Allelic loss on chromosome 22 in oral cancer: possibility of the existence of a tumor suppressor gene on 22q13.

Miyakawa, Akihisa; Wang, X L; Nakanishi, Hiroshi; Imai, Fabiana Lica; Shiiba, Masashi; Miya, Toshimichi; Imai, Yumiko; Tanzawa, Hideki

doi:10.3892/ijo.13.4.705

Cited by 36 publications

(39 citation statements)

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“…Nine out of 10 patients with deletion in the Miyakawa et al (1998) described loss of heterozygosity (LOH) involving this microsatellite marker in 11 out of 27 (40%) of informative cases from the oral cavity. However, the authors did not find any statistically significant correlation with the clinical and histopathological parameters of patients.…”

Section: Resultsmentioning

confidence: 99%

“…LOH has been frequently detected on the long arm of chromosome 22 in a variety of human solid tumors, especially in tumor cells of embryonic-neural-crest origin, including meningiomas (Ueki et al, 1999), astrocytomas (Oskam et al, 2000), schwanomas (Twist et al, 1995) and pheochromocytomas (Shin et al, 1993), but also in thyroid carcinomas (Kitamura et al, 2000), colorectal cancers (Castells et al, 1999), ovarian carcinomas (Englefield et al, 1994), renal rhabdoid tumors (Biegel et al, 2000), gastrointestinal metastatic cancer (Kim et al, 2000), breast cancer (Bryan et al, 2000) and head and neck squamous cell carcinomas from different anatomic sites (Bockmu¨hl et al, 1998). In particular, LOH restricted to the 22q13.31 region has been detected in oral cavity carcinomas (Miyakawa et al, 1998;Poli-Frederico et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Quantitative real-time PCR identifies a critical region of deletion on 22q13 related to prognosis in oral cancer

et al. 2002

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Quantitative real-time PCR identifies a critical region of deletion on 22q13 related to prognosis in oral cancer

et al. 2002

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“…12,14 The other MCRD/P2 region was confined to a 3 Mb physical distance at 22q13.31 that partially overlaps with an area of deletion previously detected by Oskam et al 13 The cytogenetic band at 22q13.1-3 appears to be a focal 'hot spot' for LOH in many types of human cancer, including breast, colon, ovarian, and head and neck cancers. 11,[36][37][38][39] Lida et al 10 were, in fact, able to map a 2 cM region of allelic loss in breast cancer to the same cytogenetic band. Similarly, Allione et al 11 reported six regions along chromosome 22q, ranging from 3 to 6 cM in size, two of which overlap those intervals identified in this study, and, in oral squamous cell carcinoma, allelic deletion seems to be restricted to D22S274, 39 a marker included within the region of deletion identified in our study.…”

Section: Discussionmentioning

confidence: 99%

“…11,[36][37][38][39] Lida et al 10 were, in fact, able to map a 2 cM region of allelic loss in breast cancer to the same cytogenetic band. Similarly, Allione et al 11 reported six regions along chromosome 22q, ranging from 3 to 6 cM in size, two of which overlap those intervals identified in this study, and, in oral squamous cell carcinoma, allelic deletion seems to be restricted to D22S274, 39 a marker included within the region of deletion identified in our study. Thus, the commonality and number of deletions at 22q13.1-3 suggest the presence of either a cluster of TSGs, each of which is involved in one tumor type, or a few TSGs involved in the etiology of many tumor types.…”

Section: Discussionmentioning

confidence: 99%

Frequent LOH on 22q12.3 and TIMP-3 inactivation occur in the progression to secondary glioblastomas

