Tongue cancer secondary prevention
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Risk calculators and risk factors for Tongue cancer secondary prevention |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]
Overview
Secondary prevention strategies following tongue cancer include monthly follow-ups for the first 12-18 months following therapy.
Secondary Prevention
- Following therapy, postoperative patients are monitored monthly for the first 12-18 months. In patients who undergo nonsurgical treatment, follow-up diagnostic imaging studies are recommended in the first 6 months.
- According to the American Cancer Society about 1 out of every 5 cases of leukoplakia is cancerous or will develop into cancer if not treated. Erythroplakia is less common, but more serious. The majority of found erythroplakia cases are cancerous or will develop into it. After having pre-cancerous spots removed it is important that you have regular check ups with a dentist or doctor to monitor your tongue and check for a recurrence of pre-cancerous spots.
- Secondary chemoprevention Beta-carotene and alpha-tocopherol (vitamin E) have been evaluated as secondary chemopreventive agents in patients with head and neck cancer [62]. No evidence of benefit has been observed, while a possible detrimental effect of supplementation with beta-carotene plus alpha-tocopherol was suggested in a secondary prevention trial in which 540 patients undergoing radiation therapy for stage I or II head and neck cancer were randomly assigned to both agents or placebo for three years starting the first day of radiation [62]. Synthetic retinoids The most extensively studied compounds for premalignant oropharyngeal disease are the synthetic retinoids [63,64,69-71]. response rates of 59 to 92 percent. Many premalignant dysplastic lesions very low levels of the nuclear retinoid receptor [73] which may reestablish many aspects of normal growth and differentiation in the aberrantly proliferating premalignant clone [73,74]. Retinoids also have antiangiogenic activity, which may directly or indirectly contribute to their antineoplastic activity [75]. NSAID therapy Intake of aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) prevents the development of intraepithelial neoplasia in the colon and rectum. The mechanism of this chemopreventive effect is thought to be inhibition COX-2 and diminished synthesis of prostaglandins, which are overproduced in colorectal tumors and have been implicated in tumorigenesis. EGFR inhibition EGFR is expressed in a wide variety of malignant tumors, including colon, non-small cell lung, breast, kidney, head and neck, bladder, and ovarian cancers [99-101]. EGFR is highly expressed in SCCHN, suggesting that EGFR inhibition may be effective in these tumors [16,102]. Combined inhibition of EGFR and COX-2 The interaction between the EGFR and COX-2 pathways has been extensively investigated in preclinical as well as clinical studies, with evidence that targeting these two pathways can synergistically or additively reverse the progression of SCCHN [105,106] Human papilloma virus related oropharyngeal carcinoma The E6 and E7 HPV viral proteins in HPV 16 are responsible for promoting cell cycle progression and viral DNA replication in differentiated normal mucosal epithelial cells. While E6 protein binds to p53 tumor suppressor protein and induces its degradation, the E7 protein ubiquitinates the retinoblastoma tumor suppressor protein. This process leads to driving the mucosal cells into S phase and induces cellular DNA synthesis [118,119].