Localization of chromosome 8p regions involved in early tumorigenesis of oral and laryngeal squamous carcinoma

El‐Naggar, Adel K.; Coombes, Madelene M.; Batsakis, John G.; Hong, Waun Ki; Goepfert, Helmuth; Kagan, Jacob

doi:10.1038/sj.onc.1201808

Cited by 64 publications

(27 citation statements)

References 25 publications

(53 reference statements)

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“…For determination of the location of some putative tumor suppressor genes, various studies have been carried out, using polymorphic markers. To date, in head and neck cancer, including oral squamous cell carcinoma (OSCC), LOH has frequently been identified on chromosomes 2q, 4q, 7q, 8p, 9p, 10q, 11q, 13q, 14q, 17p, 18q, and 22q (Uzawa et al 1996;Jares et al 1997;Matsuura et al 1998;Pearlstein et al 1998;El-Naggar et al 1998;Ransom et al 1998;Ogawara et al 1998;Mutirangura et al 1998;Miyakawa et al 1998;Wang et al 1999;Gasparotto et al 1999;Califano et al 1999). Other studies have also reported a high frequency of deletion at chromosome 3p in diverse neoplasms, as well as in oral cancer (Fullwood et al 1999;Chino et al 1999).…”

Section: Introductionmentioning

confidence: 99%

Frequent loss of heterozygosity at 3p25-p26 is associated with invasive oral squamous cell carcinoma

et al. 2001

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Recent molecular evidence suggests that allelic deletions of chromosomes are involved in the carcinogenesis of various neoplasms, including oral squamous cell carcinoma (OSCC). To determine the role of 3p deletions in Japanese OSCC and to define the localization of putative tumor suppressor genes, we initially examined loss of heterozygosity (LOH), using nine microsatellite markers in 36 OSCCs and 28 oral epithelial dysplastic lesions (OEDLs). LOH on chromosome 3p was observed at one or more loci in 72% of OSCCs and 18% of OEDLs. Fourteen (61%) of 23 OSCC patients informative at D3S2450 (3pter-p24.2) showed LOH most frequently, in contrast to OEDL, where LOH was never seen at this locus. Interestingly, we found a significant association between an allelic deletion at this locus and the histologic grade of mode of tumor invasion. Therefore, we also examined allelic deletion on chromosome 3p telomeric to where D3S2450 was located. A common deletion region was identified between D3S2450 and D3S3591. Our results provide evidence for the presence of a tumor suppressor gene in a 0.8-cM region bordered by D3S2450 and D3S3591 at 3p25-p26, which may play a role in carcinogenesis and invasion of OSCC.

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Section: Introductionmentioning

confidence: 99%

Frequent loss of heterozygosity at 3p25-p26 is associated with invasive oral squamous cell carcinoma

et al. 2001

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“…Consequential critical events in the evolution of tumors include the loss of proliferative control and the failure to undergo cellular differentiation. Genes located at chromosome 8p21.3-22 near marker D8S254 participate in tumor progression in colorectal cancer, pancreatic cancer, breast cancer, esophageal cancer, hepatocellular carcinoma, lung cancer, prostate cancer, urinary bladder carcinoma and head and neck squamous cell carcinoma (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). We previously identified a new gene named MTSG1, only <0.9 Mb apart from the D8S254 marker locus, regulating tumor cell proliferation (16).…”