Nakamura

Ishida

Shimada

et al. 2005

Laboratory Investigation

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Frequent allelic losses on the long arm of chromosome 22 (22q) in gliomas indicate the presence of tumor suppressor gene (TSG) at this location. However, the target gene(s) residing in this chromosome are still unknown and their putative roles in the development of astrocytic tumors, especially in secondary glioblastoma, have not yet been defined. To compile a precise physical map for the region of common deletions in astrocytic tumors, we performed a high-density loss of heterozygosity (LOH) analysis using 31 polymorphic microsatellite markers spanning 22q in a series of grade II diffuse astrocytomas, anaplastic astrocytomas, primary glioblastomas, and secondary glioblastomas that had evolved from lower grade astrocytomas. LOH was found at one or more loci in 33% (12/36) of grade II diffuse astrocytomas, in 40% (4/10) of anaplastic astrocytomas, in 41% (26/64) of primary glioblastomas, and in 82% (23/28) of secondary glioblastomas. Characterization of the 22q deletions in primary glioblastomas identified two sites of minimally deleted regions at 22q12.3-13.2 and 22q13.31. Interestingly, 22 of 23 secondary glioblastomas affected shared a deletion in the same small (957 kb) region of 22q12.3, a region in which the human tissue inhibitor of metalloproteinases-3 (TIMP-3) is located. Investigation of the promoter methylation and expression of this gene indicated that frequent hypermethylation correlated with loss of TIMP-3 expression in secondary glioblastoma. This epigenetic change was significantly correlated to poor survival in eight patients with grade II diffuse astrocytoma. Our results suggest that a 957 kb locus, located at 22q12.3, may contain the putative TSG, TIMP-3, that appears to be relevant to progression to secondary glioblastoma and subsequently to the prognosis of grade II diffuse astrocytoma. In addition, the possibility of other putative TSGs on 22q12.3-13.2 and 22q13.31 that may also be involved in the development of primary glioblastomas cannot be ruled out.

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“…The following microsatellite markers purchased from Research Genetics (Huntsville, AL, USA) were selected based on previous reports (Uzawa et al, 1994(Uzawa et al, , 1996Gonzalez et al, 1995;Watanabe et al, 1997;Miyakawa et al, 1998;Ogawara et al, 1998;Nakanishi et al, 1999): D5S178 (5q21), D9S104 (9p21), IFNA (9p22), D11S910 (11q23), D11S1356 (11q25), D13S273 (13q14 -21), TP53 (17p13), D18S46 (18q21), and D22S274 (22q13). Polymerase chain reaction (PCR) amplification was carried out in a 25-ml final volume containing 0.6 U of Taq polymerase in PCR buffer (50 mM KCl, 10 mM Tris-Cl (pH 8.0), 1.5 mM MgCl 2 ), 80 mM of each dNTP, and 10 pmol of each primer.…”

Section: Microsatellite Analysismentioning

confidence: 99%

Monitoring of circulating tumour-associated DNA as a prognostic tool for oral squamous cell carcinoma

et al. 2005

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Frequent allelic imbalances (AIs) including loss of heterozygosity and microsatellite instability on a specific chromosomal region have been identified in a variety of human malignancies. The objective of our study was to assess the possibility of prognostication and monitoring of oral squamous cell carcinoma (SCC) by microsatellite blood assay. DNA from normal and tumorous tissues and serum DNA obtained at three time points (preoperatively, postoperatively, and 4 weeks postoperatively) from 64 patients with oral SCC was examined at nine microsatellite loci. In all, 38 (59%) DNA samples from tumorous tissues and 52% from serum showed AIs in at least one locus. Patterns of AIs in the serum DNA were matched to those detected in tumour DNA. Of them, AIs were frequently detected preoperatively (44%, 28 of 64), and postoperatively (20%, 13 of 64). Moreover, among 12 cases with AIs during the postoperative period, six had no evidence of an AI 4 weeks postoperatively, and they had no recurrence and were disease free. In contrast, six patients with AI-positive DNA 4 weeks postoperatively have died with distant metastasis within 44 weeks. Thus, our results suggest that the assessment of microsatellite status in the serum DNA could be a useful predictive tool to monitor disease prognosis.

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Allelic loss on chromosome 22 in oral cancer: possibility of the existence of a tumor suppressor gene on 22q13.

Cited by 36 publications

References 0 publications

Quantitative real-time PCR identifies a critical region of deletion on 22q13 related to prognosis in oral cancer

Quantitative real-time PCR identifies a critical region of deletion on 22q13 related to prognosis in oral cancer

Frequent LOH on 22q12.3 and TIMP-3 inactivation occur in the progression to secondary glioblastomas

Monitoring of circulating tumour-associated DNA as a prognostic tool for oral squamous cell carcinoma

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