Loss of heterozygosity at chromosome 6q23–25 correlates with clinical and histologic parameters in salivary gland adenoid cystic carcinoma

Stallmach, Ingrid; Zenklusen, Petra; Komminoth, Paul; Schmid, Stephan; Perren, Aurel; Roos, Małgorzata; Zhao, Jianming; Heitz, Philipp U.; Pfaltz, Madeleine

doi:10.1007/s004280100523

Cited by 51 publications

(35 citation statements)

References 33 publications

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“…Exclusive of these translocations, interstitial deletions and frequent loss of heterozygosity using microsatellite markers at the 6q regions have also been reported [17][18][19][20][21]. In some of these studies, deletions in this region have been associated with aggressive clinical features [21].…”

Section: Discussionmentioning

confidence: 99%

“…The majority of the translocations consisted of balanced swapping between chromosome 6q sites and different chromosomal partners including 9q, 12q 14q, 15q and Xp regions [3-5, 8-11, 13]. Collectively, the data indicates that an important locus on chromosome 6q may house a critical gene(s) associated with the development and/or progression of ACC [17][18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

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Translocation t(6;14) as the Sole Chromosomal Abnormality in Adenoid Cystic Carcinoma of the Base of Tongue

Bell

Zhao

Rao

et al. 2007

Head and Neck Pathol

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We present an adenoid cystic carcinoma of the base of tongue in a 48-year-old male with a restricted chromosomal alteration by cytogenetic and spectral karyotypic analysis (SKY). SKY and G-banding analyses identified the t(6;14)(q25;q13) as the sole structural aberration in all metaphases analyzed. This finding supports a critical role for this event in the development of this tumor. The implications of chromosome 6q translocation in this case and in previously reported adenoid cystic carcinomas are highlighted and discussed.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Translocation t(6;14) as the Sole Chromosomal Abnormality in Adenoid Cystic Carcinoma of the Base of Tongue

Bell

Zhao

Rao

et al. 2007

Head and Neck Pathol

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“…4,5 Although the 5-year survival rate is high for patients with SACC, probably because of the slow growth of the tumor, the 10-and 15-year prognoses are poor because of the frequent local recurrences and distant metastases. [6][7][8] Although multiple genetic and epigenetic alterations have been detected in SACC, 3,[9][10][11][12][13] the precise molecular mechanisms of progression and metastasis of SACC remain unknown.…”

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confidence: 99%

miR-21 regulates tumor progression through the miR-21-PDCD4-Stat3 pathway in human salivary adenoid cystic carcinoma

Jiang

Hou

et al. 2015

Laboratory Investigation

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miR-21, which is a putative tumor onco-miR and frequently overexpressed microRNA in various tumors, has been linked to tumor progression through targeting of tumor-suppressor genes. In this study, we sought to determine whether miR-21 has any role on tumor progression of salivary adenoid cystic carcinoma (SACC) and the possible mechanisms. We found that the level of miR-21 expression was significantly higher in SACC than that in normal salivary tissues, and it is also higher in tumors with metastasis than that without metastasis. Using an anti-miR-21 inhibitor in an in vitro model, downregulation of miR-21 significantly decreased the capacity of invasion and migration of SACC cells, whereas a pre-miR-21 increased the capacity of invasion and migration of SACC cells. To explore the potential mechanisms by which miR-21 regulate invasion and migration, we identified one direct miR-21 target gene, programmed cell death 4 (PDCD4), which has been implicated in invasion and metastasis Salivary adenoid cystic carcinoma (SACC) is one of the most common malignancy of the salivary gland, accounting for 10% of salivary gland tumors and 30% of human salivary gland malignancies. 1,2 SACC is characterized by slow but aggressive growth, nerve and blood vessel invasion, multiple recurrences, and distant metastases. 3-5 Lung metastasis and nerve metastasis are the biological characteristics of SACC. [6][7][8] It has been reported that the incidence of SACC with distant metastasis ranged from 35 to 50% of all cases. Lung was the most common organ of its distant metastasis, and lung metastasis is still the leading death cause of patients with SACC. 4,5 Although the 5-year survival rate is high for patients with SACC, probably because of the slow growth of the tumor, the 10-and 15-year prognoses are poor because of the frequent local recurrences and distant metastases. [6][7][8] Although multiple genetic and epigenetic alterations have been detected in SACC, 3,9-13 the precise molecular mechanisms of progression and metastasis of SACC remain unknown.MicroRNAs (miRNAs) are small non-coding RNA molecules, with a length of 20-22 nucleotides, that regulate gene expression by either translational inhibition or mRNA degradation. miRNAs function as either oncogenes or tumor suppressors by inhibiting the expression of target genes, some of which are either directly or indirectly involved with canonical signaling pathways. 13,14 The roles and function of some selected miRNAs in SACC have been reported. 15

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“…Adenoid cystic carcinoma with solid subtypes has shown the worst prognosis. Stallmach et al (2002) reported that loss of heterozygosity at chromosome 6q23 -25 was frequently found in the histological solid subtype of ACC. Yamamoto et al (1996) also demonstrated that the loss of heterozygosity in the p53 gene was higher in the solid subtype than in the cribriform subtype.…”

Section: Discussionmentioning

confidence: 99%

Frequent downregulation of 14-3-3 σ protein and hypermethylation of 14-3-3 σ gene in salivary gland adenoid cystic carcinoma

Uchida

Almofti

et al. 2004

Br J Cancer

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14-3-3 σ , a target gene of the p53 tumour suppressor protein, has been shown to regulate the cell cycle at the G2/M checkpoint. Recent studies have demonstrated that 14-3-3 σ is downregulated by hypermethylation of the CpG island in several types of cancer. In this study, we investigated the expression and methylation status of 14-3-3 σ in human salivary gland adenoid cystic carcinoma (ACC) and mucoepidermoid carcinoma (MEC). Immunohistochemical analysis revealed that the positive expression rate of 14-3-3 σ in ACC (one out of 14) was markedly lower than that in MEC (ten out of 10). Since most of the ACCs carried the wild-type p53 protein, downregulation of 14-3-3 σ in ACC may not be due to the dysfunction of p53 pathway. Microdissection–methylation-specific PCR revealed that frequent hypermethylation of the 14-3-3 σ gene was observed in ACC when compared to that in MEC. In cultured-ACC cells, we confirmed the downregulation of 14-3-3 σ via hemimethylation of the gene by sequencing analysis after sodium bisulphite treatment. Furthermore, re-expression of 14-3-3 σ in the ACC cells was induced by the treatment with DNA demethylating agent, 5-aza-2′-deoxycytidine. Irradiation apparently induced the enhanced expression of 14-3-3 σ and G2/M arrest in normal salivary gland cells; however, in the ACC cells, neither induction of 14-3-3 σ nor G2/M arrest was induced by irradiation. These results suggest that downregulation of 14-3-3 σ might play critical roles in the neoplastic development and radiosensitivity of ACC.

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Loss of heterozygosity at chromosome 6q23–25 correlates with clinical and histologic parameters in salivary gland adenoid cystic carcinoma

Cited by 51 publications

References 33 publications

Translocation t(6;14) as the Sole Chromosomal Abnormality in Adenoid Cystic Carcinoma of the Base of Tongue

Translocation t(6;14) as the Sole Chromosomal Abnormality in Adenoid Cystic Carcinoma of the Base of Tongue

miR-21 regulates tumor progression through the miR-21-PDCD4-Stat3 pathway in human salivary adenoid cystic carcinoma

Frequent downregulation of 14-3-3 σ protein and hypermethylation of 14-3-3 σ gene in salivary gland adenoid cystic carcinoma

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