Genomic profiling of sinonasal squamous cell carcinoma

López, Fernando; Llorente, José Luís; García‐Inclán, Cristina; Alonso-Guervós, Marta; Cuesta-Albalad, Mari Paz; Fresno, Manuel; Álvarez-Marcos, César; Suárez, Carlos; Hermsen, Mario

doi:10.1002/hed.21417

Cited by 36 publications

(26 citation statements)

References 30 publications

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“…The genome-wide profile of gains and losses of the cell lines was similar to what has been described in primary sinonasal SCC35, including losses at chromosomal bands 3p, 4q, 8p, 10p, 13q, 18q and 21q, gains at 3q, 7p, 8q, 11q, 14q, 18p and 20q and amplification at 11q13. Most of these aberrations are also recurrent in head and neck SCC.…”

Section: Discussionsupporting

confidence: 71%

“…Most of these aberrations are also recurrent in head and neck SCC. A curious exception are gains at chromosome 5p and loss at 5q, these are very frequent in head and neck SCC but not so in sinonasal SCC35. Aside from recurrent genetic changes, we found several focal aberrations in the cell lines, both high level amplifications and homozygous deletions.…”

Section: Discussionmentioning

confidence: 67%

“…Focal aberrations are important because usually they concern very few genes and may indicate aberrant cellular pathways that could be useful targets for new anticancer drugs36. Amplification of chromosomal region 11q13, observed in four of the six cell lines, is a frequent event in sinonasal SCC35 as it is in head and neck SCC3738 and other tumors39. Apart from reports on the prognostic significance of this alteration373839, recent studies have indicated a role for amplification of CTTN and overexpression of cortactin (coded by CTTN ) in the progression from premalignant lesions to invasive carcinoma40.…”

Section: Discussionmentioning

confidence: 99%

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Establishment and genetic characterization of six unique tumor cell lines as preclinical models for sinonasal squamous cell carcinoma

García‐Inclán

López-Hernández

Alonso-Guervós

et al. 2014

Sci Rep

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Sinonasal squamous cell carcinomas (SCC) are rare tumors, etiologically related to occupational exposure to wood and leather dust. In spite of surgical and radiotherapeutic advances, the 5 year survival is still 30–50%. Therefore, alternative treatment options are needed. We report the establishment and characterization of six unique human sinonasal SCC cell lines, named SCCNC1, 2, 4, 5, 6 and 7. In vitro growth and invasion characteristics were evaluated and genetic profiles were compared to those of the original primary tumors. The population doubling times ranged from 21 to 34 hours. Cell lines SCCNC2 and 7 were highly invasive in matrigel. Five cell lines carried a high number of copy number alterations, including amplifications and homozygous deletions, while one showed only three abnormalities. Sequence analysis revealed three cell lines with TP53 mutation and none with KRAS or BRAF. Overexpression of p53 was observed in five, and of EGFR in four cell lines. None of the cell lines showed strong immunopositivity of p16 or presence of human papilloma virus. In conclusion, we have created six new cell lines that are clinically and genetically representative of sinonasal SCC and that will be a useful tool for the preclinical testing of new therapeutic agents.

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Section: Discussionsupporting

confidence: 71%

Section: Discussionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

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Establishment and genetic characterization of six unique tumor cell lines as preclinical models for sinonasal squamous cell carcinoma

García‐Inclán

López-Hernández

Alonso-Guervós

et al. 2014

Sci Rep

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“…In contrast, tobacco, a major risk factor for head and neck squamous cell carcinoma (HNSCC) does not have an important role in MSSCC (Zheng et al , 1993; Holt, 1994). It has been suggested that molecular mechanisms of carcinogenesis might be different for these cancers (Lopez et al , 2011). Although analyses of major cancer-related genes, such as TP53 and K-ras, mutation were reported (Bornholdt et al , 2008; Holmila et al , 2010), relatively few genome-wide gene expression analyses of MSSCC have been conducted and no analyses of microRNAs (miRNAs) have been performed for this disease.…”

