Oral cancer: reviewing the present understanding of its molecular mechanism and exploring the future directions for its effective management

Nagpal, Jatin; Das, Bibhu Ranjan

doi:10.1016/s1368-8375(02)00162-8

Cited by 119 publications

(81 citation statements)

References 77 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…While minimum allelic imbalance was observed for the normal keratinocytes, several frequent LOH regions were identified for HNSCC cases (Table 1). Chromosome arms 3p, 4p, 4q, 5q, 8p, 9p, 10p, 11q, 17p exhibit the frequent LOH, which is in agreement with various previous finds [6,11,24]. The complete LOH profile for chromosome 8 was shown in Figure 1, where a region of approximately 7 Mb at 8p22−8p21.3 exhibits the most frequent allelic imbalance.…”

Section: Resultssupporting

confidence: 90%

“…Tobacco, alcohol, viral infections as well as genetic polymorphisms on genes that metabolize carcinogens are common risk factors for HNSCC [4,5]. Several chromosome regions have been identified to be frequently altered in HNSCC, including 3p, 4q, 5q21−22, 8p21−23, 9p21−22, 11q13, 11q23, 13q, 14q, 17p, 18q and 22q [6]. However, significant improvement of functional mapping is needed to move the HNSCC diagnosis, treatment and research forward.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Genomic assessments of the frequent loss of heterozygosity region on 8p21.3∼p22 in head and neck squamous cell carcinoma

Pungpravat

Huang

et al. 2007

Cancer Genetics and Cytogenetics

View full text Add to dashboard Cite

Most human cancers are characterized by genetic instabilities. Chromosomal aberrations include segments of allelic imbalance identifiable by loss of heterozygosity (LOH) at polymorphic loci, which may be used to implicate regions harboring tumor suppressor genes. Here we performed whole genome LOH profiling on over 40 human head and neck squamous cell carcinoma (HNSCC) cell lines. Several frequent LOH regions have been identified on chromosomal arms 3p, 4p, 4q, 5q, 8p, 9p, 10p, 11q, and 17p. A genomic region of ∼7 Mb located at 8p22-p21.3 exhibits the most frequent LOH (87.9%), which suggested that this region harbors important tumor suppressor gene(s). Mitochondrial tumor suppressor gene 1 (MTUS1) is a recently identified candidate tumor suppressor gene that resides in this region. Consistent down-regulation in expression was observed in HNSCC for MTUS1 as measured by real-time quantitative RT-PCR. Sequence analysis of MTUS1 gene in HNSCC revealed several important sequence variants in the exon regions of this gene. Thus, our results suggested that MTUS1 is one of the candidate tumor suppressor gene(s) reside in 8p22-p21.3 for HNSCC. The identification of these candidate genes will facilitate the understanding of tumorigenesis of HNSCC. Further studies are needed to functionally evaluate those candidate genes.

show abstract

Section: Resultssupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Genomic assessments of the frequent loss of heterozygosity region on 8p21.3∼p22 in head and neck squamous cell carcinoma

Pungpravat

Huang

et al. 2007

Cancer Genetics and Cytogenetics

View full text Add to dashboard Cite

show abstract

“…Despite recent progress in the diagnosis of and therapeutic modalities for OSCC, the prognosis has not been improved, reflecting the ineffectiveness of current treatment regimens (Parkin et al, 2005). A more comprehensive understanding of the molecular pathogenesis of OSCC is urgently needed to identify new targets and strategies for effective therapy, and the opportunity to recognize early OSCC and/or premalignant lesions may provide insight into the phase of new strategies for chemoprevention of this disease (Nagpal and Das, 2003;Brinkman and Wong, 2006). Although OSCC is believed to arise through the accumulation of numerous genetic and epigenetic alterations, which may impair the function of oncogenes or tumor suppressor genes (TSGs) that play a crucial role in the development of this disease (Scully et al, 2000;Ha and Califano, 2006), little is still known about the genes associated with oral carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation

et al. 2007

View full text Add to dashboard Cite

Array-based comparative genomic hybridization (array-CGH) has good potential for the high-throughput identification of genetic aberrations in cell genomes. In the course of a program to screen a panel of oral squamouscell carcinoma (OSCC), cell lines for genomic copynumber aberrations by array-CGH using our in-house arrays, we identified a 3-Mb homozygous deletion at 10p12 in 1 of 18 cell lines (5.6%). Among seven genes located within this region, expression of PRTFDC1 mRNA was not detected in 50% (9/18) or decreased in 5.6% (1/18) of OSCC cell lines, but detected in normal oral epithelia and restored in gene-silenced OSCC cells without its homozygous loss after treatment with 5-aza-2 0 -deoxycytidine. Among 17 cell lines without a homozygous deletion, the hypermethylation of the PRTFDC1 CpG island, which showed promoter activity, was observed in all nine cell lines with no or reduced PRTFDC1 expression (52.9%). Methylation of this CpG island was also observed in primary OSCC tissues (8/47, 17.0%). In addition, restoration of PRTFDC1 in OSCC cells lacking its expression inhibited cell growth in colony-formation assays, whereas knockdown of PRTFDC1 expression in OSCC cells expressing the gene promoted cell growth. These results suggest that epigenetic silencing of PRTFDC1 by hypermethylation of the CpG island leads to a loss of PRTFDC1 function, which might be involved in squamous cell oral carcinogenesis.

show abstract

“…Despite improvements in surgery, radiotherapy and chemotherapy, the survival of patients with oral cancer has remained unchanged over the last 3 decades (2). Moreover, it is still not known how many of the OSCCs arise from premalignant lesions even though it is well established that OSCC is preceded by premalignant lesions such as leukoplakia, erythroplakia, lichen planus and oral submucous fibrosis (3). This has led to an increasing awareness of the potential value of screening for oral cancer and oral premalignant lesions to reduce the morbidity and mortality.…”

Section: Introductionmentioning

confidence: 99%

Molecular Alterations in Oral Carcinogenesis: Significant Risk Predictors in Malignant Transformation and Tumor Progression

et al. 2007

View full text Add to dashboard Cite

Oral cancer: reviewing the present understanding of its molecular mechanism and exploring the future directions for its effective management

Cited by 119 publications

References 77 publications

Genomic assessments of the frequent loss of heterozygosity region on 8p21.3∼p22 in head and neck squamous cell carcinoma

Genomic assessments of the frequent loss of heterozygosity region on 8p21.3∼p22 in head and neck squamous cell carcinoma

PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation

Molecular Alterations in Oral Carcinogenesis: Significant Risk Predictors in Malignant Transformation and Tumor Progression

Contact Info

Product

Resources

About