Abnormalities of the adenomatous polyposis coli gene in human oral squamous‐cell carcinoma

Uzawa, Katsuhiro; Yoshida, Hidehiko; Suzuki, Hiroyoshi; Tanzawa, Hideki; Shimazaki, Jun; Seino, Susumu; Sato, Kenichi

doi:10.1002/ijc.2910580611

Cited by 61 publications

(47 citation statements)

References 17 publications

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“…Even though there is frequent LOH on 13q (Yoo et al, 1994) there does not appear to be inactivation of the retinoblastoma gene, and it has been argued by these authors that there may be another tumour-suppressor locus at 13ql4. Also, the APC/ MCC locus on 5q, which has been demonstrated to be involved in colorectal carcinomas (Kinzler et al, 1991) and has previously been shown to have a high LOH in SCCHN (Ah-See et al, 1994), may not in fact be the target locus, as mutations in the APC gene have rarely been found in oral cancers (Uzawa et al, 1994).…”

Section: D6cusonmentioning

confidence: 99%

Allelotype of squamous cell carcinoma of the head and neck: fractional allele loss correlates with survival

Field

Kiaris²,

Risk³

et al. 1995

Br J Cancer

113

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Lasko et al., 1991;Latif et al., 1992;Cunningham et al., 1993;Adamson et al., 1994). A number of oncogenic and tumoursuppressor gene functions have been demonstrated in squamous cell carcinoma of the head and neck (SCCHN) (Field et al., 1989(Field et al., , 1991Field, 1992) To date only two global analyses of the whole genome have been undertaken with the view to determine the fractional allele loss (FAL) of specific tumours and thus provide information concerning the 'genetic burden' of the disease during its progression as measured by clinicopathological parameters and survival data. This type of analysis has been undertaken in colorectal (Vogelstein et al., 1989) and bladder cancers (Knowles et al., 1994), and provides an indication of interacting genetic mechanisms in the development of these diseases. In addition, the results of such detailed allelotypes may aid the interpretation of carcinogenesis and the development of molecular progression models for specific tumours.We have undertaken a very comprehensive allelotype of SCCHN using 145 microsatellite markers in order to identify common regions of allelic imbalance and to analyse the interactions of these regions by calculating the fractional allele loss (FAL) in these tumours. Materias and methods Specimens

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Section: D6cusonmentioning

confidence: 99%

Allelotype of squamous cell carcinoma of the head and neck: fractional allele loss correlates with survival

Field

Kiaris²,

Risk³

et al. 1995

Br J Cancer

113

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“…All patients had OSCC that was histologically confirmed, and tumour samples were checked to ensure the presence of tumour tissue in more than 80% of specimens. Genomic DNA was extracted as described previously (Uzawa et al, 1994); total RNA was prepared using Trizol Reagent (Invitrogen Corp., Carlsbad, CA, USA), according to the manufacturer's protocol.…”

Section: Tissue Samples and Nucleic Acid Isolationmentioning

confidence: 99%

Ubiquitous mitochondrial creatine kinase downregulated in oral squamous cell carcinoma

et al. 2006

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In this study, we performed two-dimensional electrophoresis (2-DE) and matrix-assisted laser desorption/ionisation time of fly mass spectrometry to identify the protein(s) associated with the development of oral squamous cell carcinomas (OSCCs) by comparing patterns of OSCC-derived cell lines with normal oral keratinocytes (NOKs), and found that downregulation of ubiquitous mitochondrial creatine kinase (CKMT1) could be a good candidate. Decreased levels of CKMT1 mRNA and protein were detected in all OSCC-derived cell lines examined (n ¼ 9) when compared to those in primary normal oral keratinocytes. Although no sequence variation in the coding region of the CKMT1 gene with the exception of a nonsense mutation in exon 8 was identified in these cell lines, we found a frequent hypermethylation in the CpG island region. CKMT1 expression was restored by experimental demethylation. In addition, when we transfected CKMT1 into the cell lines, they showed an apoptotic phenotype but no invasiveness. In clinical samples, high frequencies of CKMT1 downregulation were detected by immunohistochemistry (19 of 52 (37%)) and quantitative real-time RT -PCR (21 of 50 (42%)). Furthermore, the CKMT1 expression status was significantly correlated with tumour differentiation (Po0.0001). These results suggest that the CKMT1 gene is frequently inactivated during oral carcinogenesis and that an epigenetic mechanism may regulate loss of expression, which may lead to block apoptosis.

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“…with the possible exception of Ki-ras mutations in pancreatic cancer. the earliest genetic alteration in these malignancies has not yet been discovered (Honi et al 1992a: b;McKie et al 1993;Ogasawara et al 1994: Seymour et al 1994: Uzawa et al 1994; Yashima et al 1994: Hahn et al 1995.…”

mentioning

confidence: 99%

Chromosome 5 allelic losses are early events in tumours of the papilla of Vater and occur at sites similar to those of gastric cancer

Achille

A²,

Zamboni³

et al. 1998

Br J Cancer

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Summary During our studies of DNA fingerprinting of tumours of the pancreas and papilla (ampulla) of Vater, using arbitrarily primed polymerase chain reaction (AP-PCR), we noticed two bands showing a decreased intensity in six of ten ampullary tumours with respect to matched normal tissues. Those bands were both assigned to chromosome 5. Such a finding was somewhat in contrast with the reportedly low frequency of APC gene mutations in ampullary cancers, located at chromosome 5q21, and suggested that loci different from that of APC might be the target of chromosome 5 allelic losses (LOH) in these tumours. Therefore, we analysed chromosome 5 LOH in a panel of 27 ampullary tumours, including eight adenomas, four earty-and 15 advanced-stage cancers, using 16 PCR-amplified CA microsatellite polymorphic markers spanning the entire chromosome. Nineteen cases (70%/a) showed LOH, and the interstital deletions found in these tumours described two smallest common deleted regions, in which putative suppressor genes might reside. They were at 5q13.3-q14 and at 5q23-q31 respectively, which correspond to those found in gastic tumours. In additon, the presence of 5q LOH in six of eight adenomas and in three of four earty-stage cancers suggests that such phenomena occur at earty stages of neoplastic progression of the ampullary epithelium.

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Abnormalities of the adenomatous polyposis coli gene in human oral squamous‐cell carcinoma

Cited by 61 publications

References 17 publications

Allelotype of squamous cell carcinoma of the head and neck: fractional allele loss correlates with survival

Allelotype of squamous cell carcinoma of the head and neck: fractional allele loss correlates with survival

Ubiquitous mitochondrial creatine kinase downregulated in oral squamous cell carcinoma

Chromosome 5 allelic losses are early events in tumours of the papilla of Vater and occur at sites similar to those of gastric cancer

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