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Summary Article: Oral Cancer
from Encyclopedia of Cancer

Lesion on tongue, lip, and other areas in the mouth


Oral cancer is cancer of the mouth. It is a common form of head and neck cancer.


Oral cancer is amongst the most commonly diagnosed cancers worldwide and its incidence high in developing countries. The main etiological factors for oral cancer are tobacco and alcohol use, with 75% of those diagnosed with disease described as current or ex-smokers. Regular combined use of tobacco and alcohol significantly increases the chance of developing this type of tumor; those who both smoke and drink have a 15 times greater risk of developing oral cancer than the overall population. While the majority of people are over the age of 40 at the time of diagnosis, oral cancer may also occur in younger individuals. Exact causes for those affected at a younger age have been linked to young men and women who use “smokeless” chewing or spit tobacco. It is also a possibility that those in this younger age group have a causal link which is viral based, as their exposure to tobacco and other known causative agents is short in time. The human papillomaviruses, particularly versions 16 and 18, are implicated in the increasing incidence of young nonsmoking oral cancer patients. These are the same viruses that are the causative agents in more than 90% of all cervical cancers.

Oral cancer carries a poor prognosis and a high rate of recurrence; second primary tumors are estimated to occur at an annual rate of 3–10% and their presence is known to greatly impact survival. Despite the development of new therapeutic options, the overall survival rate for oral cancer has not changed in the last two decades.


Oral cancer progresses through various histopathological stages – from hyperplasia, various stages of dysplasia, and carcinoma in situ (CIS) to invasive disease. There are two types of precancerous oral lesions: leukoplakia and erythroplakia. Both show varying degrees of dysplastic change. In general, erythroplakia contains more severe dysplasia and is more likely to progress, while incidence of leukoplakia is much higher.

Oral leukoplakia is a white-plaque mucosal lesion that confers increased risk for the development of oral squamous cell carcinoma (OSCC). Five to fifteen percent of oral white patches are classified as dysplasia. Of these, only 15–20% develop into invasive carcinoma. Treatment for oral leukoplakia is removal via surgery or laser. Because histology of low-grade dysplastic lesions is of limited prognostic value, therapeutic intervention is considered only where there is evidence of transition to CIS or invasion. Hence there is a need to identify molecular markers that predict progression for individual preinvasive lesions.


Oral tumors have been proposed to arise through “field cancerization,” a process where whole tissue exposure to a carcinogen leads to increased risk of multiple premalignant lesions or invasive tumors. The frequent occurrence of tumors with dissimilar histology in the same individual as well as distinct genetic signatures in these tissues are evidence for this phenomenon. With field cancerization, each tumor is thought to arise by clonal evolution of a cell population that is accumulating cancer-causing genetic and epigenetic changes.

Oral cancer generally arises through dysregulation of oncogenes and tumor suppressor genes (TSGs) that drive cell proliferation. Oncogenes are altered growth-promoting regulatory genes that govern cell signal transduction pathways. Mutation of these genes leads to either overproduction or increased function of the resulting protein. TSGs, on the other hand, are “gatekeepers” of cellular proliferation. They can either inhibit cell growth or promote cell death. Mutations in a number of TSGs and oncogenes are commonly observed in oral cancer. These include RAS, MYC, CCND1 (cyclinD1), EGFR (epidermal growth factor receptor), TP53, CDKN2A (cyclin dependent kinase inhibitor 2A), and FHIT (fragile histidine triad).

See also Allelic loss involving chromosome arm 3p is one of the most frequent and earliest genetic events in the development of HNSCC. This loss is significant as several potential TSGs fall in this region. For oral cancer, multiple discontinuous regions of allelic loss support the idea that there are multiple TSGs on this chromosome arm. There is evidence that several genes residing on chromosome 3p are important for tumorigenesis, however the exact role each of these genes plays in the development of disease is still being determined. One gene residing on chromosome 3p that has been implicated in oral cancer is FHIT. This large gene, located at 3p14.2, also spans one of the most widely characterized fragile sites in the human genome, FRA3B. The FHIT gene, a member of the histidine triad gene family, is a target of tyrosine phosphorylation by the SRC protein kinase.


Treatment for oral cancer is usually surgery and radiotherapy. Chemotherapy may be added to sensitize the malignant cells to radiation, to decrease the possibility of metastasis, or to treat patients with confirmed distant metastases. The stage of the disease at diagnosis dictates which treatment modality is used. Patients who are treated for early-stage cancer may have little in the way of posttreatment disfigurement. For those diagnosed with later stage cancer, the results of surgical removal of the disease may require reconstruction of portions of their oral cavity or facial features.

See also Oral Squamous Cell Carcinoma

  • 1. Ragin, CC; Modugno, F; Gollin, SM (2007) The epidemiology and risk factors of head and neck cancer: a focus on human papillomavirus. J Dent Res 86(2):104-114 (PubMed) (CrossRef).
  • 2. Lung, T et al (2007) Head and neck cancer, epidemiology and histological aspects - Part 1: a decade’s results 1993-2002. J Craniomaxillofac Surg 35(2):120-125 (PubMed) (CrossRef).
  • 3. Epstein, JB; Zhang, L; Rosin, M (2002) Advances in the diagnosis of oral premalignant and malignant lesions. J Can Dent Assoc 68(10):617-621 (PubMed).
  • 4. Suarez, P; Batsakis, JG; EL-Naggar, AK (1998) Leukoplakia: still a gallimaufry or is progress being made? - a review. Adv Anat Pathol 5(3):137-155 (PubMed) (CrossRef).
  • 5. Ha, PK; Califano, JA (2003) The molecular biology of mucosal field cancerization of the head and neck. Crit Rev Oral Biol Med 14(5):363-369 (PubMed) (CrossRef).
  • Cathie Garnis
    MIT Center for Cancer Research, Cambridge, MA, USA
    Wan L. Lam
    Department of Cancer Genetics and Developmental Biology, British Columbia Cancer Research Centre, Vancouver, BC, Canada
    © Springer-Verlag Berlin Heidelberg 2011, 2009, 2001

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