Progression of precancerous lesions to oral cancer: Results based on the Taiwan National Health Insurance Database

Lian, Ie Bin; Tseng, Yao Ting; Su, Chin-Chuan; Tsai, Kuo-Yang

doi:10.1016/j.oraloncology.2012.12.004

Cited by 73 publications

(62 citation statements)

References 12 publications

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“…Patients with chronic inflammatory diseases can develop cancer after variable latency periods. For example, a long-term follow-up of patients with oral pre-cancerous lesions demonstrated an increased risk for oral cancers after 5 and 10 years of about 5% and 10%, respectively [118]. …”

Section: Presentation Of the Hypothesismentioning

confidence: 99%

Epistemology of the origin of cancer: a new paradigm

2014

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BackgroundCarcinogenesis is widely thought to originate from somatic mutations and an inhibition of growth suppressors, followed by cell proliferation, tissue invasion, and risk of metastasis. Fewer than 10% of all cancers are hereditary; the ratio in gastric (1%), colorectal (3-5%) and breast (8%) cancers is even less. Cancers caused by infection are thought to constitute some 15% of the non-hereditary cancers. Those remaining, 70 to 80%, are called “sporadic,” because they are essentially of unknown etiology. We propose a new paradigm for the origin of the majority of cancers.Presentation of hypothesisOur paradigm postulates that cancer originates following a sequence of events that include (1) a pathogenic stimulus (biological or chemical) followed by (2) chronic inflammation, from which develops (3) fibrosis with associated changes in the cellular microenvironment. From these changes a (4) pre-cancerous niche develops, which triggers the deployment of (5) a chronic stress escape strategy, and when this fails to resolve, (6) a transition of a normal cell to a cancer cell occurs. If we are correct, this paradigm would suggest that the majority of the findings in cancer genetics so far reported are either late events or are epiphenomena that occur after the appearance of the pre-cancerous niche.Testing the hypothesisIf, based on experimental and clinical findings presented here, this hypothesis is plausible, then the majority of findings in the genetics of cancer so far reported in the literature are late events or epiphenomena that could have occurred after the development of a PCN. Our model would make clear the need to establish preventive measures long before a cancer becomes clinically apparent. Future research should focus on the intermediate steps of our proposed sequence of events, which will enhance our understanding of the nature of carcinogenesis. Findings on inflammation and fibrosis would be given their warranted importance, with research in anticancer therapies focusing on suppressing the PCN state with very early intervention to detect and quantify any subclinical inflammatory change and to treat all levels of chronic inflammation and prevent fibrotic changes, and so avoid the transition from a normal cell to a cancer cell.Implication of the hypothesisThe paradigm proposed here, if proven, spells out a sequence of steps, one or more of which could be interdicted or modulated early in carcinogenesis to prevent or, at a minimum, slow down the progression of many cancers.

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Section: Presentation Of the Hypothesismentioning

confidence: 99%

Epistemology of the origin of cancer: a new paradigm

2014

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“…Over the past several decades the survival rate for patients with TSCC has not significantly improved despite the progress in treatment. Local or regional relapse and cervical lymph node metastasis are considered to be the most prevalent causes of death in these patients [2]. It was revealed by several researches that epithelial-mesenchymal transition (EMT) plays a significant role during TSCC metastasis and progression [3, 4].…”

Section: Introductionmentioning

confidence: 99%

miR-373-3p Targets DKK1 to Promote EMT-Induced Metastasis via the Wnt/β-Catenin Pathway in Tongue Squamous Cell Carcinoma

Weng

Zhang

Wang

et al. 2017

BioMed Research International

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MicroRNAs (miRNAs) regulate gene expression and at the same time mediate tumorigenesis. miR-373-3p has diverse effects in tumors, but its role in tongue squamous cell carcinoma (TSCC) remains unknown. The purpose of this study is to determine the function of miR-373-3p in the progression of TSCC. Our results brought to light that miR-373-3p is markedly upregulated in clinical TSCC tissues compared with paired adjacent normal tissues and has significant correlation with a more aggressive TSCC phenotype in patients. Gain-of-function and loss-of-function studies revealed that ectopic miR-373-3p overexpression promoted the metastasis of TSCC cells. Notably, Wnt/β-catenin signaling was hyperactivated in TSCC cells overexpressing miR-373-3p, and this pathway was responsible for the epithelial-mesenchymal transition (EMT) induced by miR-373-3p. Furthermore, miR-373-3p directly targeted and suppressed Dickkopf-1 (DKK1), a negative regulator of the Wnt/β-catenin signaling cascade. These results demonstrate that, by directly targeting DKK1, miR-373-3p constitutively activated Wnt/β-catenin signaling, thus promoting the EMT-induced metastasis of TSCC. Taken together, our findings reveal a new regulatory mechanism for miR-373-3p and suggest that miR-373-3p might be a potential target in TSCC therapy.

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“…Betel‐nut chewing with or without tobacco (smoking or chewing) is the major risk factor for high‐prevalence oral premalignant disease. In 1 recent nationwide Taiwanese survey, the oral leukoplakia incidence rate was high, and the mean patient age was 47.36 years. The high premalignancy rate and the younger patients in the study population might have affected the course and outcomes of oral cancer treatment.…”

Section: Introductionmentioning

confidence: 99%