Cancer of the base of the tongue: Past and future

Brunin, F.; Mosseri, Véronique; Jaulerry, C; Point, D; Cosset, J.M.; Rodriguez, José

doi:10.1002/(sici)1097-0347(199912)21:8<751::aid-hed11>3.3.co;2-w

Cited by 70 publications

(31 citation statements)

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“…12,13 Five to 15% of oral white patches are histologically classified as dysplasias. 14,15 Of these, a substantial part (15-20%) is reported to develop into carcinomas.…”

Section: Clinical Course Of Oral Cancer Precursor Lesionsmentioning

confidence: 99%

Retracted: The evolution of predictive oncology and molecular‐based therapy for oral cancer prevention

Sudbø

Reith

2005

Intl Journal of Cancer

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More than 300,000 new cases worldwide are being diagnosed with oral squamous cell carcinoma annually. This aggressive epithelial malignancy is associated with a high mortality and severe morbidity among the long-term survivors. The ability to intervene prior to this advanced stage may improve treatment results. This requires the early identification of molecular events that represent early phases of malignant transition, which is possible through measurement of DNA ploidy in epithelial cells of oral leukoplakia. Recently, we showed that patients with aneuploid dysplastic oral lesions had a 96% rate of oral cancer (26 of the 27 patients received the diagnosis) with a 70% rate within three years, an 81% rate of subsequent cancer (22 of 27), a 74% rate of death from cancer (21 of 27) and virtually no help from complete resection-all hallmarks of biologically aggressive cancer. Standard treatment of oral leukoplakia-a precursor lesion of oral cancer-varies from watchful waiting to complete resection. We have recently demonstrated that complete resection of aneuploid oral leukoplakia does not prevent the occurrence of clinically aggressive and highly lethal oral cancer. Oral carcinogenesis is a complex multifocal process of multiclonal field carcinogenesis and intraepithelial clonal spread. The multifocal nature of early oral carcinogenesis may hinder local treatment modalities. Inhibitors of cyclooxygenase-2 (COX-2) and epidermal growth factor receptor (EGFR), either alone or in combination, may be used for reversing or stopping the oral carcinogenesis at an early stage of disease. The failure of standard treatment to control aneuploid oral leukoplakia justifies clinical trials with new treatment modalities, such as systemic therapy with molecular targeting agents, which in patients with aggressive leukoplakia is tantamount to cancer therapy. ' 2005 Wiley-Liss, Inc.Key words: leukoplakia; cancer prevention; molecular-based therapy; targeted therapy; predictive oncology; aneuploidy EpidemiologyMore than 300,000 new cases worldwide are being diagnosed with oral squamous cell carcinoma annually. This aggressive epithelial malignancy is associated with severe morbidity and less than 50% long-term survival despite advances in treatment with surgery, radiation and chemotherapy. The poor prognosis of oral cancer has not improved significantly over the last 4 decades.

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“…12,13 Five to 15% of oral white patches are histologically classified as dysplasias. 14,15 Of these, a substantial part (15-20%) is reported to develop into carcinomas.…”

Section: Clinical Course Of Oral Cancer Precursor Lesionsmentioning

confidence: 99%

Retracted: The evolution of predictive oncology and molecular‐based therapy for oral cancer prevention

Sudbø

Reith

2005

Intl Journal of Cancer

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“…12,13 Five to 15% of oral white patches are histologically classified as dysplasias. 14,15 Of these, a substantial part (15% to 20%) is reported to develop into carcinomas.…”

Section: Clinical Course Of Oral Cancer Precursor Lesionsmentioning

confidence: 99%

Novel Management of Oral Cancer: A Paradigm of Predictive Oncology

Sudbø¹

2004

Clinical Medicine & Research

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The rationale for molecular-targeted prevention of oral cancer is strong. Oral cancer is a major global threat to public health with 300,000 new cases diagnosed worldwide on an annual basis. Notably, the great morbidity and mortality rates of this devastating disease have not improved in decades. Oral cancer development is a tobacco-related multistep and multifocal process involving field carcinogenesis and intraepithelial clonal spread. Biomarkers of genomic instability, such as aneuploidy and allelic imbalance, can accurately measure the cancer risk of oral premalignant lesions or intraepithelial neoplasia (IEN). Retinoid-oral IEN studies (e.g., retinoid acid receptor-β, p53, genetic instability, loss of heterozygosity, and cyclin D1) have advanced the overall understanding of the biology of intraepithelial carcinogenesis and preventive agent molecular mechanisms and targets, important advances for monitoring preventive interventions, assessing cancer risk, and pharmacogenomics. Clinical management of oral IEN varies from watchful waiting to complete resection, although complete resection does not prevent oral cancer in high-risk patients. New approaches, such as interventions with molecular-targeted agents and agent combinations in molecularly defined high-risk oral IEN patients, are urgently needed to reduce the devastating worldwide consequences of oral cancer.

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“…Carcinomas of tongue base are often diagnosed when the disease is already advanced and lymph node metastases are present in 50% of the patients [3]. Optimal treatment of squamous cell carcinoma of the base of tongue has not been defined.…”

Section: Introductionmentioning

confidence: 99%