print copies: Available from the Agency for Healthcare Research and Quality Publications Clearinghouse. For more information, go to http://www.ahrq.gov/news/pubsix.htm or call 1-800-358-9295 (U.S. only).

The Electronic Preventive Services Selector (ePSS), available as a PDA application and a web-based tool, is a quick hands-on tool designed to help primary care clinicians identify the screening, counseling, and preventive medication services that are appropriate for their patients. It is based on current recommendations of the USPSTF and can be searched by specific patient characteristics, such as age, sex, and selected behavioral risk factors.

PATIENT RESOURCES

The following is available:

— The pocket guide to good health for adults. Rockville (MD): Agency for Healthcare Research and Quality (AHRQ); 2003.

Electronic copies: Available from the U.S. Preventive Services Task Force (USPSTF) Web site. Copies also available in Spanish from the USPSTF Web site.

Print copies: Available from the Agency for Healthcare Research and Quality (AHRQ) Publications Clearinghouse. For more information, go to http://www.ahrq.gov/news/pubsix.htm or call 1-800-358-9295 (U.S. only).

Please note: This patient information is intended to provide health professionals with information to share with their patients to help them better understand their health and their diagnosed disorders. By providing access to this patient information, it is not the intention of NGC to provide specific medical advice for particular patients. Rather we urge patients and their representatives to review this material and then to consult with a licensed health professional for evaluation of treatment options suitable for them as well as for diagnosis and answers to their personal medical questions. This patient information has been derived and prepared from a guideline for health care professionals included on NGC by the authors or publishers of that original guideline. The patient information is not reviewed by NGC to establish whether or not it accurately reflects the original guideline’s content.

NGC STATUS

This summary was completed by ECRI on June 30, 1998. The information was verified by the guideline developer on December 1, 1998. This summary was updated by ECRI on April 8, 2004. The updated information was verified by the guideline developer on April 22, 2004.

COPYRIGHT STATEMENT

Requests regarding copyright should be sent to: Gerri M. Dyer, Electronic Dissemination Advisor, Agency for Healthcare Research and Quality (formerly the Agency for Health Care Policy and Research), Center for Health Information Dissemination, Suite 501, Executive Office Center, 2101 East Jefferson Street, Rockville, MD 20852; Facsimile: 301-594-2286; E-mail: gdyer@ahrq.gov.

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Those at high risk for oral cancer include tobacco users, African-American men and heavy drinkers, but anyone can develop oral cancer. According to the Oral Cancer Consortium, 25 percent of people diagnosed with oral cancer have no risk factors. Studies have also determined there may be a link between HPV (human papilloma virus) and oral cancer.

Your dentist and hygienist usually screen you for any signs of oral cancer at your regular checkups, but some symptoms of oral cancer can be invisible to the naked eye.

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The FDA has recently approved a device to detect oral cancer called a VELscope. The VELscope is non-invasive and uses a bright blue light to emphasize any changes in the mouth that a dentist or hygienist could not normally see.

Dr. Kenneth Magid, a professor at New York University College of Dentistry, states on the Oral Cancer Foundation website, “The problem, for the most part, is that early oral cancer looks like everything else. It looks like a million other injuries and changes in the tissue in the mouth. It’s a red spot or a white spot. We see them all the time.” But using the VELscope to detect oral cancer can make abnormalities stand out like sore thumbs, according to Dr. Magid.

The Oral Cancer Foundation estimates that 34,000 Americans will be diagnosed with oral cancer this year alone, with only 50 percent still being alive in 5 years. The problem is much larger worldwide. Even with these statistics, the experts agree that early diagnosis pushes the five-year survival rate to an astonishing 80 percent.

Since oral cancer can affect anyone, without regard to age or gender, it is very important to have regular screenings for this deadly disease. Talk with your dentist about the latest developments and technologies for diagnosing oral cancer.

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Cancer Research Institute, Advanced Center for Treatment, Research and Education in Cancer, Tata Memorial Center, Kharghar, Navi Mumbai 410 208, India
¹ BTIS Advanced Center for Treatment, Research and Education in Cancer, Tata Memorial Center, Kharghar, Navi Mumbai 410 208, India
² Zoology Department, University of Pune, Ganesh Khind, Pune 411007, India

^* To whom correspondence should be addressed. Tel: +91 22 2740 5000, Ext 5049; Fax: +91 22 27405085/5058; Email: mmahimkar@actrec.gov.in

Oral cancer is the leading cancer type among Southeast Asian men and is causally associated with the use of tobacco. Genetic polymorphisms in xenobiotic-metabolizing enzymes modify the effect of environmental exposures, thereby playing a significant role in gene–environment interactions and hence contribute to the high degree of variance in individual susceptibility to cancer risk. This study investigates the role of polymorphisms at CYP1A1, GSTM1 and GSTT1 to oral squamous cell carcinoma (OSCC) in a case–control study involving 155 patients with precancerous lesions, 458 cancer patients and 729 age and habit-matched controls. Genotypes at these loci were determined by polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism performed on genomic DNA extracted from peripheral blood lymphocytes. Risk to oral cancer was estimated among different tobacco exposure groups and doses using logistic regression analysis. GSTM1 null genotype conferred 1.29-fold increased risk [95% confidence interval (CI), 1.04–1.65] to OSCC. GSTT1 null genotype, however, conferred 0.57 times reduced risk to OSCC (95% CI, 0.39–0.83), specifically among tobacco chewers (odds ratio 0.27; 95% CI, 0.14–0.53). This risk was further reduced to 0.13 times (95% CI, 0.04–0.46) with increase in lifetime exposure to tobacco. We also investigated risk conferred by these genotypes at two different intra-oral sites, buccal mucosa and tongue. We found increased susceptibility to buccal mucosa cancer among individuals carrying these genetic markers. These results support the finding that GSTM1 null genotype is a risk factor to OSCC among Indian tobacco habits; GSTT1 null genotype, however, emerged as a protective factor.

Abbreviations: CI, confidence interval; CYP, cytochrome p450; GSH, glutathione; GST, glutathione S-transferase; OR, odds ratio; OSCC, oral squamous cell carcinoma; PAH, polycyclic aromatic hydrocarbon; PCL, precancerous lesion; PCR, polymerase chain reaction; SCE, sister chromatid exchange.

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