Novel Management of Oral Cancer: A Paradigm of Predictive Oncology

Sudbø, Jon

doi:10.3121/cmr.2.4.233

Cited by 43 publications

(36 citation statements)

References 76 publications

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“…Oral squamous cell carcinoma (OSCC) is a common malignancy that affects 300,000 individuals per year worldwide (1). A number of etiologic factors have been implicated in the development of OSCCs, such as the use of tobacco, alcohol or betel nut chewing, human papillomavirus infection, and the presence of incompatible prosthetic materials.…”

Section: Introductionmentioning

confidence: 99%

Copy number changes of CRISP3 in oral squamous cell carcinoma

Sugahara

Sakuma

et al. 2011

Oncology Letters

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Abstract. The aim of this study was to identify tumor suppressor genes (TSGs) in oral squamous cell carcinoma (OSCC) using whole-genome analysis of microarray technology and real-time quantitative polymerase chain reaction (QPCR). We applied whole-genome analysis of TSGs in the specimens from 3 patients of OSCC by microarray technology. A total of 11 genes, CRISP3, SCGB3A1, AGR2, PIP, C20orf114, TFF1, STATH, AZGP1, MUC7, DMBT1 and LOC389429, were found to be down-regulated, and 2, matrix metallopeptidase (MMP) 1 and MMP3, were found to be up-regulated in the 3 OSCC patients using microarray technology. In this study, we selected the CRISP3 gene. CRISP3 belongs to the cystein-rich secretary protein gene family in chromosome 6p12.3. CRISP3 has been found in the salivary gland, spleen and prostate gland and is a prominent biomarker in the gene expression of prostate cancer. Down-regulation of this gene was previously observed in OSCC. No studies examining the DNA copy number of CRISP3 in detail exist. We analyzed the DNA copy number of CRISP3 in 5 OSCCderived cell lines (SAS, KON, HSC2 and HSC4) and 60 OSCC tissues by real-time QPCR. The DNA copy number loss of CRISP3 was observed in 2 of the 5 OSCC-derived cell lines (SAS, HSC2) and in 24 of 60 patients (40.0%) using real-time QPCR. A significant statistical correlation between the copy number loss and gender and T classification was observed. These results indicate that the inactivation of CRISP3 is an early event in OSCC, since the T1/T2 classification is correlated with DNA copy number loss of CRISP3, whereas T3/T4 classification is not. We conclude that CRISP3 may be involved in the carcinogenesis of OSCC.

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Section: Introductionmentioning

confidence: 99%

Copy number changes of CRISP3 in oral squamous cell carcinoma

Sugahara

Sakuma

et al. 2011

Oncology Letters

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“…Other molecules that have been associated with OSCC are cyclo-oxygenase 2 (COX-2), which has been found in high levels in dysplastic lesions (56); the human trophoblast cell-surface antigen (TROP2), which appears to be associated with shorter survival (57); and the epithelial adhesion molecule (EpCAM), which has been associated with tumor size, regional lymph node metastasis, histologic differentiation, and an invasive pattern (31). The connective tissue growth factor, CCN2 (also known as CTGF), was recently associated with head and neck squamous cell cancer; findings included high levels of messenger RNA (mRNA) and its protein in stromal fibroblasts, tumor cells, and vascular endothelial cells (58).…”

Section: Other Molecules Associated With Osccmentioning

confidence: 99%

Genetic and molecular alterations associated with oral squamous cell cancer (Review)

Pérez-Sayáns¹

2009

Oncol Rep

101

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Abstract. The development of oral squamous cell cancer (OSCC) is a multistep process involving the accumulation of multiple genetic alterations modulated by genetic predisposition and environmental influences such as tobacco and alcohol use, chronic inflammation, and viral infections. All of these factors can lead to a wide range of genetic and molecular alterations that can be detected using a range of molecular studies. The alterations mostly affect two large groups of genes: oncogenes and tumor suppressor genes, which can be either inactivated or overexpressed through mutations, loss of heterozygosity, deletions, or epigenetic modifications such as methylation. Other molecules that are closely associated with tumor pathogenesis and prognosis also exist and warrant further study. Important advances in molecular biology are helping to shed light on oral cancer and thus aiding in the early diagnosis and development of new personalized treatment approaches. The purpose of the review is to explore the genetic and molecular alterations associated with OSCC.

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“…This aggressive epithelial cancer is associated with severe morbidity and a 5-year survival rate of less than 50%, despite advances in surgical treatment, radiotherapy and chemotherapy. 2,3 Indeed the high rates of morbidity and mortality associated with this devastating disease have not improved in decades. Agents for the molecular targeting of OSCC treatment are urgently needed.…”

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confidence: 99%