Section: Introdutionmentioning

confidence: 99%

Down-regulation of MTUS1 in human colon tumors

Zuern

Heimrich²,

Kaufmann³

et al. 2009

Oncol Rep

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Abstract. Loss of proliferative control and failure to undergo cellular differentiation are key events during carcinogenesis. We recently identified a new potential tumor suppressor gene named MTUS1 (mitochondrial tumor suppressor 1), downregulated in undifferentiated tumor cell lines, inhibiting tumor cell proliferation after recombinant over-expression. The aim of this study was to investigate whether MTUS1 is also down-regulated in human tumor tissues, and whether reduced expression of MTUS1 enhances cellular proliferation. Expression of MTUS1 in human colon cancer tissues was compared with corresponding normal colon tissues using Western blot analysis and RT-PCR. Investigation of the DNA sequence and methylation pattern was performed using bisulfite reaction and DNA sequencing. Promotor activity was measured by promoter assays. Silencing of MTUS1 was carried out by siRNA transfection. Proliferation was measured by cell count. MTUS1 expression is significantly down-regulated in colon cancer tissues, compared to the corresponding normal tissues, on protein and mRNA level. No mutations of MTUS1 were detected in the coding sequence or the predicted promoter region in cancer tissues. No difference of CpG methylation, but an altered CpNpG methylation was found in the predicted promoter region. Functional significance of the predicted promoter region was demonstrated by promoter assays. Down-regulation of the MTUS1 expression by siRNA transfection significantly increased cellular proliferation. This study demonstrates a significant down-regulation of the MTUS1 expression in human colon cancer tissues. Since reduced expression of MTUS1 results in increased cellular proliferation, these data suggest that MTUS1 could be involved in the loss of proliferative control in human colon cancer. IntrodutionThe multistage process of carcinogenesis includes the progressive acquisition of genetic alterations, resulting in activation of proto-oncogenes and inactivation of tumor suppressor genes. Consequential critical events in the evolution of tumors include the loss of proliferative control and the failure to undergo cellular differentiation. Genes located at chromosome 8p21.3-22 near marker D8S254 participate in tumor progression in colorectal cancer, pancreatic cancer, breast cancer, esophageal cancer, hepatocellular carcinoma, lung cancer, prostate cancer, urinary bladder carcinoma and head and neck squamous cell carcinoma (1-15). We previously identified a new gene named MTSG1, only <0.9 Mb apart from the D8S254 marker locus, regulating tumor cell proliferation (16). In accordance with the Guidelines for Human Gene Nomenclature it was recommended to change the gene name to MTUS1 (mitochondrial tumor suppressor 1), as it meanwhile appears in most databases. MTUS1 was discovered by investigating the molecular regulation during cellular transition from proliferation to senescence and differentiation in a three-dimensional collagen type I cell culture model. We thereby observed a transient up-regulation of MTUS1 during the init...

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“…Allelic losses of the chromosome 8p21-22 have been reported as a frequent event in Oncogene (2001) (El-Naggar et al, 1998;Emi et al, 1992;Kagan et al, 1995;Mitelman et al, 1997;Monni et al, 1996;Wistuba et al, 1999;Yaremoko et al, 1996). These data strongly indicate that the chromosome 8p21-22 may harbor one or more tumor suppressor genes and suggest that TRAIL-R1 and TRAIL-R2 genes might be the candidate tumor suppressor genes in this region.…”

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confidence: 99%

Somatic mutations of TRAIL-receptor 1 and TRAIL-receptor 2 genes in non-Hodgkin's lymphoma

et al. 2001

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Tumor necrosis factor-related apoptosis-inducing ligandreceptor 1 (TRAIL-R1) and tumor necrosis factor-related apoptosis-inducing ligand-receptor 2 (TRAIL-R2) are cell-surface receptors involved in tumor necrosis factorrelated apoptosis-inducing ligand (TRAIL)-induced celldeath signaling. TRAIL-R1 and TRAIL-R2 genes have recently been mapped to chromosome 8p21-22, which is a frequent site of allelic deletions in many types of human tumors, including non-Hodgkin's lymphoma (NHL). Because TRAIL/TRAIL receptor system plays an important role in lymphocyte homeostasis, we hypothesized that the mutations of TRAIL-R1 and TRAIL-R2 may be involved in the development of NHL and that such mutations may be responsible for the allelic losses of 8p21-22 in NHL. In this study, we analysed the entire coding region of TRAIL-R2 gene and the death domain region of TRAIL-R1 gene for the detection of the somatic mutations in a series of 117 human NHLs using polymerase chain reaction (PCR)-based single strand conformation polymorphism (SSCP) analysis. Overall, eight tumors (6.8%) were found to have two TRAIL-R1 gene mutations or six TRAIL-R2 gene mutations. Interestingly, of the eight mutations, six missense mutations (two TRAIL-R1 and four TRAIL-R2) were detected in the death domains and one nonsense mutation of TRAIL-R2 was detected just before the death domain. Our data suggest that somatic mutations of TRAIL-R1 and TRAIL-R2 genes may play a role in the pathogenesis of some NHLs and that TRAIL-R1 and TRAIL-R2 genes might be the relevant genes to the frequent loss of chromosome 8p21-22 in human NHL. Oncogene (2001) 20, 399 ± 403.

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Localization of chromosome 8p regions involved in early tumorigenesis of oral and laryngeal squamous carcinoma

Cited by 64 publications

References 25 publications

Frequent loss of heterozygosity at 3p25-p26 is associated with invasive oral squamous cell carcinoma

Frequent loss of heterozygosity at 3p25-p26 is associated with invasive oral squamous cell carcinoma

Down-regulation of MTUS1 in human colon tumors

Somatic mutations of TRAIL-receptor 1 and TRAIL-receptor 2 genes in non-Hodgkin's lymphoma

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