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

Kayahara, Hiroaki; Yamagata, Hidehisa; Tanioka, Hiroaki; Miki, Tetsuro; Hamakawa, Hiroyuki

doi:10.1007/s100380170069

Cited by 14 publications

(5 citation statements)

References 23 publications

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“…Regions A, B, D, E, and F coincide with reported allelic losses identified by microsatellite analysis or copy number loss by conventional CGH (5, 6, 8, 22, 24, 25). The improved resolution in the current work has further fine-mapped these regions and allows us to name specific gene candidates (25).…”

Section: Resultssupporting

confidence: 61%

Multiple Aberrations of Chromosome 3p Detected in Oral Premalignant Lesions

Tsui

Rosin

Zhang

et al. 2008

Cancer Prevention Research

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The study of oral premalignant lesions (OPL) is crucial to the identification of initiating genetic events in oral cancer. However, these lesions are minute in size, making it a challenge to recover sufficient DNA from microdissected cells for comprehensive genomic analysis. As a step toward identifying genetic aberrations associated with oral cancer progression, we used tiling-path array comparative genomic hybridization to compare alterations on chromosome 3p for 71 OPLs against 23 oral squamous cell carcinomas. 3p was chosen because although it is frequently altered in oral cancers and has been associated with progression risk, its alteration status has only been evaluated at a small number of loci in OPLs. We identified six recurrent losses in this region that were shared between high-grade dysplasias and oral squamous cell carcinomas, including a 2.89-Mbp deletion spanning the FHIT gene (previously implicated in oral cancer progression). When the alteration status for these six regions was examined in 24 low-grade dysplasias with known progression outcome, we observed that they occurred at a significantly higher frequency in low-grade dysplasias that later progressed to later-stage disease (P < 0.003). Moreover, parallel analysis of all profiled tissues showed that the extent of overall genomic alteration at 3p increased with histologic stage. This first high-resolution analysis of chromosome arm 3p in OPLs represents a significant step toward predicting progression risk in early preinvasive disease and provides a keen example of how genomic instability escalates with progression to invasive cancer.

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Section: Resultssupporting

confidence: 61%

Multiple Aberrations of Chromosome 3p Detected in Oral Premalignant Lesions

Tsui

Rosin

Zhang

et al. 2008

Cancer Prevention Research

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“…The chromosome 3p25 region of the human genome was associated with LOH and was deleted at a high frequency in oral squamous cell carcinoma [20], breast carcinoma [21,22], renal cell carcinoma [23][24][25], bladder tumour [26], pancreatic acinar cell carcinoma [27] and cervical cancer [28][29][30]. The location of the gene for CIDE-3 at chromosome 3p25 implicated that CIDE-3 might play an important role in prevention of tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

Molecular cloning and characterization of CIDE-3, a novel member of the cell-death-inducing DNA-fragmentation-factor (DFF45)-like effector family

Liang

Zhao

et al. 2003

Biochemical Journal

101

113

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DNA fragmentation is one of the critical steps in apoptosis, which is induced by DNA fragmentation factor (DFF). DFF is composed of two subunits, a 40 kDa caspase-activated nuclease (DFF40) and a 45 kDa inhibitor (DFF45). Recently a novel family of cell-death-inducing DFF45-like effectors (CIDEs) has been identified. Among CIDEs, two from human (CIDE-A and CIDE-B) and three from mouse (CIDE-A, CIDE-B and FSP27) have been reported. In this study human CIDE-3, a novel member of CIDEs, was identified upon sequence analysis of a previously unidentified cDNA that encoded a protein of 238 amino acids. It was shown to be a human homologue of mouse FSP27, and shared homology with the CIDE-N and CIDE-C domains of CIDEs. Apoptosis-inducing activity was clearly shown by DNA-fragmentation assay of the nuclear DNA of CIDE-3 transfected 293T cells. The expression pattern of CIDE-3 was different from that of CIDE-B. As shown by Northern-blot analysis, CIDE-3 was expressed mainly in human small intestine, heart, colon and stomach, while CIDE-B showed strong expression in liver and small intestine and at a lower level in colon, kidney and spleen. Green-fluorescent-protein-tagged CIDE-3 was revealed in some cytosolic corpuscles. Alternative splicing of the CIDE-3 gene was also identified by reverse transcription PCR, revealing that two transcripts, CIDE-3 and CIDE-3alpha, were present in HepG2 and A375 cells. CIDE-3 comprised a full-length open reading frame with 238 amino acids; in CIDE-3alpha exon 3 was deleted and it encoded a protein of 164 amino acids. Interestingly the CIDE-3alpha isoform still kept the apoptosis-inducing activity and showed the same pattern of subcellular localization as CIDE-3. Consistent with its chromosome localization at 3p25, a region associated with high frequency loss of heterozygosity in many tumours, CIDE-3 may play an important role in prevention of tumorigenesis.

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“…We also searched for disease locus data in major genetics or related journals published in the past 4 years with the last date searched being 7 May 2003. For diseases in which genetic intervals were less than 5 cM or 5 Mb, the disease locus data from the references were re‐extracted (Table 2, only the data for less than 1 cM or 1 Mb are shown; data for 1−5 cM are not shown) 21−60 . Redundant data from the LocusLink‐OMIM search were discarded.…”

Section: Resultsmentioning

confidence: 99%