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confidence: 99%

Tumour suppressive microRNA-874 regulates novel cancer networks in maxillary sinus squamous cell carcinoma

et al. 2011

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Background:On the basis of the microRNA (miRNA) expression signature of maxillary sinus squamous cell carcinoma (MSSCC), we found that miR-874 was significantly reduced in cancer cells. We focused on the functional significance of miR-874 in cancer cells and identification of miR-874-regulated novel cancer networks in MSSCC.Methods:We used PCR-based methods to investigate the downregulated miRNAs in clinical specimens of MSSCC. Our signature analyses identified 23 miRNAs that were significantly reduced in cancer cells, such as miR-874, miR-133a, miR-375, miR-204, and miR-1. We focused on miR-874 as the most downregulated novel miRNA in our analysis.Results:We found potential tumour suppressive functions such as inhibition of cancer cell proliferation and invasion. A molecular target search of miR-874 revealed that PPP1CA was directly regulated by miR-874. Overexpression of PPP1CA was observed in MSSCC clinical specimens. Silencing of the PPP1CA gene significantly inhibited cancer cell proliferation and invasion.Conclusion:The downregulation of miR-874 was a frequent event in MSSCC, which suggests that miR-874 functions as a tumour suppressive miRNA, directly regulating PPP1CA that has a potential role of an oncogene. The identification of novel miR-874-regulated cancer pathways could provide new insights into potential molecular mechanisms of MSSCC oncogenesis.

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“…[8] Recently, accumulating evidence suggests that a number of genetic alterations may contribute to the initiation and progression of SNSCC. [9–12] The p53 gene is a tumor suppressor gene mapped to chromosome 17p13, encodes the p53 protein, which involves in the regulation of the cell cycle, the inhibition of DNA synthesis, the function of DNA repair and apoptosis. [13–15] The p53 mutation is the most commonly found genetic alterations in various human carcinomas, [16,17] and the overexpression of p53 detected by immunohistochemistry (IHC) in most of cases (85%) is consistent with an underlying mutation.…”

Section: Introductionmentioning

confidence: 99%

Clinical effects of p53 overexpression in squamous cell carcinoma of the sinonasal tract

Wang

et al. 2017

Medicine

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Background:The level of p53 protein expression in sinonasal squamous cell carcinoma (SNSCC) has been estimated, but the results remain inconsistent and the point of consensus has not been reached. This study was first determined to evaluate the clinical effects of p53 expression in SCC of the sinonasal tract.Methods:According to the preferred reporting items for systematic reviews and meta-analyses (PRISMA) statement criteria, the potential literature was searched from diverse databases. The pooled odds ratios (ORs) with corresponding 95% confidence intervals (CIs) were calculated to assess the strength of association between p53 expression and SNSCC.Results:Final 17 eligible studies were included in a total of 258 cases and 748 controls. The result of p53 expression was shown to be notably higher in SNSCC than in benign sinonasal papillomas and normal sinonasal mucosa (OR = 26.93, P < 0.001; OR = 39.79, P < 0.001; respectively). Subgroup analyses of ethnicity revealed that p53 expression had significant association with SNSCC in Asian and Caucasian populations in cancer versus benign sinonasal papillomas or normal sinonasal mucosa. The expression of p53 was notably higher in moderately or poorly differentiated SNSCC than in well-differentiated SNSCC (OR = 3.51, P = 0.021), while p53 expression was not associated with histological type.Conclusion:The results suggested that p53 overexpression may be correlated with the carcinogenesis and progression of SNSCC. The p53 gene may become a novel drug target of SNSCC. Additional studies on the correlation of p53 expression with clinicopathological features are needed.

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Genomic profiling of sinonasal squamous cell carcinoma

Abstract: The genomic profile of sinonasal SCC showed a number of chromosomal regions with copy number changes similar to those known in HNSCC, in spite of the differences in etiology.

Cited by 36 publications

References 30 publications

Establishment and genetic characterization of six unique tumor cell lines as preclinical models for sinonasal squamous cell carcinoma

Establishment and genetic characterization of six unique tumor cell lines as preclinical models for sinonasal squamous cell carcinoma

Tumour suppressive microRNA-874 regulates novel cancer networks in maxillary sinus squamous cell carcinoma

Clinical effects of p53 overexpression in squamous cell carcinoma of the sinonasal tract

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