DNA Content as a Prognostic Marker in Patients with Oral Leukoplakia

Sudbø, Jon; Kildal, Wanja; Risberg, Bjørn; Koppang, Hanna Strömme; Danielsen, Håvard E.; Reith, Albrecht

doi:10.1056/nejm200104263441702

Cited by 240 publications

(158 citation statements)

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“…Our prognostic study 26 did not indicate whether standard treatment in the form of preventive excision of leukoplakia would be adequate treatment. Conceivably, local treatment in the form of surgical excision could prevent later carcinomas.…”

Section: Surgical Resection Of Leukoplakiamentioning

confidence: 68%

“…Therefore, reliable predictive markers that may be used for making treatment decisions at an early stage of disease development are greatly needed. A number of such markers have evolved during the past decade, [23][24][25][26] and some of them are finding their way into the clinical work-up of patients with oral putatively premalignant lesions. 26 …”

Section: Traditional Prognostic Markersmentioning

confidence: 99%

“…In a recent report, we demonstrated that aneuploidy in dysplastic oral leukoplakia was a powerful prognostic marker to identify which lesions would progress to carcinoma. 26 Ploidy analysis has also been shown to predict, with a considerable degree of certainty, which non-dysplastic oral epithelial lesions will progress into carcinomas. 33 In Norway, ploidy analysis is now a part Novel management of oral cancer …”

Section: Criteria For the Classification Of Dna Contentmentioning

confidence: 99%

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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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Section: Surgical Resection Of Leukoplakiamentioning

confidence: 68%

Section: Traditional Prognostic Markersmentioning

confidence: 99%

Section: Criteria For the Classification Of Dna Contentmentioning

confidence: 99%

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Novel Management of Oral Cancer: A Paradigm of Predictive Oncology

Sudbø¹

2004

Clinical Medicine & Research

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“…Chen et al (2002) demonstrated that chewing tobacco (areca quid) resulted in the formation of ROS in the oral cavity causing oxidative DNA damage to the surrounding tissues. Further support can be found in a report demonstrating that premalignant mucosal lesions and low-grade carcinomas express DNA aberrations following a pathway of exposure to free radicals (Sudb et al, 2001). Moreover, Bloching et al (2001) recently found increased genotoxic activity in the saliva of smokers with a highly significant additional increase of genotoxicity measured in smoking and drinking individuals.…”

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confidence: 67%

Saliva – a pivotal player in the pathogenesis of oropharyngeal cancer

2004

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Oropharyngeal (OP) cancer, which is usually squamous cell carcinoma, is the most common head and neck malignancy and accounts for 2 -4% of all new cancers. It is primarily induced by exposure to tobacco. The paradigm of cigarette smoke (CS)-induced OP cancer's pathogenesis is based on the assumption that a constant direct attack of various CS carcinogens causes widespread accumulating cellular and DNA aberrations in the OP mucosal cells, in turn eventually resulting in malignant transformation. However, there is never a direct contact between CS and the OP mucosa. Saliva, bathing the mucosa from the oral cavity to the larynx, always intervenes, and CS must first interact with saliva before it reaches the mucosa. The current study investigated the role of saliva in the pathogenesis of OP cancer. A synergistic effect of CS and saliva on oral cancer cells was demonstrated. This synergism is based on the reaction between redox active metals in saliva and low reactive free radicals in CS, which results in the production of highly active hydroxyl free radicals. Thus, when exposed to CS, salivary behavior is reversed and the saliva loses its antioxidant capacity and becomes a potent prooxidant milieu. The devastating role of CS-borne aldehydes was demonstrated as well. Based on these results and on our recent reports demonstrating that CS destroys various salivary components, including protective ones such as peroxidase, the most important salivary antioxidant enzyme, a comprehensive view of the pivotal role of saliva in the pathogenesis of CS-induced OP cancer is suggested. Oropharyngeal (OP) cancer, which is usually squamous cell carcinoma, is the most common head and neck malignancy, having a worldwide incidence of over 300 000 new cases each year and accounting for 2 -4% of all new cancers (Bross and Coombes, 1976;McGinnis and Foege, 1993;Collins et al, 1994;Ko et al, 1995;Piyathilake et al, 1995;Zheng et al, 1997;Nagler et al, 1999; Lippman and Hong, 2001). The commonly accepted paradigm for cigarette smoke (CS)-induced OP cancer pathogenesis is based on the assumption that a constant and direct attack of various CS carcinogens causes widespread accumulating cellular and DNA aberrations in the OP mucosa eventually leading to malignant transformation and cancer development. The CS-borne carcinogens are often thought to be free radicals. The process is initially expressed by dysplastic mucosal lesions which are then transformed into in situ carcinoma lesions, eventually resulting in fullblown infiltrating and metastasising OP cancer (Holleb et al, 1991). Chen et al (2002) demonstrated that chewing tobacco (areca quid) resulted in the formation of ROS in the oral cavity causing oxidative DNA damage to the surrounding tissues. Further support can be found in a report demonstrating that premalignant mucosal lesions and low-grade carcinomas express DNA aberrations following a pathway of exposure to free radicals (Sudb et al, 2001). Moreover, Bloching et al (2001) recently found increased genotoxic activity in the saliv...

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“…При этом наличие тетраплоидных клеток не явля-ется фактором неизбежного прогрессирования заболевания. Опухоли, содержащие тетраплоидные клетки, с равной вероят-ностью могли и регрессировать [14,15]. Были также представле-ны доказательства, что полиплоидизация является распростра-ненной причиной опухолевой эволюции генома у человека и коррелирует с прогрессированием заболевания [16,17].…”

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